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mccoy

Caloric or proteic restriction?

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Sibiriak, I might ditch the eggs since they are really not necessary, although they make up a good unexpensive source of organic protein-based food. However, for the sake of methionine reduction, it can be done and that's a good idea.

 

Since I can only eat 2 times a day, I should optimize my 2 meals, by making the 1st one fruit-based and the 2nd one vegetables+protein based. the days I don't work out I've started to do that.

 

As far as I could see, the only leucine threshold coming from an authoritative source is the 2002/2005 exhaustive NAS publication, where the media (EAR) value is 34/mg/kg/d and RDA is EAR+2Cov ,42/mg/kg/d. I assume the weight is an ideal weight, not a lean mass weight. That is an estimated high percentile based on statistical considerations. The cronometer value I must ascertain since in my settings it's related to exercise, but it should be the 34 value. 

 

Actually, the NAS study considered 3 different studies, each came out with the following EAR values in mg/kg/d: 24.5; 38.3; 40

 

 

Messing with Leucine is probably not advisable, So I'd say to stick to a RDA (safe value) would be best, even because it's close to the higher of the 3 different values determined by different studies.

 

Best of all would be to practice regular exercise so that Leucine is sequestered for muscle protein synthesis(MPS), being hijacked to fuel mTORC1 in muscles and left in non-redundant amounts for mTORC1 to remain quiescent in other organs.

 

It all takes some observation and sensitivity, and that's what I'm doing now. The cronometer reference remains a good one though.

 

Another strategy would be as Dr Attia does, to drink 3 or 5 grams of pure Leucine powder during workouts, boosting muscular mTORC1 hence MPS. I do not share this strategy since I'm a natural guy who prefers to tinker with real food only. 

 

NAS Median value for protein in general is 0.66 g/kg/d, whereas its safe value (RDA) is 0.8 g/kg/d, which corresponds to about the 65th percentile, since the reference distribution is pretty skewed.

 

Since the inter individual variability is large, we can only observe what happens in our case while starting at the median or at the RDA value.

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If you choose legumes as your primary protein source, then track consumption on cronometer, you may find that you may both get plenty-o-protein while reducing methionine to boot (e.g., RDA +\~ 100%)

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If you choose legumes as your primary protein source, then track consumption on cronometer, you may find that you may both get plenty-o-protein while reducing methionine to boot (e.g., RDA +\~ 100%)

I wish I may have that option. As a matter of fact, I only eat twice a day. First meal is fruit+nuts, with added yogurt especially after workouts. no room for legumes here.

 

2nd meal is about 500 grams or more vegetables, then I'm not so much hungry to eat a 200 grams serving. I'm starting to change my habits, eating legumes twice a week together with enzymes. But I doubt I'll ever be able to eat legumes every day, notwithstanding that's one food recognized to promote longevity by just about everyone.

/

IGF-1 is boosted by methionine but probably by insuline as well. A diet with moderate carbs and moderate proteins is unlikely to upregulate the insuline IIS/signaling since fat is neutral insuline-wise (although Dr. Greger thinks otherwise).

 

In my case, I might make up for the relative abundance of methionine with the low AUC values of insulin. 

 

The above reasoning may just be a rational delusion.

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I have been thinking about % protein in the diet lately ( and posting this also to prove I get get just as bogged down in details and thinking about optimization as the true CR diehards out here), and there may be some good news.  Would be interested in forum thoughts on (1) the paper and (2) personal protein restriction practices.  

 

But first, for fun, a little review and example:

 

Background reading supporting the premise that protein and/or amino acid restriction exert substantial independent impact on longevity, these are gems:

(1) (2) (3)

 

It is easy for the average omnivore to overdo protein, even if they do not follow the SAD which exceeds even the conventional guidelines by 2-3 fold:

 

Dr. Longo advises "[...]The ideal diet is a plant and fish based diet that is low in protein, about 0.37 grams per kilogram body weight and that may increase a little bit in proteins after age 65 or 70, depending on the need" [ source ]. 

 

 

Using some round numbers to illustrate, for a small/petite individual), lean body weight ~ 100 pounds = 45.36 kilograms.  So, (45.36 kilograms)*(0.37) =  16.78 grams of protein a day.  The 100 pound figure is not only round but also convenient: a more common weight is a multiple of 1.5 or 2 of that.  So if your lean body mass is around 200 pounds or a little over 75 kilograms, then that translates to a limit of around 33-34 grams of protein a day.  So basically a range of between around 17-34 grams of protein per day.

 

We can be a bit more generous depending on how far you would like to take protein restriction.  Ron Rosedale suggested a minimal protein restriction of about 0.75 mg/kg, roughly double the allowance above.  But this is a minimal number deemed "restriction."

 

So now we are talking 17-34 grams of protein a day if you are very petite, or 34-68 grams a day of protein if you are taller and/or more robust, with greater weight behind the low end of those ranges.

 

For the omnivore looking to follow fish guidelines "A 3-ounce serving of six types of fish -- cod, haddock, tuna, flounder, perch and halibut -- has 90 to 130 calories and 19 to 26 grams of protein. "  Arbitrarily using 25 grams ( on the larger size of the spectrum but if you eat out portions tend to be on the higher side), so only two servings of fish a week recommended by the AHA ( if anything this is an underestimate since their serving sizes are larger - 3.5 ounce cooked, or about ¾ cup of flaked fish - and they recommend two servings a week as a minimum).  Now granted, this is over a week, not a day, but it is easy to overdo protein in a day: a cup of cooked beans would be typically around 15 or up to 20 grams of protein, a 51 gram package of natto adds another 8 grams, another 5-7 grams protein from a cup of grains or an egg, another 8-16 grams of protein from a half cup of seeds/nuts (I may have a full cup = 16-24 grams), etc.  This list does not include any non-fish meats or dairy which in most diets ( not mine ) would then make up the Lion's Share of protein.  It is no wonder "The low-methionine content of vegan diets may make methionine restriction feasible as a life extension strategy" .  Vegan diets are also lower, for a given gram of protein, in the essential amino acids that drive the mTOR pathway hypothesized to be one of the major drivers and mechanism of accelerated aging averted via protein restriction so these numbers may be less applicable but with 20 grams of protein per cup of tofu even many a vegan exceed these numbers.

 

Now, for the potentially good news:

 

"Calories or Protein? The effect of dietary restriction on lifespan in rodents is explained by calories alone."

 

From the conclusion of the paper 

 

" [...] there is an independent impact of dietary protein reduction on lifespan, but it operates over a different range of restriction (50 to 85%: relative to a reference intake of 18-26% protein in the diet) than that over which CR is effective (10-65% relative to ad libitum intake), and has a much smaller impact. Hence, reducing protein levels by 80% (from 20% to 4%) increases median lifespan by about 15%, while reducing calories by half this amount (40%) increases median lifespan by on average twice as much (30%)."

 

We can poke holes here, but based on the quality of data we have across different organisms, the science of PR is in its infancy.  

 

Footnote: Would be interested in other opinions -- my personal take is that looking at the range of % protein in the Blue Zones is a more reliable indicator of % protein impact on longevity.  Only 9% of calories are derived from protein in Okinawa, but my sense from reading secondary sources is that the Blue Zones in general ( would love to see a table with the direct comparison of % macronutrients across the blue zones but have not come across it yet if it exists) while they consume much lower protein than in the SAD, not as low as Dr. Longo's recommendations.

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Dr. Longo advises "[...]The ideal diet is a plant and fish based diet that is low in protein, about 0.37 grams per kilogram body weight and that may increase a little bit in proteins after age 65 or 70, depending on the need" [ source ].

 

 

I've seen that quote, but I wonder about it given that 1) 0.37g/kg is extraordinarily low,  and 2) Dr. Longo advises  the more normal 0.7-0.8 g/kg (up to 65-70 years old) in his currently prescribed  "Longevity Diet"  (https://www.crsociety.org/topic/11883-valter-longo-interviewed-by-rhonda/).

Edited by Sibiriak

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Dr. Longo advises "[...]The ideal diet is a plant and fish based diet that is low in protein, about 0.37 grams per kilogram body weight and that may increase a little bit in proteins after age 65 or 70, depending on the need" [ source ].

 

 

I've seen that quote, but I wonder about it given that 1) 0.37g/kg is extraordinarily low,  and 2) Dr. Longo advises  the more normal 0.7-0.8 g/kg (up to 65-70 years old) in his currently prescribed  "Longevity Diet"  (https://www.crsociety.org/topic/11883-valter-longo-interviewed-by-rhonda/).

 

Yes I have noticed the same thing and comment about this and the author have contacted Professor Longo.

Long story short, it is 0.37g per pound as I have noticed -> roughly 0.8 grams per kilogram,

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Thank you Tasbin, that makes more sense though did not rule out the original numbers since Ron Rosedae described his own figure of 0.75 mg/kg as an "upper limit"rather than as an ideal, and perhaps Longo get it a legal liability to use the "ideal" rather than "conservative, safer" guidelines for optimal protein intake.

 

I wonder though about operationalizing thte recommendations.  As noted   Ron Rosedale 

, and at the very end of the talk I linked to he basically advised to be obtaining most of your energy from burning fat ( as opposed to carbohydrate) which he emphasizes may or may not involve ketosis as ketone bodies may still be low.  This is to minimize mTOR activation.

 

Contrasting his recommendations with the Okinawa experience, the traditional Okinawa diet, rather than "mostly fat," fat intake represented only about 6% of traditional Okinawan caloric needs.  Could this be because although carbohydrates represent by far the lion's share of the Okinawa diet, due to their low caloric intake overall ( 1785 vs 2068 calories in the Japanese control), most of their "burned" calories were still obtained from fat due to their relatively fasted state?  I do not have a background in nutrition to assess this, is this hypothesis an absurd nonsensical contradiction, or alternatively what we would expect ( i.e., high % of calories burned from fat on a low calorie diet even in the presence of a very high % of consumed calories obtained from carbohydrates ).  Inquiring minds want to know  :)xyz 

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Tasbin, I too found the linked presentation by Rosedale extremely fascinating and went through it several times. During my life of health buff I came across many insights from different authors which suggested the idea that the body can live with far fewer proteins than affirmed by the official science. Today, very recent research provides a rational conceptual framework which appears to be satisfactory. We can vary the amount of dietary proteins and by that we can actuate powerful metabolic masterswitches like mTOR. 

 

As far as I can see though, there is some imprecision in the suggestions given on the reccomended daily protein threshold which avoids mTOR signaling.

 

1st of all, there is some confusion about the concepts of 'lean body mass' and 'ideal body weight'. In his blogs Dr. Rosedale, for example, reccomends 0.6 to 0.75 g/kg lean mass, whereas in his book (the Rosedale diet) it results clear, the concept is an 'ideal weight' concept, that is a lean weight with ideal bodyfat percentge (not specified, but it is agreed in males it's about 10 to 15%). Maybe it's easier to relate the ideal weight to an ideal BMI of 20 to 23 maybe, but this reasoning is faulty in very muscular individuals.

 

The above is important, since quantities of proteins would/might result in lesser than minimum requirement to avoid starvation. Dr. Garth Davis in his Proteaholic book refers to lean weight but to me that appears wrong and potentially unsafe.

 

The official reference all appear to fall back to is the WHO/FAO 2002 n=235 metanalysis, whose results I posted previously and am going to post again here. The authors refer clearly to an effective weight of the studied individuals, which was corrected when it went beyond an ideal BMI range (not specified).

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This is the WHO, 2002 lognormal distribution of minimum protein intake in the human being, expressed in mgN/kg effective bodyweight/day, for a mixed diet (animal+plant based proteins) and with an adequate energetic substrate (adequate calories from carbs or fats).

The conversion is usually 6.25 (widely valid approximation for all foods). So the modal value would be about 0.63 k/kg/d, the median value a little higher=0.66, the 97.5% value, which is the safe RDA value, would be the 0.8 k/kg/d value given by Longo (or, with redundant precision, 0.825).

 

28988355354_b3dfcb479f_b.jpg

Edited by mccoy

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My bottom line is that, according to Longo, abundance of proteins is not reached at the safe RDA intake of 0.8 g/kg/d, more is needed until the mTOR sensor sense abundance and swithces to the growth & proliferation mode.

 

Arguably, Prof. Longo might just be playing safe here, aware that to suggest less would mean to expose some not negligible percentile of the population to potential starvation.

 

Whereas Dr. Rosedale (and Dr. Fung follows suit) approach tend to suggest the median value of 0.66 g/kg/d.

 

The real stuff that none seems to consider appropriately aside Dr Attia, is that the minimum protein requirement is not a deterministic number, rather a probabilistic number hence it changes from person to person. What is abundance for me might be deficiency for you. Consequently, the mTOR activation issue has no solution valid for everyone.

Our personal zero nitrogen balance point (minimum protein requirement) should be estabilished on an individual basis. Significantly more than that, we have abundance= mTOR ON-

At that personal requirement, or not much more, mTOR goes in the OFF mode.

 

As far as I understood, nobody knows exactly when mTOR will go ON. The authors speak widely of 'abundance' of protein. How much is abundance we don't know. We have a few references though:

 

-Dr Rosedale, Dr. Fung: we have abundance definitely some value beyond 0.8, sometimes over 0.7 and for diabetic people it is highly suggested to stop at 0.6.

-Dr Longo: we have abundance some value beyond 0.8

-Dr Attia: we have abundance a significant value above our individual zero nitrogen value, which must be determined individually.

 

All above considerations are valid for sedentary people. Exercise shifts the 'abundance' threshold by various amounts (5 to 10 g proteins/day Dr Rosedale; 30 grams proteins every workout Longo; 20 grams proteins every workout Davis; 3 grams pure Leucine per workout Attia).

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RE Ron Rosedale: I studied his proposed diet. his most recent suggestiosn are as follows:

 

1- Restrict proteins to 0.6-0.8 g/kg/d and most of them should be fish.

2-Restrict carbs as much as possible, avoiding simple sugars, fruit, cereals and so on; just eat plenty of vegetables

3- Satisfy the caloric need mainly by fats.

 

His suggested diet hence is a low carb-low proteins-hi fat - pescetarian diet, with plenty vegetables.

He also suggests ample supplementation, very ample when metabolic syndrome or diabetes are involved.

 

I'm a little  puzzled by the negative connotation he assigns to fructose and fruit. In his opinion, fruit is damaging because of fructose and consequent glycosis phenomena.

 

In my 40 years of healthy nutrition experience, fruit is the healthiest food and has always served me well.

Edited by mccoy

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This post may be useful here:

 

http://www.livingthecrway.com/home/blog/living-the-cr-way/2014/03/11/try-ketogenesis-this-week!

 

Paul McGlothin achieves a level of ketosis while using a very complex carbohydrate approach, meanwhile Dave Brauer on the same thread uses a high fat approach. Each have sample menus posted.

Drewab, apparently the posts are visible only to the registered members.

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Thank you Drewab. I am not a member so it looks like no access to the links but will look out elsewhere on the internet for the work of Dr. Tom Seyfried on ketogenic diets.

 

Mccoy, lots of interesting points and resources, thanks. I have a few thoughts/clarifications, and questions from what we garnered so far.

 

1) I stated earlier that Ron Rosedale suggested a minimal protein restriction of about 0.75 mg/kg, and you provided a great summary of the various recommendations by different experts on daily restricted protein regimens. In the same video, he actually posted 0.75 mg/kg as an upper limit that "everyone" should have at a maximum. His preferred number on the slide dubbed "What's High?" is 0.6/kg lean mass/day, especially in the context of specific conditions as it "may be even better after adaptation to treat DM, Cancer." He did not explicitly state that this is viable for the long-term, but he did imply it by making a statement to the effect that the body adapts to such lower levels of protein intake by conserving more protein. That seems to be our (or at least his) answer to the question of ideal versus lean body mass as well. So for every 100 pounds or 45.36 kg of lean body mass, that's about 27 - 34 grams of protein a day.

 

2) In that same video Dr. Rosedale emphasizes at about 33:34 , that it isn't ketogenesis we are after, it is fat burning / burning fatty acids for fuel rather than other macronutrients in metabolism. He notes that 4+ ketone bodies is not what we are looking for and may not be required - it may be an indication that you are in ketogenesis, but ketogenesis may occur under non-ideal conditions such as with a higher protein diet which would defeat the purpose as this would still rev-up mTOR. Ketone bodies, when present may be in indication that you are burning fat ( which is good by his premise), the ketone bodies simply indicate the state and high levels of ketone bodies are not inherently healthiful. This last point was interesting for me as I have seen studies showing benefit at least in the CNS for higher levels of ketosis. This may indeed be the case for some situations, but with his focus was on mTOR and keeping that pathway low. To underscore the point the ketone bodies are not necessarily beneficial overall, at least for some circumstances, he cited a study with the ominous title Ketone body utilization drives tumor growth and metastasis

 

3) He also cited as evidence that low protein diets reduce mTOR activation with increased longevity with the manuscript ominously titled: The ratio of macronutrients, not caloric intake, dictates cardiometabolic health, aging, and longevity in ad libitum-fed mice. The title says it all, but from the abstract: "Longevity and health were optimized when protein was replaced with carbohydrate to limit compensatory feeding for protein and suppress protein intake." What I find interesting here is that although the actual paper found benefits from removing the protein and adding carbohydrates in it's place, in Rosedale's talk he quickly added there that carbohydrate as the primary fuel to burn is not optimal and it would be much better to burn fat instead. While his conjecture has biological plausibility from our understanding of mTOR activators, he skips any data or evidence to support his claim. It may not be difficult to cite studies demonstrating that carbohydrates activate mTOR whereas lipids/fats/fatty acids are neutral, without a direct study comparing carbohydrates to fatty acids as fuel, I do not feel we adequatly surmise the effect size (ie difference between a low-protein, modest calorie carbohydrate based diet versus the same diet low in carbohydrates but high in fat). Is the difference in outcomes 300%? Or is it 5%? The data he presented was for replacement with carbs not fat, and if we are going to commit to a ketogenic diet with a very high percentage fat, which for many would represent a significant departure from dietary preferences, I would like to see the data and convince myself it is worth the difference ( perhaps for 200% but not a chance for a 10% difference!). So essentially I find his argument persuasive that lower protein intake is a good idea, but I am not convinced it must be ketogenic.

 

4) In addition to the leap of faith described in in #3 above, I see examples like in Okinawa where fats only make up 6% of caloric intake. Barring a genetic anomaly ( which seems increasingly less plausible with migration studies and changes in morbidity/mortality with Okinawa cohorts adapting a more Western-style diet albeit this is not the same thing as showing the reverse), it seems to me that ketogenic diets may offer little if any advantage over other methods ( i.e., a diet and lifestyle more closely resembling a Blue Zone diet/lifestyle) of arriving at the same point in longevity and health. This brings me back to my initial query which at this point is outside of my nutritional/metabolic background (sorry, quoting myself here): Could this be because although carbohydrates represent by far the lion's share of the Okinawa diet, due to their low caloric intake overall ( 1785 vs 2068 calories in the Japanese control), most of their "burned" calories were still obtained from fat [ rather than from their primarily carbohydrate-centered diet] due to their relatively fasted steady state? ( is anybody here a nutritional scientist who can comment? A mere amateur & relative newbie here, and I am far short of the 10,000 hours of labor to achieve nutritional proficiency... if nothing else I hope amusing to the true expert legacy posters here).

 

5) Blue Zones median longevity and vitality already closely approximate the upper limit of aging, so I am skeptical dietary interventions that depart substantially from them can do much simply based on the emperical observation that the curve for our species ( just like for every other) drops off abruptly over a decade or two. In this diverse planet of cultures and individual preferences there are innumerable Dean-like pioneers self-experimenting with unique diets and the survival curve only stretches out so far. Outliers are few in number, and only go so far, and the outliers identified for the most part are variations on a theme diet-wise rather than doing something truly unusual diet-wise... this suggests the few extreme outliers such as longevity record-holders are more the byproduct of what is already known ( plant-based, not too many calories, lower protein, exercise, etc.) plus an additional bonus factor of genes and stoachastic luck factor (someone needs to fill the tail of a probability distribution).

 

Of course, there is another interpretation, cited above, that it may not matter so much: "Calories or Protein? The effect of dietary restriction on lifespan in rodents is explained by calories alone."

 

PS - Agree intuitively with comment regarding fructose from natural sources being unjustifiably vilified provided ( would add provided no strong tendency towards metabolic syndrome as they can elevate triglycerides disproportionately albeit even higher triglycerides from fruit sources may not be so bad provided insulin levels are low due to qualitative differences in metabolism based on some more recent data < citation missing here - trouble finding the study > ) -- this summary from Kris Kressler is a bit dated but supports your contention. I would have more confidence if we had more observational data in already very healthy populations ( many epidemiologic studies, some cited by Dr. Greger, show potential benefit in the context of SAD, including for morbidity such as lower AD risk with berries, etc. ). I suspect his concern is more along the lines of fructose being more insulinogenic and thus higher IGF-1 which is a driver of mTOR, but I could be mistaken. In any case, ancestral diet school of thought emphasize historically this was only available seasonably, and I would be more reassured if a Blue-zone like area ( in absence of unique genetics) had a higher fructose consumption. Having said that, without better data, I still enjoy my 200-300 g of berries a day and other assorted fruit.

Edited by Mechanism

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Could this be because although carbohydrates represent by far the lion's share of the Okinawa diet, due to their low caloric intake overall ( 1785 vs 2068 calories in the Japanese control), most of their "burned" calories were still obtained from fat [ rather than from their primarily carbohydrate-centered diet] due to their relatively fasted steady state?

 

As I understand the glucose from carbohydrates is first converted to glycogen and stored in skeletal muscles and the liver and only when those stores are full does much get converted and burned/stored as fat.  Fructose I think is more readily converted to triglycerides than glucose, but unless they are alternately binging and fasting I would expect most of their carbs to be burnt as carbs.

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Could this be because although carbohydrates represent by far the lion's share of the Okinawa diet, due to their low caloric intake overall ( 1785 vs 2068 calories in the Japanese control), most of their "burned" calories were still obtained from fat [ rather than from their primarily carbohydrate-centered diet] due to their relatively fasted steady state?

As I understand the glucose from carbohydrates is first converted to glycogen and stored in skeletal muscles and the liver and only when those stores are full does much get converted and burned/stored as fat. Fructose I think is more readily converted to triglycerides than glucose, but unless they are alternately binging and fasting I would expect most of their carbs to be burnt as carbs.

Maybe through fasting to a more ketogenic state, or through a fat-dominated diet, the percentage shifts? Also, and maybe this is semantics, but does the body "burn" carbs and fat, or does the body expel calories through respiration? For some reason I find this a better visual for my imagination: we aren't furnaces, as someone wrote. We're breathing things, I think a poet said, and every yoga teacher I've ever met.

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1) I stated earlier that Ron Rosedale

, and you provided a great summary of the various recommendations by different experts on daily restricted protein regimens. In the same video, he actually posted 0.75 mg/kg as an upper limit that "everyone" should have at a maximum. His preferred number on the slide dubbed "What's High?" is 0.6/kg lean mass/day, especially in the context of specific conditions as it "may be even better after adaptation to treat DM, Cancer." He did not explicitly state that this is viable for the long-term, but he did imply it by making a statement to the effect that the body adapts to such lower levels of protein intake by conserving more protein. That seems to be our (or at least his) answer to the question of ideal versus lean body mass as well. So for every 100 pounds or 45.36 kg of lean body mass, that's about 27 - 34 grams of protein a day.

 

 

I'll refer to the WHO technical report series 935, 2002: PROTEIN AND AMINO ACID REQUIREMENTS IN HUMAN NUTRITION

 

section 14.1 Derivation fo requirements

 

14.1.4 Relation to body weight

Protein requirements are derived as amounts per kg body weight of subjects whose weight is within the acceptable range for height (adults) or age (children). The requirements per person within the acceptable ranges of body weights may either be based on the actual weight or normalized to the median weight for height or age, as given in the appropriate tables, according to the objectives for which they are to be used

 
It is clear from the above that the official requirements refer to actual bodyweight, sometimes corrected and not to lean body mass.
 
By the Rand et al. Metanalysis portrayed in the study, it results that 0.66 grams of proteins per actual body weight per day is the median minimum requirement.
 
When Rosedale says that 0.6 per LBM is the ideal requirement, he speaks of a less then median value, a value which might mean starvation for about 60 or 65% of the population according to the Rand et al. metanalysis.
 
The above does not consider adaptation.
 
My bottom line is that Dr. Rosedale might have misspoken. Otherwise, he would imply that downregulation of mTOR is only possible by starvation for most people.
 
It makes more sense to construe Dr. Rosedale's words by reference to 'ideal weight' and not 'lean body mass'.
 
Otherwise: whence did Dr. rosedale take those values? What's his database and why it should be more valid than the Radd et al. n=235 database, considered by official agencies?
Edited by mccoy

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Great point McCoy.  I think the greatest issue, as you pointed out, is the interpersonal variability and need for individualized testing.  I am now sure how much this varies by year for an individual 

 

What do you think of Tod's and Sthira's interpretation of whether a high carb diet can still burn a high % fatty acids as a percentage of mobilized macronutrients?  I suspect this to be the case, but cannot find any smoking guns or confirmation.  

 

I still see no point in adapting a ketogenic diet based on theory when the best real life centenarian populations are carb-centered, and even the mTOR study I described above, mentioned by Dr. Rosedale, reduced protein in place of carbs (not fat) instead to get that benefit.

 

The devil is in the details.  I did detailed chron-o-meter analysis on myself and was surprised my protein intake was so high - a little over 100 grams a day.  Then I drilled down and found my % calories from protein was 11-13% which is just a bit higher than Dean's 9% (which is more ideal and between / on a par with 9% protein in Okinawa ( like Dean, hurray!) vs. 13% for a mediterranean diet which is higher protein than mine.  Moreover, when I pushed the numbers only about 6% of my protein comes from fish on days when I have 1/4 a can of sardines, and on the other days 100% of my protein is plant-based and this has a more favorable amino acid profile than plant sources.  

 

You cited some experts suggesting different protein fudge factors based on activity levels - there does not seem to be great agreement here so the influence of total ( for a given ideal vs lean body weight) versus % caloric intake from protein is a significant question.  If your % calories from protein is low but total amount of protein high, will you have the same benefits, provided your other biomarkers like CRP and IGF-1 are good?  I don't think we have the data to say one way or another.

 

An interesting comparison which raises some issues on what details count:

 

Dean justifiably consumes 3400 calories a day with his intense exercise, with similar BMI, age, and stature I have nearly identical caloric intake ( did detailed check yesterday and today: 3193 and 3454 calories respectively but I am an order of magnitude less active - a decent amount of standing during day but not a ton of movement ( clinician seeing patients going between rooms), three or four 30-40 minute fairly intense anerobic weight resistance workouts a week, 1 30-60 minute moderate-paced walk at lunch on weekdays (not running), and perhaps 10-20 minutes of biking on a stationary bike most days with some weekend hiking on and off versus street walking and a modest and variable amount on weekends.  So while Dean's diet is one step removed from the data ( higher calorie, but higher energy expendure), I am two steps removed ( like Dean, but only moderately active and order of magnitude less so than Dean so not nearly enough to offset my nearly identical caloric intake... in the past I consumed maybe 2500 calories but I was not so active then and weighed less with no muscle to speak of).  Probably better to be one step removed than two...

 

However my hs-CRP is low, modestly low IGF-1, & endocrine markers are CR-like despite high caloric intake, and, now, my primary concern of post-prandial BG is better than most CR practitioners (and respectable fasting BG) following some diet and lifestyle self-experimenting.  

 

Moreover, I find that I need to eat this much just to keep my BMI at respectable levels, now on a par with Dean's.  Skinny my whole life despite a voracious apetite, I have only through workouts have been able to gain some weight ( I know, first world problem for many), hence no plans to reduce calories - I eat to satiation which is my primary guide) up to a desirable level. The muscle mass was secondary but probably helps with improved post-prandial BG and is likely to have raised my BMR to even higher levels requiring even more calories just to sustain it - the irony.

Edited by Mechanism

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What do you think of Tod's and Sthira's interpretation of whether a high carb diet can still burn a high % fatty acids as a percentage of mobilized macronutrients?  I suspect this to be the case, but cannot find any smoking guns or confirmation.  

 

 

 

Re: burning of fatty acids by carbs: I cannot express myself about the involved biochemistry but it appears that a diet with some caloric restriction, high in carbs but poor in fats and moderate in proteins may actually constitute a weight loss diet. This is just the opposite of a traditional low-carb diet which is also known to cause weight loss. So there is hard evidence. I saw it myself very recently. A coleauge of mine asked me how to loose weight. I suggested to him a low carb diet first since he has the signs of insulin resistance. As soon as I realized that it was just not his lifestyle nor ancestry (his ancestors are pure farmers from the mediterranian region) I advised to him to try a starch and vegetables rich diet, with very few fats, 30% less calories than his BMR. 

The thing, to my surprise, worked almost instantaneously (with full and sedulous adherence of my coleauge of course).

 

So I should conclude that yes, like in philosophy it seems that the opposites touch, there is evidence that a high carbs healthy diet with caloric restriction can effectively burn fats.

I don't know if I misunderstood your question but sure the biochemistry beats me. My wife is on a low-carbs, moderate proteins, hi fats diet and is loosing weight (having constitutional insulin sensitivity).

My colleauge is on an opposite track and is loosing weight as well. I myself, will loose weight either on a low-fat, hi carbs low calories diet and on a low-carbs, hi fat diet, as experimented.

Edited by mccoy

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I still see no point in adapting a ketogenic diet based on theory when the best real life centenarian populations are carb-centered, and even the mTOR study I described above, mentioned by Dr. Rosedale, reduced protein in place of carbs (not fat) instead to get that benefit.

 

 

 
Ketogenic diets are extreme diets which, conceptually, should find application in extreme cases of difficult weight loss, therapeutic conditions such as epilepsy, cancer, general metabolic syndrome.
Ps note that many voices started to speak up against the undiscriminate intake of proteins. We saw rosedale, then Fung, Attia, James Moore, the ones I know. Too many proteins are glycogenetic hence they eliminate ketogenesis and are apparently more or less unhealthy. Also, as per Dr. Attia affirmations, some people do not tolerate ketogenic diets. They tend to develop, as far as I understood, unfavourable and worrying lipid profiles.
 
Dr Rosedale supports a low-carbs, moderate-proteins, hi fats diet with lots of vegetables. The purpose, as described in detail in his presentation, is to have all the metabolic signals unfavourable to longevity and degenerative disease downregulated. I do not understand his remarks on ketosis but I do understand his overall logic. 
I do not agree with everything in his dietary suggestions but agree with his purpose. Now, re. the centenarian populations: do they possess an inherent genetical makeup such that IGF-1 is low and on top they eat little proteins? In such a way they would not suffer an high IIS signaling by favourable genetics. I do not know that.
It makes sense that people who have not a favourable genetic makeup should try and consciously dicrease both IIS and mTOR signaling, by decreasing carbs and proteins.
The details then are related to the individual.
Edited by mccoy

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The devil is in the details.  I did detailed chron-o-meter analysis on myself and was surprised my protein intake was so high - a little over 100 grams a day.  Then I drilled down and found my % calories from protein was 11-13% which is just a bit higher than Dean's 9% (which is more ideal and between / on a par with 9% protein in Okinawa ( like Dean, hurray!) vs. 13% for a mediterranean diet which is higher protein than mine.  Moreover, when I pushed the numbers only about 6% of my protein comes from fish on days when I have 1/4 a can of sardines, and on the other days 100% of my protein is plant-based and this has a more favorable amino acid profile than plant sources.  You cited some experts suggesting different protein fudge factors based on activity levels - there does not seem to be great agreement here so the influence of total ( for a given ideal vs lean body weight) versus % caloric intake from protein is a significant question.  If your % calories from protein is low but total amount of protein high, will you have the same benefits, provided your other biomarkers like CRP and IGF-1 are good?  I don't think we have the data to say one way or another.

 

Conceptually speaking, with reference to the detailedly reasoned Rosedale's presentation, % of proteins is not the factor which governs mTOR signaling. The mTOR sensor senses a general 'abundance' of dietary aminoacids into the cell environemnt.

Now the question you should pose according to such logic is: "Will my 100 gr of daily proteins be construed by mTOR as abundance?" 

You didn't specify your ideal bodyweight but from comparison with Dean you are ingesting a lot of proteins.  Ps correct me but you should be at around 55 kg weight.so you are almost 2 g/kg/d and that should certainly be construed as abundance by mTOR,  Unless you are an utter outlier, which we cannot rule out.

The amount of exercise you carry out, I doubt would imply more than 5 or 10 g/day of proteins sequestered for MPS. 

 

So an objective suggestion would be: maybe your proteins are too high. On the other side, an ancillary suggestion would be: check if you are going to loose muscle mass with a lower amount of proteins, leaving calories unvaried. If so, you are in negtive nitrogen balance, hence you need more. 1 g/kg/d maybe your zero nitrogen balance or close to it.

 

Another issue: since vegetable proteins seem to have a lower nitrogen-to proteins conversion factor with respect to animal proteins, then it means you may have slightly higher amounts of proteins if they are vegetable. But not all of them have the same conversion factor and the results may be tricky. According to Rosedale, in one of his blogs, the difference is significant though, around 30%. I tend to reason more by numbers and the numbers I have seen would grant just a slight increase in daily minimum proteic intake. 

Edited by mccoy

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An interesting comparison which raises some issues on what details count:

 

 

Dean justifiably consumes 3400 calories a day with his intense exercise, with similar BMI, age, and stature I have nearly identical caloric intake ( did detailed check yesterday and today: 3193 and 3454 calories respectively but I am an order of magnitude less active - a decent amount of standing during day but not a ton of movement ( clinician seeing patients going between rooms), three or four 30-40 minute fairly intense anerobic weight resistance workouts a week, 1 30-60 minute moderate-paced walk at lunch on weekdays (not running), and perhaps 10-20 minutes of biking on a stationary bike most days with some weekend hiking on and off versus street walking and a modest and variable amount on weekends.  So while Dean's diet is one step removed from the data ( higher calorie, but higher energy expendure), I am two steps removed ( like Dean, but only moderately active and order of magnitude less so than Dean so not nearly enough to offset my nearly identical caloric intake... in the past I consumed maybe 2500 calories but I was not so active then and weighed less with no muscle to speak of).  Probably better to be one step removed than two...

However my hs-CRP is low, modestly low IGF-1, & endocrine markers are CR-like despite high caloric intake, and, now, my primary concern of post-prandial BG is better than most CR practitioners (and respectable fasting BG) following some diet and lifestyle self-experimenting.  

Moreover, I find that I need to eat this much just to keep my BMI at respectable levels, now on a par with Dean's.  Skinny my whole life despite a voracious apetite, I have only through workouts have been able to gain some weight ( I know, first world problem for many), hence no plans to reduce calories - I eat to satiation which is my primary guide) up to a desirable level. The muscle mass was secondary but probably helps with improved post-prandial BG and is likely to have raised my BMR to even higher levels requiring even more calories just to sustain it - the irony

 

 

 

Now, I've seen Dean's diet and it is fascinating. His case constitutes undoubtedly an outlier, the Rand et al. distribution is surely not representative of his particular condition of BMI, diet, lifestyle, temperature exposure, physical activity. He's probably a case on his own and I would be dumbstruck if mTOR is upregulated in his case, notwithstanding the large amount of proteins.

 

Now, your case seems similar, skinny and with a voracious appetite bespeaks of some peculiar metabolic state with a systemic necessity for larger amounts of food.

In your case the Rand et al. distribution may not be applicable too, and you should play by ear so to speak, that is behave by instinct and self experimentation.

 

My BMI is higher (22.5 presently) but I too have difficulties in gaining weight if not by exercise, and strenuos to boot. I too am wondering about my personal threshold for mTOR activation. I've been monitoring my calories and proteins for a while now and apparently muscle mass is not increasing at equal bodyweight and notwithstanding exercise, so maybe my present intake of proteins, 0.8 g/kg/d is around the zero nitrogen point, including exercise in the balance.

 

Other more direct ways would be careful monitoring of protein intake + 24 hours urine nitrogen measures, repeated for a few days. By some corrections you may be able to determine if you are in negative, zero or positive N-balance.

Or monitoring your lean body mass by DEXA scans, and checking when it decreases by parallel decrease of proteins. When your lean muscle mass starts decreasing, then you are in negative balance and are starving. You may by interpolation determine your exact zero-N point which is a benchmark fo rthe mTOR threshold.

 

According to logic, mTOR should sense an abundance of proteins, hence a significatively higher intake than the zero-N balance intake.

 

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Thank you Todd & Sthira, and thank you McCoy for the elaborate and helpful reply.

 

I agree that you can lose weight on high carb implies you can consume high carb yet net burn mostly fats. My question is whether you can still burn high % fats in a high carb diet if your energy intake and expenditure are in balance such that your BMI does not change over time. Not all consumed calories are stored as adipose tissue, and thermogenesis, etc. can be increased with higher caloric intake. Likewise two twins can consume different # of calories indefinitely and after one loses weight relative to the other ( or the other gains weight ) they can maintain BMI equilibrium at their respective different BMIs. In theory one may be on a CR diet and the other in a SAD, for example. So I wonder / speculate whether lower calorie diets with the same % macronutrient intake of P/C/F, burn a higher % of calories from adipose relative to identical diets that are higher calories. This may explain longer lived societies such as Okinawa with very high % calorie intake from carbs yet more carb fuel for mTOR. Alternatively it may be simply that the carb intake while large as a proportion to other macronutrients, is small enough in absolute numbers ( less of a carb signal via eating less ) that even if most energy "burned" is from carbs ( not fat ) that mTOR signaling is diminished this way. If it is the latter not the former, then Rosedale's high fat diet approach may not at all be required to achieve his goal of less mTOR activation providered that total calories are low.

 

Another question if interpretation 2 is correct: to have low mTOR signaling on a high carb diet, does absolute carb amount need to be low, or in the case of Dean just low compared to energy requirements? Do his healthy biomarkers ( which include CRP and various CR measures) speak for themselves? None of these measures mTOR activation directly and IGF-1 is only one of a multitude of potential mTOR activators.

 

One step further removed from this question is another ( from the example of myself, with about Dean's BMI and energy intake but apparently very high metabolism as I exercise much less but have not gained weight until recently... only to roughly catch up with his BMI as I increased muscle mass )---- whether mTOR can remain low under Dean's diet with BMI stable rather than with exercise ( as Dean does), but instead from having by luck alone the genetics of possessing a high baseline BMR as I seem to always have had - no unusually high level of exercise, large muscle mass, or large amounts of cold exposure to account for inherently apparently genetically determined high BMR --- presumably the more I eat the more my body successfully dissipates it via thermogenesis and other metabolic processes rather than storage of calories as adipose tissue, etc.

 

To be fair, I have now recently intentionally and successfully gained weight and meal size can be habitual so I can't say that 3400 kcal is my baseline. However even prior to this period when I was substantially less active and had no muscle to speak of, I was not gaining weight and was consuming at a minimum of ~2700 kcal/day which is a lot for my 5 foot 8.5 inch frame and BMI at the time we'll into the underweight category. BMI as low as about 16 before gaining 10-15 pounds lately through a very concerted effort with intense anaerobic exercises and even greater caloric intake to gain muscle mass. Even then, prior to the intentional weight gain, my BMR must have been extraordinary high to consume so much and with a lot less activity ( no daily hour walk, no weight resistance) and no muscle at all to boot. (All of this of course assumes no bioabsorption issues - out of curiosity I got tested and no stool steatorrhea or other signs of malabsorption ). So the basic question remains -

 

**how the above may apply to an individual such as myself with very high caloric intake relative to a low ( near low normal/underweight) and stable BMI yet no increases in BMI**,

 

since that described me up until very recently: even 2700 calories is quite a lot in a 5 foot 8.5. inch individual in his early 40's with only moderate physical activity and BMI in the 16 - 18.5 range.

 

Nevertheless I would not go below that caloric high intake with such low-side BMI, as adequate BMI is more important to me based on epidemiological data on outcomes with low BMI especially as one gets older not to mention metabolic and glycemic load buffer protection that some degree of muscle and fat impart.

 

With regard to your protein intake , it is only 11-13% of my caloric intake hence my question in the last thread whether absolute vs relative protein are the #s that count really count with regard to mTOR activation and it's impact on overall health. Both Dean & I have about 100 grams of protein a day, mine with only 6% from animal sources on those days days that a have around 1/4 of a 4.25 ounce serving of sardines or salmon, etc. (0% on others, and Dean of course with 0% every day).

Edited by Mechanism

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PS- Dean, don't mean to invoke your name in the 3rd person, by way of comparison and illustration here ... know you are busy with your AI endeavors...

Edited by Mechanism

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With regard to your protein intake , it is only 11-13% of my caloric intake hence my question in the last thread whether absolute vs relative protein are the #s that count really count with regard to mTOR activation and it's impact on overall health. Both Dean & I have about 100 grams of protein a day, mine with only 6% from animal sources on those days days that a have around 1/4 of a 4.25 ounce serving of sardines or salmon, etc. (0% on others, and Dean of course with 0% every day).

 

The absolute rather than the relative amount of proteins would govern. So, just by sheer numbers you would inevitably fall into the growth and proliferation mode. However, yours seems a case of augmented BMR don't know if driven by hypertyroidism, who knows how the proteins are metabolized in your system. Lean as you are and with all those difficulties in gaining weight, it is hard to imagine any real growth & proliferation mode ruling. So maybe you have inherent, genetic propensity to a downregulated mTOR. Maybe, just speculating. Another issue is the high BMR and thermogenesis, that according to Rosedale may not be such a desirable condition for longevity, implying what he calls an higher rate of organic wear and tear.

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