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mccoy

protein RDAs for vegans

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By the way, I can show some results for the physical activity, although only by a moderate growth. Sarcopenia and osteopenia are being hopefully avoided. Pic only if the shredded look shows well, LOL

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Pls note that Longo advocates the RDA of 0.8 g/kg/d plus 30 g of protein as a post workout meal.

 

My understanding was that a single 30g protein meal was meant to come out of the .7- .8g/kg/day protein total,  not be an addition to it.

 

That was my interpretation of the summary of Longo's  "Longevity Diet" posted here:

https://www.crsociety.org/topic/11883-valter-longo-interviewed-by-rhonda/?do=findComment&comment=18952

 

That interpretation would be consistent with the theory outlined by Longo and colleagues in this article:

 

Low Protein Intake is Associated with a Major Reduction in IGF-1, Cancer, and Overall Mortality in the 65 and Younger but Not Older Population

.

...low protein intake during middle age followed by moderate protein consumption in old subjects may optimize healthspan and longevity.

 

...we propose that up to age 65 and possibly 75, depending on health status, the 0.7 to 0.8 grams of proteins/kg of body weigh/day reported by the Food and Nutrition Board of the Institute of Medicine, currently viewed as a minimum requirement, should be recommended instead of the 1–1.3 g grams of proteins/kg of body weigh/day consumed by adults ages 19–70 (Fulgoni, 2008

 

We also propose that at older ages, it may be important to avoid low protein intake and gradually adopt a moderate to high protein possibly mostly plant based consumption to allow the maintenance of a healthy weight and protection from frailty (Bartali et al., 2006; Ferrucci et al., 2003; Kobayashi et al., 2013).

 

I haven't seen Longo et al. arguing that the same pro-longevity and anti-cancer effects of a low protein diet  can be obtained by a higher protein diet + resistance training.  I haven't read Longo's book, though.

Edited by Sibiriak

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Sibiriak, I'm just checking longo's book.

 

He suggests a close to RDA protein approach, that is: 0.7 to 0.8 g/kg/d, on a pescovegan diet, with fish possibly limited to 2 or 3 meals per week.

 

More animal protein (fish, eggs, cheese) after 65-70 years for those who start loosing weight, strength and muscle mass

 

After 65-70 years 10-20% more protein for people who start loosign weight and muscle mass

 

RE protein after meals. Actually, it's not very clear, he says that meals with 30 g of protein should be consumed 1-2 hours after exercise. Maybe it's part of the daily intake.

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In my case, right now I'm trying to bulk as much as it's possible with light weights, stimulating mTOr by metabolic stress. Esercise plus CE make me ravenous. These same things though, plus lots of xenohormetic compounds, keep AMP-kinase pretty active, which tends to inhibit a systemic overamplification of mTOR. Whereas mTOR is stimulated in muscle  tissues, which absorb most amminoacid in the blood when there is demand, especially after strenous exercise. Plus bone tissues, which are stimulated by similar mechanoreceptors as the muscle tissues.

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Igf-1 levels take a dive in old age and so it may just be too low. Thats a recipe for frailty so upping protein makes sense.

 

Mccoy, thanks for the great discussion.

 

Just noting that I agree with Mike's concern above.

 

I also want to submit that many people digest nuts badly (partly because they may be chewing them too little). This means that the amount of protein in dietary anal. software might, in effect, read low, for people, like me, who get most of their protein from nuts.

 

I've upped my protein to 1.4 g / kg body weight based on my IGF-1 levels. I'm assuming a lot of my nut protein protein ends up in the toilet. My goal is to have IFG-1 levels in the 20th or so percentile.

 

Brian

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By the way, last month I averaged 2900 kCal and 98 grams protein /day, notwithstanding such abundance of nutrients (I'm 5'7", 140 lbs)  I didn't gain any weight. Probably some muscle tissue has displaced fat tissue, but I would have expected more growth, that's why I'm thinking about high AMP-kinase activity and a tendency of my metabolism to attenuate mTOR activity.

 

Brian's considerations about the poor digestibility of nuts might also stand true for myself, since my average protein quota from nuts and seeds is about 25%

 

I'm considering to check my IGF-1 levels for the first time in my life, together with other basic health benchmarks. Going to search the forums for the suggested ones, otherwise going to open a new thread.

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Current Concepts and Unresolved Questions in Dietary Protein Requirements and Supplements in Adults

Front Nutr. 2017; 4: 13

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5420553/
 

The RDA for protein at 0.80 g/kg/day is recommended to come from mixed sources of proteins of generally high quality. Until recently, protein quality was estimated using the PDCAAS. An expert recommendation has, however, been that the PDCAAS be replaced in favor of a new scoring system called the DIAAS (24). There are some notable differences between PDCAAS and DIAAS, and the main reasons to advocate DIAAS as a replacement for PDCAAS are around the shortcomings of the PDCAAS method, specifically:

  1. protein digestibility-corrected amino acid score uses fecal protein digestibility, and there is significant bacterial (colonic) metabolism of amino acids that can falsely enhance values of true protein digestibility;
  2. truncation of PDCAAS values at 1.0 does not account for the bioavailability of individual indispensable amino acids that may have specific roles, and thus, proteins of higher quality are not identified;
  3. protein digestibility-corrected amino acid score values are overestimated because of limited bioavailability of specific forms of amino acids such as lysine (25); and
  4. fecal protein digestibility values are determined using rats, which have a different requirement for amino acids for growth and maintenance versus humans.

Table Table11 lists the PDCAAS and DIAAS of some commercially available isolated protein sources and some commonly consumed protein-containing foods. The limiting amino acids in the proteins and foods listed in Table Table11 differ, but an important point is the reference for PDCAAS is egg protein, whereas in DIAAS, it is a theoretical best protein.

 

 

DCAAS and DIAAS for selected isolated proteins and foods.

 

Food PDCAAS DIAAS Limiting AA
 
MPCa  1.00   1.18 Met + Cys
WPIa   1.00   1.09 Val
SPIa     0.98   0.90 Met + Cys
PPCa   0.89   0.82 Met + Cys
RPCa   0.42   0.37 Lys
Whole milkb             1.00   1.14 Met + Cys
Chicken breastb      1.00   1.08 Trp
Egg (hard boiled)b  1.00   1.13 His
Cooked peasa         0.60 0  .58 Met + Cys
Cooked ricea           0.62     0.59 Lys
Almondsb              0.39    0.40 Lys
Chickpeasb             0.74     0.83 Met + Cys
Tofub                        0.56     0.52 Met + Cys
Corn-based cereala 0.08    0.01 Lys
Hydrolyzed collagenc 0.0 0.0 Trp

 

PDCAAS, protein digestibility-corrected amino acid score; DIAAS, digestible indispensable amino acid score; MPC, milk protein concentrate; WPI, whey protein isolate; SPI, soy protein isolate; PPC, pea protein concentrate; RPC, rice protein concentrate; Trp, tryptophan.

aValues from Ref. (26).

bValues from Ref. (24).

cHydrolyzed collagen has a PDCAAS and DIAAS of 0 since it contains no Trp and is very low in methionine (27).

 

 

Edited by Sibiriak

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Very interesting article, Sibiriak.

 

Also, in table 2 there are the reference ratios values (AARRs) for leucine.

Whey protein isolate overwhelms all, whereas pea protein concentrate is almost one half of it.

This would support the massive use of whey protein by bodybuilders to boost MPS

 

The above goes cheek to cheek with a lesser risk of mTOR overamplification by using plant-based protein supplements 

 

Table 2:  Leucine amino acid reference ratio (AARR) for selected isolated proteins.

 
Milk protein concentrate 1.77
Whey protein isolate 2.57
Whey protein concentrate 1.93
Soy protein concentrate 1.29
Pea protein concentrate 1.37
Rice protein concentrate 1.11
Edited by mccoy

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Mccoy:  RE protein after meals. Actually, it's not very clear, he says that meals with 30 g of protein should be consumed 1-2 hours after exercise. Maybe it's part of the daily intake.

 

Frankly, I don't see the ambiguity;  the 30g of protein is part of the daily total, not in addition to it.  I bought Longo's book so I could  get it straight from the horse's mouth:

 

Consume low but sufficient proteins. Consume 0.31 to 0.36 grams of protein per pound of body weight per day. If you weigh 130 pounds, that comes to about 40 to 47 grams of protein per day, of which 30 grams should be consumed in a single meal to maximize muscle synthesis. If you weigh 200 to 220 pounds and have 35 percent body fat or higher, 60 to 70 grams of protein per day is sufficient, since fat cells require lower levels of protein than muscles. Since this minimum requirement can change from person to person, it is preferable to occasionally consult a dietitian, to make sure that a healthy, lean body mass is maintained. Protein intake should be increased slightly after age sixty-five in individuals who are losing weight and muscle. For most people, a 10 to 20 percent increase (5 to 10 grams more per day) is sufficient. Finally, the diet should be free of animal proteins (red meat, white meat, cheese) with the exception of proteins from fish, but relatively high in vegetable proteins (legumes, nuts, etc.) to minimize the former’s negative effects on diseases and maximize the latter’s nourishing effects.

 

Valter Longo,  The Longevity Diet: Discover the New Science Behind Stem Cell Activation and Regeneration to SlowAging, Fight Disease, and Optimize Weight (Kindle Locations 846-854).

 

It would radically undermine Longo's low-protein pro-longevity dietary philosophy if he were to prescribe 30grams of protein in addition to the .31-.36g/lb/day low-but-sufficient amount.   For people of smaller stature in particular, an additional 30 grams  would constitute a fairly drastic increase in protein.

 

I've just gotten into the book, but I presume the 30g of protein in a single meal prescription is based on the  “leucine trigger”  concept (the idea that a ≈2g leucine dose is required for maximal muscle protein synthesis.)

 

I did some fresh calculations on my own diet and I seem to be getting about .7g/kg/day protein.  I do use a soy protein/cacao/cinnamon concoction fairly often to make it easier to get 30g of that protein in one meal.

 

Mccoylast month I averaged 2900 kCal and 98 grams protein /day, notwithstanding such abundance of nutrients (I'm 5'7", 140 lbs)

 

That would be 1.54g/kg/day protein.    Seems quite high--if the goal is health/longevity.  Almost double Longo's maximum recommendation.

Edited by Sibiriak

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Mccoy: [Exercise and cold exposure],  plus lots of xenohormetic compounds, keep AMP-kinase pretty active, which tends to inhibit a systemic overamplification of mTOR. Whereas mTOR is stimulated in muscle  tissues, which absorb most amminoacid in the blood when there is demand, especially after strenous exercise.

 

A few questions:

 

1) That strategy for muscle-tissue specific mTOR stimulation seems to be based on  “mechanistic speculation”, to use one of Michael Rae’s favorite expressions—have you run across compelling empirical evidence that supports that strategy?

 

[Michael  Rae:  "...recent findings have substantially brought me 'round to something much closer to Dr. Luigi Fontana's (and Paul McG's) position: that while the case remains uncertain, and by far the most important issue is 'Calories, Calories, Calories' as it has always been, the best bet, for long-term Calorie restriction practice, is probably to limit oneself to not much more than RDA levels of protein, and to monitor IGF1 as a likely mediator of the effects of CR — if CR is initiated in middle age or before, and if a lower-protein diet and lower-IGF1 metabolic state is sustainable by the individual without substantial decrements in quality of life or health risks".  (Blue emphasis added)   http://www.longecity.org/forum/topic/41691-low-protein-the-real-way-to-go/?do=findComment&comment=428539 ]

 

2)  Dr. Attia and others who are pursuing the same aim (maximizing muscle growth while avoiding the downsides of increased protein intake) have adopted a strategy of  taking 3-5 grams of free form leucine during resistance training workouts.  https://www.ihmc.us/stemtalk/episode001/   [25:19]

 

I noticed that you adopted that strategy as well for a short time, then dropped it.    Dr. Attia points out that it is quite “challenging to hack the system”, and he argues that high protein intake should be avoided and that  pure leucine supplementation is necessary for muscle-tissue specific mTOR activation. So I’m wondering why you don't think Attia's approach is necessary, given that you share his goal of  tissue-specific mTOR activation.

 

3) You focus on tissue-specific mTOR stimulation,  but what about IGF-1?    IGF-1 promotes cell proliferation and differentiation and inhibits apoptosis, potentially increasing tumor growth IGF‐1 inhibition down-regulates growth pathways and up-regulates autophagic and apoptotic pathways,  increasing resistance to multiple toxic agents, and increasing genome stability (Fontana, 2015),  

 

Protein restriction lowers IGF-1 (along with mTOR), potentially inhibiting tumor growth.  This anti-cancer  effect of protein restriction is independent of body weight and body fat content (Fontana, 2008).   Furthermore,  IGF-1 down-regulation has important anti-aging effects apart from specific anti-cancer effects.  We also know that exercise (in lean people) increases IGF-1. 

 

According to Valter Longo, "high consumption of protein before age sixty-five is associated with a 75 percent increase in risk of death and a fourfold increase in risk of death from cancer."  (The Longevity Diet, Kindle Locations 993-994)

 

Do you believe that resistance training/CE/hormetics etc. can counteract those negative aspects of high protein intake?  Is it worth the risk?

 

 

References:

 

Fontana et al. (2008)  "Long-term effects of calorie or protein restriction on serum IGF-1 and IGFBP-3 concentration in humans"   https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2673798/

 

Fontana et al. (2015) "Effects of 2‐year calorie restriction on circulating levels of IGF‐1, IGF‐binding proteins and cortisol in nonobese men and women: a randomized clinical trial"   https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4717266/

Edited by Sibiriak

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Mccoy: I would have expected more growth, that's why I'm thinking about high AMP-kinase activity and a tendency of my metabolism to attenuate mTOR activity.

 

Well, AMPK is known to inhibit  mTOR and muscle protein synthesis.    [Fujita et al. (2007) "Nutrient signalling in the regulation of human muscle protein synthesis" https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2075348/ ]

 

It could also be that you are simply a low-responder.

 

Role of Ingested Amino Acids and Protein in the Promotion of Resistance Exercise–Induced Muscle Protein Anabolism

Paul T Reidy and Blake B Rasmussen*

J Nutr. 2016 Feb; 146(2): 155–183.
PMCID: PMC4725426
 

Unfortunately, only 2 of ∼50 studies actually showed the individual responses after protein supplementation and RET 9 [resistance exercise training]  186, 196). This is unfortunate because there is marked variability in the responses, and useful information for clinical practice could be gained by understanding the reasons behind the variant responses. We pooled the data from our laboratory and the 2 previously described studies (186, 196) and another study in a milk-protein-only group (94) to generate a diagram of the individual responses in whole-body lean mass after RET with protein or carbohydrate supplementation (Figure 3A, B).

 

Although the exercise-training protocols and the protein type given (blend, whey, or milk protein) were diverse, the pattern of magnitude of the change and especially the extreme variability in the change was remarkably similar across studies, so we pooled the data into 2 groups (protein and carbohydrate) (Figure 3A). The variability in the response is remarkable, and it is clear that some individuals do not respond to protein/AAs (Figure 3A, bottom left) and some natural responders do quite well, even with carbohydrate, and are likely to experience minimal benefit from protein/AAs (Figure 3A, top right). These groups represent a third of the sample who experience minimal to no effect of protein/AAs 

 

[…]it is very doubtful that protein/AAs or any form of nutritional supplementation can turn a low responder into a high responder.  (Reidy et al.  2016)

 

There is also the issue of diminishing returns with increased training.

 

It is well known that physiologic adaptation to a given stress changes over time. What is clear is that the “law of diminishing returns” exerts a strong precedent on the acute MPS response as an individual becomes more trained (199). Interestingly, this effect has been suggested to occur rather quickly (102, 253). These data could theoretically suggest that the “upper limit” or “set point” of hypertrophy is approaching and that various mechanisms may start to attenuate the anabolic response. (Reidy et al.  2016)

 

Even untrained persons quickly hit a hypertrophic plateau:

 

The longest-running RET and protein supplement study in young  adults to date evaluated participants at 12, 24, and 36 wk of a periodized RET program (186). In contrast to popular belief, the authors showed that lean mass gain clearly reached a plateau at  12 wk with protein and further supplementation throughout a progressively difficult RET program had no additional effect. A similar pattern was shown when using ultrasound to assess  muscle thickness at 10.5 and 21 wk of progressive RET and protein supplementation (200). Collectively, these data suggest a slowing or limit of muscle growth (hypertrophic plateau) at 6–12 w of RET, even when using untrained participants. This duration coincides with the time course of muscle hypertrophy (201, 202), indicating that 90% of the muscle hypertrophy occurs in the first 2 mo of RET.   (Reidy et al.  2016)
Edited by Sibiriak

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Hi Sibiriak, glad to see you have reasoned about this vital topic, here are furthed considerations, I'm going to answer with multiple posts since it's going to be easier to me to organize answers in such a way.

 

 

Basic point is that official RDAs are already cautious values, that is are probably amounts in ecess of the minimum requirement.

 

So it makes perfect sense that Longo does not reccomand more than the RDA. Let's remind that this reasoning is rigorous only for 97.5% of the population, so exceptions are possible. Longo However considers a pescetarian diet, so animal protein is included in his guidelines, which are not meant to be strictly for vegan groups.

 

At this point, we should consider the subpopulation of Vegan individuals. The Randd et al., 2003 study on RDAs (the metanalysis upon which the official values have been taken, which are also considered by Longo himself) considers mixed diets, that is diets which both animal and plant-based proteins. So his conclusions are not necessariy true for vegans.

As I reported in the OP, some literature sources, which Brenda Davis and Velina Monsanto cite in their treatise "Becoming Vegan", point out that plant based proteins seem to be less digestible, so a vegan RDA for protein would be 0.9 g/kg/d, or even 1 g/kg/d. So when speaking about a purely vegan diet, these should be the reference values (I can trace the original articles but not now).

 

So, the premise for all the following considerations is that if the starting point is the RDA, or something below the RDA, closer to the average value, such a benchmark is different if only plant-based proteins are ingested (RDA +10 to 20%). I consider my personal RDa to be 1 g/kg/d only by personal observation of my difficulties in gaining weight and the ease by which I loose weight. An index of poor absorption or high subjective nutrient requirements.

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Re. additional or inclusive 30 g/day. The part you underlined in red leaves no doubt, so 30 additional grams as a post workout meal is not his suggestion, that remains a suggestion for strict bodybuilders in bulking mode.

 

Your explanation about the reason why those 30g (/leucine trigger) makes sense to me.

 

My present RDA of 1.5 g/kg/day lies within the 1.3 to 1.9 g/kg/day for vegan strength athletes. Although I'm by no means a strength athlete, I'm doing regular resistance plus aerobic exercise which might involve intense amminoacids breakdown and utilization (my almost always sore muscles testify to that!). Since my present target is to increase muscle mass, I'm trying to understand if a constraint was given by protein requirement. In a few words, by eating lots of protein, I can subjectively eliminate a potential constraint to muscle growth. By springtime I'll start back my cycles of FMD, cease cold exposure and most probably be back to a more moderate regime of calories and proteins.

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Mccoy:  As I reported in the OP, some literature sources, which Brenda Davis and Velina Monsanto cite in their treatise "Becoming Vegan", point out that plant based proteins seem to be less digestible, so a vegan RDA for protein would be 0.9 g/kg/d, or even 1 g/kg/d. So when speaking about a purely vegan diet, these should be the reference values

 

 

 

Your point about pure vegan diet protein requirements is  a good one.   As a matter of fact, I have the book "Becoming Vegan  The Complete Reference to Plant-based Nutrition"  by Brenda Davis and Vesanto Melina (I avoid Monsanto like the plague),  and I'll take another look at it.

 

It does makes sense that a vegan's  0.9-0.1 g/kg/d  would be  roughly equivalent to an omnivore's .07-.08 g/kg/day  and I appreciate your stressing that point.

 

My main concern, however, is with the question of whether or not higher strength-athlete-recommended levels of protein + high volume resistance training can be justified from a long-term health and longevity standpoint.   

 

You've made it clear now that you intended to return  in springtime to a "more moderate regime of calories and proteins" .  That answers, at least in part, my  question in a previous post:  "Are you engaging in intermittent stimulation of IGF-1, mTOR  etc. (periods of general growth and proliferation mode), conserving muscle gains with (reduced) resistance training alone during periods of down-regulated growth factors (periods of repair and maintenance mode)?"

Edited by Sibiriak

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Dr. Attia and others who are pursuing the same aim (maximizing muscle growth while avoiding the downsides of increased protein intake) have adopted a strategy of  taking 3-5 grams of free form leucine during resistance training workouts.  https://www.ihmc.us/...alk/episode001/   [25:19]

 

I noticed that you adopted that strategy as well for a short time, then dropped it.    Dr. Attia points out that it is quite “challenging to hack the system”, and he argues that high protein intake should be avoided and that  pure leucine supplementation is necessary for muscle-tissue specific mTOR activation. So I’m wondering why you don't think Attia's approach is necessary, given that you share his goal of  tissue-specific mTOR activation.

 

I simply reasoned that there is a risk of unreported side effects which I do not accept, given the fact that it's not an urgent necessity to me to gain muscle mass, I'll take my time.

 

Artificial leucine causes a transitory, hi-intensity peak in the blood which is not observed with natural leucine. The unnatural peak may be deleterious, who knows. Sure I've no risk appetite to that regard.

 

Some higher protein intake is probably  necessary to provide the raw material to build new muscle tissue or make the existing one grow or to repair the one damaged by exercise.

 

Also, I reason that when there is a strong growth signal driven by the mechanoreceptors in the muscles and bones, by the virtue of adaptive response that becomes a priority with respect to the organs, so it makes sense that the abundance in Leucine and other amminoacids is sequestered by muscle and bones, not organs

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Mccoy:  I'm trying to bulk as much as it's possible with light weights, stimulating mTOr by metabolic stress.

 

Why aim for maximal muscular hypertrophy?  If it’s for strictly aesthetic reasons, okay.    But you suggested you were trying to maximize muscle mass as a buffer against sarcopenia in old age.

 

I’m wondering what evidence is there that  during middle age RDA levels of protein intake (or the increased vegan versions)  + moderate resistance training are not sufficient to maintain a reasonable amount of muscle mass heading into old age?   Why not wait until one is 65+ years old before increasing protein intake levels,  as recommended by Longo and others?   Is it really necessary to bulk up in one’s 50s or earlier in order to avoid old age sarcopenia?   Maybe it is, but I’d like to see some scientific evidence to back up that idea.   Which longevity experts are promoting that notion?

 

Michael Rae makes an interesting point about sarcopenia:

 

sarcopenia is not a simple problem of loss of muscle mass, but of muscle structure and function as well. CR, in mice, rats, and nonhuman primates, preserves that low level of mass steadily with age, whereas in AL it goes down; and, CR preserves the structure (fiber breakage, mitochondrial deletions, neuromuscular junctions) and function (strength output per unit mass) of that muscle, whereas aging causes a steady erosion, even in master athletes.

 

If you want to gain muscle mass in advanced age, you can always exercise, eat more, and up your protein then, but there's no way (yet) to get back the lost structure and function: you can (as yet, and only if translatable, blah blah blah) only reduce its deterioration in the first place it with CR.

 

http://www.longecity.org/forum/topic/41691-low-protein-the-real-way-to-go/?do=findComment&comment=417605

 

 

Whether or not CR in humans does everything MR claims,  it’s certainly true the age-related muscular decline involves far more than just the loss of muscle mass.  He also may be wrong that there is no way to get back "lost structure and function"--but that would surely involve more  than a hypertrophy-oriented resistance exercise program.

 

In an earlier thread I wrote: "… it's important to keep in mind that as we grow older  what really matters is the loss of functional ability brought about by the loss of strength, power, agility, balance, coordination flexibility etc.  The loss of muscle mass is involved in that, of course,  but strength and power, for example,  are not strictly determined by muscle mass,  and resistance training (including neuromuscular training) for functional strength /power uses  different methods than resistance training  strictly for muscle hypertrophy."  https://www.crsociety.org/topic/11905-weight-gaining-while-on-cr/page-2?do=findComment&comment=22927

 

Longitudinal Muscle Strength Changes in Older Adults: Influence of Muscle Mass, Physical Activity, and Health

 

https://academic.oup.com/biomedgerontology/article/56/5/B209/554584

 

The total amount of muscle is a major determinant of the force-generating capacity of the muscle, as demonstrated by the high correlation between muscle mass and strength in a cross-sectional analysis (4). This has led some to conclude that the loss in muscle strength is due entirely to the loss in muscle mass (30). However, a significant association between the change in muscle strength and mass with exercise training or restricted activity is rarely observed (31)(32). This, along with the finding of disproportionately greater loss of strength compared to lean tissue declines over 11 to 15 years and no correlation between muscle strength and fiber area changes (7)(10), suggests that other neuromuscular changes may mediate muscle strength change. In our cohort, muscle mass changes explained a small (5%) part of the variance in knee strength.   Because only a small amount of the variance in strength was explained by muscle mass loss and because of the lack of association with physical activity, there is a need to explore the relative contribution of other cellular, neural, or metabolic mediators of changes in muscle function.

.

 

The Loss of Skeletal Muscle Strength, Mass, and Quality in Older Adults: The Health, Aging and Body Composition Study

https://academic.oup.com/biomedgerontology/article/61/10/1059/600461

 

Conclusions. Although the loss of muscle mass is associated with the decline in strength in older adults, this strength decline is much more rapid than the concomitant loss of muscle mass, suggesting a decline in muscle quality. Moreover, maintaining or gaining muscle mass does not prevent aging-associated declines in muscle strength.

 

 

Although it has been postulated that reduced muscle mass plays a major role in the age-related decline of strength (9,32,33), in this large cohort of older adults, initial lean mass and changes of lean mass could explain only a small portion (5%) of variability of strength decline. Moreover, even individuals who maintained their lean mass became weaker, and individuals gained weight and lean mass did not become stronger as might have been expected. This finding further suggests that alterations in muscle quality play a role in the loss of strength in old age. Hughes and colleagues (29) also reported that changes in muscle mass explained only 5% of the changes in strength.

 

The loss of strength in these older men and women was much more rapid than the concomitant loss of muscle mass, suggesting a significant decline in the quality of muscle. Additionally, individuals who maintained or even gained lean mass were not able to significantly prevent their loss of strength. Although it may be important to preserve lean mass to prevent strength decline in old age, a considerable amount of the age-dependent strength decline is not explained by the loss of muscle mass alone. Therefore, we can put forth an alternative hypothesis that, in addition to muscle quantity, muscle quality may be an important determinant of loss of strength with aging. Further studies are required to identify other risk factors for the decline in strength with aging so that more targeted interventions can be planned to prevent or slow the decline, thus maintaining overall function of older men and women.

 

Increases in  strength come from increased muscle fiber size, neurological changes in muscle fiber activation, inter-muscular coordination,  skill development, etc.    Hypertrophy is only one of those elements, and not necessarily the most important one.  Furthermore,  there are two very different types of muscular hypertrophy.

 

Science and Practice of Strength Training-2nd Edition

By Vladimir Zatsiorsky, William Kraemer

 

http://fpio.org.ru/data/50-powerlib//Science_and_Practice.pdf

http://www.humankinetics.com/products/all-products/science-and-practice-of-strength-training-2nd-edition

 

The two extreme types of muscle fiber hypertrophy can be schematically depicted: sarcoplasmic and myofibrillar hypertrophy (figure 3.2). Sarcoplasmic hypertrophy of muscle fibers is characterized by the growth of sarcoplasm (semifluid interfibrillar substance) and non-contractile proteins that do not directly contribute to the production of muscular force.   Specifically, filament area density in the muscle fiber decreases, while the cross-sectional area of the muscles fibers increases, without any accompanying increase in muscular strength.

 

Myofibrillar hypertrophy is an enlargement of the muscle fiber as it gains more myofibrils and, correspondingly, more actin and myosin filaments.

 

[…] Contractile proteins are synthesized, the proteins link to form new filaments, and filament density increases.  This type of hypertrophy leads to increased muscle force  production.

 

[…]sarcosplasmic hypertrophy is typically seen in bodybuilders.

 

According to Zatsiorsky, Kraemer and many others,  the kind of low-load /high volume resistance exercise protocol you seem to be following is most likely going to to involve  sarcoplasmic hypertrophy more than myofibrillar hypertrophy—which means at best you will be getting and increase in muscular mass with little increase in functional muscular strength.

Edited by Sibiriak

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Mccoy: Also, I reason that when there is a strong growth signal driven by the mechanoreceptors in the muscles and bones, by the virtue of adaptive response that becomes a priority with respect to the organs, so it makes sense that the abundance in Leucine and other amminoacids is sequestered by muscle and bones, not organs

 

All that still seems highly speculative to me.  Reasonableness is not evidence.   Why risk losing the  well-evidenced anti-cancer /anti-aging effects of a low-protein diet as advocated by Longo, Fontana et al. by consuming nearly double the RDA for protein intake,  especially when maximal muscle hypertrophy in middle age is probably not going to provide any great dividends when one hits old age?

Edited by Sibiriak

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Mccoy: Also, I reason that when there is a strong growth signal driven by the mechanoreceptors in the muscles and bones, by the virtue of adaptive response that becomes a priority with respect to the organs, so it makes sense that the abundance in Leucine and other amminoacids is sequestered by muscle and bones, not organs

 

All that still seems highly speculative to me.  Reasonableness is not evidence.   Why risk losing the  well-evidenced anti-cancer /anti-aging effects of a low-protein diet as advocated by Longo, Fontana et al. by consuming nearly double the RDA for protein intake,  especially when maximal muscle hypertrophy in middle age is probably not going to provide any great dividends when one hits old age?

 

 

I agree Sibiriak that it's all speculative but literature articles really do not agree on all aspects. In lieu of a consensus I have to navigate by hypotheses. Also, I'm still in an experimental and transitional stage and started this pure plant-based diet since a short time. I didn't want to loose weight so I'm rather exceeding in the direction of caloric abundance but qualitative restriction.

 

I'm not advocating a very high intake of plant based protein but pls refer to the other post where absorption of nuts was questioned. The result on myself of this abundance of vegetable protein was not such an awesome muscular growth, although the muscles seem to be a little more bulging. After this phase I'll probably try and calibrate the protein intake decreasing it gradually.

 

I'm using soymilk plus pea protein and that way it's pretty easy to add up to conspicuos amounts of protein. Spinach and broccoli are also big providers of protein.

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Sibiriak, what about strenght and mass loss. I do what I can. I am 57, have an inguinal hernya, haven't been training for 27 years due to misterious abdominal pains which recently ceased and still suffer joint and cartilage nagging aches because of forced inactivity.

But I'm feeling alive again. Whatever comes, a little mass, a little strenght, both, is welcome. Sure physical activity invigorates and improves stamina and well being and, in my case, optimism in life.

 

In general, I agree that functional strength is what matters and that should be relatively easy to mantain or even improve together with a reasonable CR regime.

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Mccoy,  yes,  optimism in life is supremely important, and we all must find our path.   All paths lead to nowhere, so optimism along the way may be the ultimate aim.

 

Please take my posts as a kind of "thinking out loud".    I have no certainty in any of this.  I was intrigued by the dea that if one combines higher protein intake with resistance training etc. one might be able to avoid the pro-cancer, pro-ageing effects of the protein-stimulated IGF-1 and mTOR upregulation.   I'm referring to the selective-tissue mTOR stimulation  ("targeted anabolism") idea you've talked about in various posts.

 

Mccoy: (Jan 2017) ...if practicing CR or protein optimization, mTORC1 would stay downregulated in the other tissues, allowing a targeted anabolism without extending the anabolic state to the whole system.

 

https://www.crsociety.org/topic/12036-new-section-on-physical-exercise-for-longevity/page-2?do=findComment&comment=20128

 

Mccoy: (October 2016) My present obsession is to gain muscle weight at the same time keeping off the anabolic, anti-longevity signals of IIS and mTOR. Easier said than done. When much younger and a gym rat, I was able to build conspicuos muscle by eating lots of ricotta cheese, rich in anabolic whey proteins, and eggs. Plus natural carbs like honey, fruit and fruit juice.

 

The above of course would irremediably trigger the main metabolic pathways we know are NOT conducive to longevity. 

 

Now, after having lost much of the former muscle due to forced inactivity, what I'm trying to do (this is an ongoing experiment) is to upregulate mTORC1 in muscle tissues, simply by supplying them with more protein than the minimum required at rest. So I lift weight at 60-70% my maximum load (maximum liftable weight single repetition), trying to stimulate muscle protein synthesis (MPS). Arguably, this is not the same as stimulating growth and reproduction (which would necessarily thwart longevity). Conceptually, we are stimulating the functional requirements of the body, which adapts itself to environmental demands by growing muscle cells, sequestering the excess proteins (amino acids, especially leucine) before they reach organs and other tissues.

 

The above is what I understand at present. I may be wrong, hopefully not too much. The tricky part is to estimate how much additional protein is needed to allow MPS without upregulating IGF-1 and mTOR in non-muscle tissues. 

 

That's tricky before we should estimate first our at-rest minimum proteins requirement, then our additional protein requirement because of exercise. It's a biochemical juggler's work.

 

https://www.crsociety.org/topic/11905-weight-gaining-while-on-cr/?do=findComment&comment=19127

 

 

Fascinating ideas--that's why I've been grilling you on them a bit.  If you are going to do this experiment, I do think it would be worthwhile to monitor IGF-1 levels.

 

In any case, I personally would need more empirical evidence before embarking on such a program.  I've kind of settled on the Longo, Fontana et al. low-protein during middle age/possibly increase after 65years approach.

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Sibiriak, probably what you are doing, following Longo's and Fontana's suggestions is the best. Actually, since the RDA in a mixed-diet, average activity person is very cautious, you might aim for about 0.6 g/kd/d (the median value in Randd et al. distribution), making sure that the following points are respected:

  1. Make sure all essential amminoacids' RDAs are met (EAAs are used in many metabolic functions)
  2. moderate, but not restrict (that is, stick to just the RDA) leucine, methionine and tryptophan, the thre EAAs which have been shown to directly contribute to proliferation and growth. 
  3. monitor your bodyweight and muscle mass strictly. Then adjust total proteic intake upward if necessary or even downward if there is not a suboptimal condition, at teh same time following the above 2 points.
  4. Allow for your usual quota of low GI carbs

# 3 is tricky because you cannot know when your zero nitrogen balance is reached, altough bodyweight and muscle mass should be a good proxy.

 

I'm planning to do the above but starting from my present intake and allowing for muscle tissue wear and tear plus some growth if possible. It's going to be a long issue but I'm not in a hurry.

 

In your case you are definitely not growing muscle, but you can become exceptionaly shredded.

Edited by mccoy

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Again on quantity of protein in a vegan diet. I'm noticing that when I eat spinachs (usually 500 g or 1.1 pounds) that becomes the main contributor to cronometer (about 20 g of protein). Broccoli are also another good source of protein.

 

The above added to nuts & seeds, cereals, beans and soy products, mushrooms, I find I'm daily exceeding my RDA of a substantial amount, even when not employing pea protein powder.

 

I'll have to redesign my diet, the fun goes on...

Edited by mccoy

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