• Log in with Facebook Log in with Twitter Log In with Google      Sign In    
  • Create Account
  LongeCity
              Advocacy & Research for Unlimited Lifespans

Photo
- - - - -

High Starch, High MUFA Diet, Moderate Protein

diet longevity monounsaturated fat carbs low protein starch health

  • Please log in to reply
22 replies to this topic

#1 Sith

  • Guest
  • 161 posts
  • 5 â‚®
  • Location:Birmingham
  • ✔

Posted 29 April 2017 - 12:57 AM


Hey everyone!

 

 

Diet seems to be a grey area on this forum, but I would appreciate some evidence based help for my dietary approach. I wanted an analysis of my daily diet as it would really help me and my quest of longevity as many of you understand.  :)

 

So my dietary emphasis is on carbs; complex, high-starch carbs. As well as this, I have a diet rich in monounsaturated fat from olive oil and avocados: this is a staple of my diet. I have a low protein intake usually from beans, legumes and fish- my protein intake is moderate to low. My diet is largely plant-based with around 2 oily fish servings a week. 

 

What is everybody's opinion of this? Can complex carb and MUFAs co-exist? Are they compatible for longevity?



#2 HaplogroupW

  • Guest
  • 101 posts
  • 67 â‚®
  • Location:Flyover country
  • NO

Posted 29 April 2017 - 07:10 AM

I'm shifting into the camp that thinks high-carb (even complex carb) diets are dangerous. I'll let Tim Noakes explain why:

 

https://www.youtube....h?v=lGKX8HoNb-0

 

I posted this on another thread, but I think it's apropo here too.

 

 

I suggest looking into a ketogenic diet (https://www.reddit.com/r/keto/wiki/faq). Your olive oil and avocados will be right at home there.


  • WellResearched x 1

sponsored ad

  • Advert
Click HERE to rent this advertising spot for NUTRITION to support LongeCity (this will replace the google ad above).

#3 Sith

  • Topic Starter
  • Guest
  • 161 posts
  • 5 â‚®
  • Location:Birmingham
  • ✔

Posted 01 May 2017 - 12:55 PM

I have looked into Keto in the past, but I'm not convinced. The advice on saturated fat consumption is unfounded and may even be dangerous. The longest lived populations on earth have low to mediocre fat consumption and their diet is based primarily on carbohydrates; with low protein.

Ketogenic diet may have small studies supporting it, carbohydrate based diets have entire epidemiological studies supporting them.


  • Good Point x 2
  • Ill informed x 1

#4 tunt01

  • Guest
  • 2,308 posts
  • 414 â‚®
  • Location:NW

Posted 01 May 2017 - 01:28 PM

IMO, Tim Noakes is not a reliable source of information about longevity and long-term outcomes of dietary and lifestyle decisions.  The guy has a PhD in exercise sciences.  He has recommended LCHF in post-weaning infants, which is flipping moronic and ignorant of basically all modern research on early infant life.  I'd be extremely wary of what he is saying without specific data on the long-term outcomes.

 

I think a lot of keto acolytes fall into the trap of short-term biomarkers, that they just assume will lead to improved long-term outcomes.  There really isn't any data and it's certainly a gamble.


Edited by prophets, 01 May 2017 - 01:31 PM.

  • like x 2

#5 misterE

  • Guest
  • 1,035 posts
  • -76 â‚®
  • Location:Texas
  • NO

Posted 10 May 2017 - 02:28 PM

I think fat and carbs don't mix well, especially unsaturated-fats, which compete for oxidation of glucose more so than saturated-fats. I tend to think of fats more of a treat, than as a primary fuel source... the primary fuel source is starch  :)


Edited by misterE, 10 May 2017 - 02:29 PM.

  • Informative x 1
  • dislike x 1

#6 mccoy

  • Guest
  • 162 posts
  • 33 â‚®
  • Location:Italy

Posted 20 May 2017 - 09:36 PM

What is everybody's opinion of this? Can complex carb and MUFAs co-exist? Are they compatible for longevity?

 

 

Why they shouldn't? As long as your carbs and fats are healthy (EVOO and avocados are). Hi-carb, Hi-fat, Low-protein is not a nutritional geometry much discussed. But low protein is definitely very compatible with longevity. I would just make sure there is plenty of fiber in the diet.

 

That geometry is the one I'm practicing now. I switched from moderate carbs, Hi-fat, Low protein to higher carbs. My fat intake has maybe more variation than yours in that I eat SAFAs (from cacao and chocolate), MUFAs from all kinds of nuts & seeds, lots of EVOO, PUFAs from seeds and n-3 from flaxseed (you take it from oily fish). 

 

The diet you are following is maybe similar to the longevity diet described by the well-known biogerontologist Valter Longo (pescovegan, negligible cheese) in his recent book and similar to some mediterranean diet variations, with lots of EVOO.


Edited by mccoy, 20 May 2017 - 09:38 PM.

  • like x 1

#7 LucasT

  • Guest
  • 17 posts
  • 7 â‚®
  • Location:Germany
  • NO

Posted 21 May 2017 - 08:48 AM

As long as you are calorie restricted and getting your micros, you can chose your carb/fat ratio as you prefer. For the protein part, and Im assuming that you believe the low protein part is necessary (Im not very convinced), it depends on your age.

Honestly, if I were to base my diet aiming for longevity, I would do it more ketogenic-like.


Sent from my iPhone using Tapatalk
  • Agree x 1

#8 LucasT

  • Guest
  • 17 posts
  • 7 â‚®
  • Location:Germany
  • NO

Posted 21 May 2017 - 08:52 AM

IMO, Tim Noakes is not a reliable source of information about longevity and long-term outcomes of dietary and lifestyle decisions. The guy has a PhD in exercise sciences. He has recommended LCHF in post-weaning infants, which is flipping moronic and ignorant of basically all modern research on early infant life. I'd be extremely wary of what he is saying without specific data on the long-term outcomes.

I think a lot of keto acolytes fall into the trap of short-term biomarkers, that they just assume will lead to improved long-term outcomes. There really isn't any data and it's certainly a gamble.


I agree, Tim Nokes has lost any credibility. He is just a keto zealot.

Re: biomarkers. What are the ones you are talking about? Unfortunately, in nutrition, we rely mostly on short-term biomarkers…


Sent from my iPhone using Tapatalk

#9 mccoy

  • Guest
  • 162 posts
  • 33 â‚®
  • Location:Italy

Posted 22 May 2017 - 06:55 PM

Honestly, if I were to base my diet aiming for longevity, I would do it more ketogenic-like.

 

Is that based upon gut-feeling or credible literature ? Pls note I believe that sometimes gut-feeling is better than literature. Also, I do not consider credible literature the articles where the authors are sponsored by the industry.

 

Fact is that a true ketogenic diet must contain lots of fats. Are there any random trials on humans on such kind of diets and what happens in the long run? 

 

An hi-protein keto diet is probably not keto because of gluconeogenesis. Hi protein has been suggested by credible literature to pose  problems and I'm not speaking about kidney problems. Although it is not clear what hi-protein means. Minimum protein requirement is a function of the individual and varies within the same individual with time. It is probably anything above 2*RDA, maybe 1.5*RDA is also high in most people who don't workout. I'll remind that RDA is presently 0.8 g kg-1d-1 and has not been revised since many years. RDA is meant to be, by its definition, already an high (cautious) value.



#10 LucasT

  • Guest
  • 17 posts
  • 7 â‚®
  • Location:Germany
  • NO

Posted 24 May 2017 - 10:18 AM

 

Honestly, if I were to base my diet aiming for longevity, I would do it more ketogenic-like.

 

Is that based upon gut-feeling or credible literature ? Pls note I believe that sometimes gut-feeling is better than literature. Also, I do not consider credible literature the articles where the authors are sponsored by the industry.

 

Fact is that a true ketogenic diet must contain lots of fats. Are there any random trials on humans on such kind of diets and what happens in the long run? 

 

An hi-protein keto diet is probably not keto because of gluconeogenesis. Hi protein has been suggested by credible literature to pose  problems and I'm not speaking about kidney problems. Although it is not clear what hi-protein means. Minimum protein requirement is a function of the individual and varies within the same individual with time. It is probably anything above 2*RDA, maybe 1.5*RDA is also high in most people who don't workout. I'll remind that RDA is presently 0.8 g kg-1d-1 and has not been revised since many years. RDA is meant to be, by its definition, already an high (cautious) value.

 

 

Well, I would say its a mix between them. Evidence-based gut feeling if you might. Im just basing my recommendation on biochemistry and bioenergetics. 

 

The high-protein-anti-keto link is not so straight forward. It depends on a lot of stuff. The metabolic response to fasting (and by extension, ketotic state) is the absence of exogenous glucose. If you fast, do exercise or both, you can consume more protein without being kicked out of ketosis. Then there are the levels of ketosis that you might (or want) achieve. For treatment of certain diseases, then yes you might have to eat more fat to induce ketosis and maintain weight (energy balance). For life-extension purposes, I don't think you need so much, as you should be calorie-restricting anyways. 

 

What are you referring with "credible literature suggesting problems of high protein"? The IGF-1 link?



#11 mccoy

  • Guest
  • 162 posts
  • 33 â‚®
  • Location:Italy

Posted 24 May 2017 - 10:30 AM

 

What are you referring with "credible literature suggesting problems of high protein"? The IGF-1 link?

 

 

yes, all the body of literature which points out to higher mortality and especially higher prevalence of degenerative disease from excess of protein.


Edited by mccoy, 24 May 2017 - 10:30 AM.


#12 LucasT

  • Guest
  • 17 posts
  • 7 â‚®
  • Location:Germany
  • NO

Posted 24 May 2017 - 11:12 AM

 

 

What are you referring with "credible literature suggesting problems of high protein"? The IGF-1 link?

 

 

yes, all the body of literature which points out to higher mortality and especially higher prevalence of degenerative disease from excess of protein.

 

 

Most literature is observational, which I wouldn't use for inferring that a particular group of foods is bad. Eating a lot of processed meat on top of high sugar/high fat diet (SAD) is different than eating only meat with vegetables. Epidemiological observations only go to some point. 

 

Re: the protein-IGF-1 link. I don't see how you think that might be "credible" (but not other sources, that I guess are not credible because they show the opposite of what you believe). It basically comes from Longo, who has interests in his FMD. Not saying that its necessarily flawd, though. But its good to keep that in mind, taking into account that IF seems to reduce IGF-1 levels even when consuming around 2g/kg of protein per day

 

More problems with Longo's interpretation:

 

https://www.facebook...hc_location=ufi



#13 mccoy

  • Guest
  • 162 posts
  • 33 â‚®
  • Location:Italy

Posted 24 May 2017 - 08:04 PM

Lucas T, the Levine et al. article sure has some gaps, the main one I believe the use of the NHANES database with a 24 hours recall. It is not reasonable that such recalls can be representative of years of dietary habits. 

Also, I'm pretty much skeptical about the 65 years threshold for larger need of protein (why such precision?). Also, the low-protein group has a very small numerosity compared to the others hence carries little statistical representativity, unless the CI includes the effect of small sample size, honestly right now I can't tell that.

 

Pls note though that the critic by Phillips is signed by authors like Donald Layman, who are sponsored by, guess who: the beef industry, the eggs industry, the dairy industry,  in a few words by the very guys who have the highest interest in selling their protein. Animal protein.

 

At this point I believe I should produce randomized double blind trials (if there are any) but I have no time now unfortunately, I wish I were retired or that I had no other commitments. I love to geek it out but sometimes I geek it out in too may fields. Suffice it to say that I agree in part that meat with lots of vegetables may not be unhealthy, if consumed in moderation. One of the reasons not to exceed with protein is thought to be a mechanistic one: the mTOR pathway that, if chronically amplified, might prevent autophagy and enhance proliferation whit subsequent cancer growth and degenerative disease. Nobody knows with precision the activation threshold for mTOR, unless biopsies in the relevant tissues of the individual are made and lab tests carried out to measure phosphorylation ratio of mTOR protein.

Also, do not let's forget that the RDA is not the average or median minimum requirement, is the 97.5% of the normal distribution of minimum requirements, which means that it is a number which guarantees from deficiencies almost all population (actually, a sample of n=235 people). Twice the RDA means that we are far above the possible minimum requirements measured in a sample of 235 people eating different diets from different geographical areas. But it deals with minimum requirements, not optimal ones. The issue is a complex one and to date I think it has not been solved.


Edited by mccoy, 24 May 2017 - 08:07 PM.


#14 LucasT

  • Guest
  • 17 posts
  • 7 â‚®
  • Location:Germany
  • NO

Posted 26 May 2017 - 07:55 AM

One of the reasons not to exceed with protein is thought to be a mechanistic one: the mTOR pathway that, if chronically amplified, might prevent autophagy and enhance proliferation whit subsequent cancer growth and degenerative disease. Nobody knows with precision the activation threshold for mTOR, unless biopsies in the relevant tissues of the individual are made and lab tests carried out to measure phosphorylation ratio of mTOR protein.

 

This is a very simplistic view of cell signalling. You know what else activates mTOR? Glucose and energy. You could argue that a high carb diet, by promoting higher levels of insulin, will also activate mTOR chronically. mTOR is not bad as AMPK is not good, they are both necessary. 

 

Overall, I think that there should be a balance between activation and inhibition of mTOR, and this should be achieved by fasting-feeding cycles. This, of course, its not what happens with current recommendations in for instance, the fitness field, in which there is an increasing interest of promoting pre-sleep protein ingestion.

 

What do you mean with "Nobody knows with precision the activation threshold for mTOR"? If you are referring to threshold for amino acid ingestion I doubt there will be one and its irrelevant. Its very context dependent (and organ dependent) and I doubt there is a difference between 30% activation vs. 60% activation (for example). As long as you have periods of low mTOR activity (and high AMPK) it should be fine. 



#15 mccoy

  • Guest
  • 162 posts
  • 33 â‚®
  • Location:Italy

Posted 26 May 2017 - 11:16 PM

 

 

This is a very simplistic view of cell signalling. You know what else activates mTOR? Glucose and energy. You could argue that a high carb diet, by promoting higher levels of insulin, will also activate mTOR chronically. mTOR is not bad as AMPK is not good, they are both necessary. 

 

 

I agree that view is sure simplified. And sure mTOr is necessary, only at death it becomes totally inactive and high doses of rapamycin suppress the immune system dowregulating mTOR too much. here are 2 possible scenarios.

 

  1. Low-protein, hi-carb scenario: AMPK is high, insulin may be high but actually is moderate in pre-diabetics. IGF-1 is lowish. The leucine signal is low. This means that few molecules of the mTOR complex are attracted to the lysosome surface and can be phsophorylated(activated). Hence, this is a condition where mTOR activity si low (phosphorylation ratio = phosporylated/unphosphorylated mtOR is low)
  2. Hi-protein, low-carb scenario: AMPK may be low but may not be so low because of gluconeogenesis-derived glucose. Insulin is high because of hi protein. IGF-1 is very high. The leucine signal is high. A moderate AMPK is overwhelmed by a huge IGF-1+Insulin signal and PIPK3-Akt signal. Overall result is an amplified mTOr activity.

 

 

Overall, I think that there should be a balance between activation and inhibition of mTOR, and this should be achieved by fasting-feeding cycles. This, of course, its not what happens with current recommendations in for instance, the fitness field, in which there is an increasing interest of promoting pre-sleep protein ingestion

 

I totally agree, life is a proper balance of growth & proliferation versus repair & manteinance. However, degenerative disease and cancer are prevented by keeping the balance toward repair & manteinance. The fitness field is really a case where strategies to grow muscle at all cost promote an overamplified mTOR activity. 

 

 

 

What do you mean with "Nobody knows with precision the activation threshold for mTOR"? If you are referring to threshold for amino acid ingestion I doubt there will be one and its irrelevant. Its very context dependent (and organ dependent) and I doubt there is a difference between 30% activation vs. 60% activation (for example). As long as you have periods of low mTOR activity (and high AMPK) it should be fine.

 

You are right, I should have written the threshold beyond which mTOR activity may become chronically amplified. As you point out, it's difficult to say which is the optimum activity (phosphorylation ratio) since it depends on organs and tissues and context. Cycles of fasting and refeeding may be good to reach a balance between growth and repair, as well as continuos caloric restriction which stresses repair & maintenance (autophagy) with the drawback of  weightloss and maybe excessively low BMI.


Edited by mccoy, 26 May 2017 - 11:17 PM.


#16 LucasT

  • Guest
  • 17 posts
  • 7 â‚®
  • Location:Germany
  • NO

Posted 28 May 2017 - 08:34 AM

I agree that view is sure simplified. And sure mTOr is necessary, only at death it becomes totally inactive and high doses of rapamycin suppress the immune system dowregulating mTOR too much. here are 2 possible scenarios.

 

  1. Low-protein, hi-carb scenario: AMPK is high, insulin may be high but actually is moderate in pre-diabetics. IGF-1 is lowish. The leucine signal is low. This means that few molecules of the mTOR complex are attracted to the lysosome surface and can be phsophorylated(activated). Hence, this is a condition where mTOR activity si low (phosphorylation ratio = phosporylated/unphosphorylated mtOR is low)
  2. Hi-protein, low-carb scenario: AMPK may be low but may not be so low because of gluconeogenesis-derived glucose. Insulin is high because of hi protein. IGF-1 is very high. The leucine signal is high. A moderate AMPK is overwhelmed by a huge IGF-1+Insulin signal and PIPK3-Akt signal. Overall result is an amplified mTOr activity.

 

This logic is flawed and not based on actual data:

 

1. AMPK is not necessarily high. Glucose increases the NADH/NAD ratio (so indirectly inhibiting AMPK) and promotes higher insulin levels. Additionally, the ratio of NADH:FADH produced by fatty acid oxidation is lower than glucose oxidation. 

 

2. GNG derived glucose doesn't increase blood glucose levels and/or insulin. I dont know where people get these interpretations of basic metabolism. Protein feeding promotes a short term pulse of insulin release, and thats it. As shown in my other post, fasting itself reduces circulating IGF-1 levels even at high protein concentrations and eucaloric conditions, compared to non-fasting. High protein feeding increases GNG, but only to produce sufficient glucose for exclusively glycolytic cells. Replacing protein for carbohydrate at the same level of calories reduces blood glucose and insulin levels. The increase of GNG is marginal, and dietary carbohydrates don´t affect the rate of GNG (so higher carbohydrates dont reduce your rate of GNG significantly; and higher protein dont increase your rate of GNG significantly). 

 

In both cases, if one assumes caloric restriction (which should be happening for life extension purposes), then clearly replacing carbohydrates for fat would be a better option, specially when considering the potential benefits of BHB. 

I totally agree, life is a proper balance of growth & proliferation versus repair & manteinance. However, degenerative disease and cancer are prevented by keeping the balance toward repair & manteinance. The fitness field is really a case where strategies to grow muscle at all cost promote an overamplified mTOR activity. 

 

Yes, no doubt that increasing muscle mass is opposite to life extension, at least at the cellular level. The exception would be the elderly. 

 

You are right, I should have written the threshold beyond which mTOR activity may become chronically amplified. As you point out, it's difficult to say which is the optimum activity (phosphorylation ratio) since it depends on organs and tissues and context. Cycles of fasting and refeeding may be good to reach a balance between growth and repair, as well as continuos caloric restriction which stresses repair & maintenance (autophagy) with the drawback of  weightloss and maybe excessively low BMI.

 

I agree with you, but there is probably no threshold, at least applicable to dietary interventions. And its not as simple as inhibiting mTOR = better health and disease prevention, although a selective mTORC1 inhibitor looks promising, 


Edited by LucasT, 28 May 2017 - 08:35 AM.


#17 mccoy

  • Guest
  • 162 posts
  • 33 â‚®
  • Location:Italy

Posted 29 May 2017 - 01:25 PM

 

I agree that view is sure simplified. And sure mTOr is necessary, only at death it becomes totally inactive and high doses of rapamycin suppress the immune system dowregulating mTOR too much. here are 2 possible scenarios.

 

  1. Low-protein, hi-carb scenario: AMPK is high, insulin may be high but actually is moderate in pre-diabetics. IGF-1 is lowish. The leucine signal is low. This means that few molecules of the mTOR complex are attracted to the lysosome surface and can be phsophorylated(activated). Hence, this is a condition where mTOR activity si low (phosphorylation ratio = phosporylated/unphosphorylated mtOR is low)
  2. Hi-protein, low-carb scenario: AMPK may be low but may not be so low because of gluconeogenesis-derived glucose. Insulin is high because of hi protein. IGF-1 is very high. The leucine signal is high. A moderate AMPK is overwhelmed by a huge IGF-1+Insulin signal and PIPK3-Akt signal. Overall result is an amplified mTOr activity.

 

This logic is flawed and not based on actual data:

 

1. AMPK is not necessarily high. Glucose increases the NADH/NAD ratio (so indirectly inhibiting AMPK) and promotes higher insulin levels. Additionally, the ratio of NADH:FADH produced by fatty acid oxidation is lower than glucose oxidation. 

 

 

Sorry Lucas, My bad, I realize I didn't properly review my post and ended up writing the opposite of what I meant as far as AMPK goes.

 

AMP-kinase is activated by an energy deficit, so of course an hi-carb scenario implies usually a low AMPK. AMPK activates the TSC complex which inhibits the mTOR-activating Rheb signal, as it results clear in the following image. My conclusions stands unchanged though, that is, even if there is energy as glucose+oxygen and in presence of a moderate Insulin signal (high dietary carbs), the lack of a sufficient Leucine signal will result in small mTOR phosphorylation ratio= small mTOR activity. that's the principle of protein moderation or restriction, a subset of the principle of caloric restriction. Also, thanks for the reference to energy from fatty acids oxydation, which I was not considering.

Attached File  12986_2012_Article_466_Fig2_HTML.jpg   55.54KB   1 downloads



#18 mccoy

  • Guest
  • 162 posts
  • 33 â‚®
  • Location:Italy

Posted 29 May 2017 - 07:59 PM

Re: gluconeogenesis. In the article you linked there are a few hints, such as the quoted one, which would suggest an active role of gluconeogenesis in providing available glucose for cell metabolism

 

Hultman and Bergstrom (30) showed that, although extremely slowly, a high-protein diet with a very low carbohydrate content restored glycogen stores.

 

 

 

Now, I do not know in detail the mechanisms of gluconeogenesis but people who follow a strict ketogenic diet (example: Jimmy Moore, the author of 'keto clarity') insist that above a certain individual protein threshold they 'go out of ketosis', attributing such condition to glucose-forming gluconeogenesis, which causes such glucose to be burned for energy instead of fats, and the subsequent drop of ketone bodies in the blood.

 

The fact that dietary carbs do not increase GNG is not relevant to our discussion, since carbs are already available.

The fact that higher protein does not increase GNG: are Jimmy Moore and the other keto practitioners all wrong??

 

Also, in theory low protein, low carb, hi fat (the Ron Rosedale proposal) should keep mTOR at a low level of activity. Insulin remains very low, IGF-1 should be low or moderate, according to protein nature. That constitutes a caloric restriction on its own, the drawback beign that the high fats, especially if saturated, may not be handled well by some people



#19 LucasT

  • Guest
  • 17 posts
  • 7 â‚®
  • Location:Germany
  • NO

Posted 30 May 2017 - 07:35 AM

Re: gluconeogenesis. In the article you linked there are a few hints, such as the quoted one, which would suggest an active role of gluconeogenesis in providing available glucose for cell metabolism

 

Hultman and Bergstrom (30) showed that, although extremely slowly, a high-protein diet with a very low carbohydrate content restored glycogen stores.

 

 

 

Now, I do not know in detail the mechanisms of gluconeogenesis but people who follow a strict ketogenic diet (example: Jimmy Moore, the author of 'keto clarity') insist that above a certain individual protein threshold they 'go out of ketosis', attributing such condition to glucose-forming gluconeogenesis, which causes such glucose to be burned for energy instead of fats, and the subsequent drop of ketone bodies in the blood.

 

The fact that dietary carbs do not increase GNG is not relevant to our discussion, since carbs are already available.

The fact that higher protein does not increase GNG: are Jimmy Moore and the other keto practitioners all wrong??

 

Also, in theory low protein, low carb, hi fat (the Ron Rosedale proposal) should keep mTOR at a low level of activity. Insulin remains very low, IGF-1 should be low or moderate, according to protein nature. That constitutes a caloric restriction on its own, the drawback beign that the high fats, especially if saturated, may not be handled well by some people

 

If you re-read my post, that is exactly what I said. The role of GNG is to provide glycolytic cells with glucose. However, if you are under a fat-based metabolism, then your glucose requirements go down. So overall, even when going down to 2% of carbohydrates in the diet, GNG goes up only 14%. This is because we are talking about a dynamic system.

 

So again, higher protein increases GNG and no one has said that it doesn't, I just said that the increase its not as straight forward in magnitude as suggested by some. If you have to go as high as you can on blood ketone levels, then yes, moderate to low protein is the way to go. But this is only mandatory, IMO, in therapeutic ketogenic diets. And your "protein tolerance" also depends on the amount of physical activity, calorie level, among others, so its not a clear-cut answer.

 

Jimmy Moore is not a reliable source of information, sorry. He is just dogmatic and his income depends on a lot of products he promotes to live a "keto" lifestyle. He promotes eating a lot of fat (fat bombs, etc) that in most people, increases calorie intake which reduce weight loss and/or increases weight, thus having the opposite effect of a healthy diet. He has literally said that eating protein is the same as eating a piece of cake.

 

The Ron Rosedale stuff certainly makes sense but I think you have to see the trade-off. Reducing protein intake (specially without resistance exercise) reduces muscle mass, which is a problem during aging. Muscle mass, among others, is directly responsible for metabolic flexibility, which IMO, should be a goal for everyone. As you mentioned, one way around would be to chose proteins with lower leucine content, but by doing so, you also reduce the sources that give you the best amino acids for muscle mass. Additionally, leucine has also other effects different from mTORC1 activation, such as increasing SIRT1 expression and intracellular NAD+ levels. It promotes mitochondrial biogenesis and fatty acid oxidation in vitro. So certainly there is probably more about it and focusing on just mTOR is missing the forest for the trees.
 



#20 mccoy

  • Guest
  • 162 posts
  • 33 â‚®
  • Location:Italy

Posted 30 May 2017 - 01:28 PM

 

 

So certainly there is probably more about it and focusing on just mTOR is missing the forest for the trees.

 

LOL, it may be so, since the aspect is so fascinating (a single, metabolically powerful protein which has remained almost unvaried thru evolution from yeasts to mammals), and some people are just captured by its utter fascination.

 

What I'm sure realizing is that mTOR is a complex issue, with variability within individuals and within organs and tissues. There is no switching ON/OFF, there is different levels of activity=phosphorylation ratios and alternating low and high activity is probably  needed, chronic amplification is bad, chronic attenuation may be all right or beneficial if moderate, whereas attenuation can be disastrous if excessive.

 

Also, thanks for the links and for reminding that Leucine deficiency might have very detrimental effects, because of its functions as a metabolic signal.

 

I agree with your conclusions that a diet too moderate in proteins might be deleterious. Sure those who follow it should stimulate some mTOR activity in skeletal muscles by resistance exercise, and take advantage to eat more protein.

 

Just to state the obvious: a proper balance is the best and the balance is different across individuals.


Edited by mccoy, 30 May 2017 - 01:30 PM.


#21 LucasT

  • Guest
  • 17 posts
  • 7 â‚®
  • Location:Germany
  • NO

Posted 30 May 2017 - 01:39 PM

 

 

 

So certainly there is probably more about it and focusing on just mTOR is missing the forest for the trees.

 

LOL, it may be so, since the aspect is so fascinating (a single, metabolically powerful protein which has remained almost unvaried thru evolution from yeasts to mammals), and some people are just captured by its utter fascination.

 

What I'm sure realizing is that mTOR is a complex issue, with variability within individuals and within organs and tissues. There is no switching ON/OFF, there is different levels of activity=phosphorylation ratios and alternating low and high activity is probably  needed, chronic amplification is bad, chronic attenuation may be all right or beneficial if moderate, whereas attenuation can be disastrous if excessive.

 

Also, thanks for the links and for reminding that Leucine deficiency might have very detrimental effects, because of its functions as a metabolic signal.

 

I agree with your conclusions that a diet too moderate in proteins might be deleterious. Sure those who follow it should stimulate some mTOR activity in skeletal muscles by resistance exercise, and take advantage to eat more protein.

 

Just to state the obvious: a proper balance is the best and the balance is different across individuals.

 

 

Yes, overall I agree with you. I have no problem with someone eating moderate or low (but adequate) protein. I just like to point plot holes and play devil's advocate, also with my own biases. That is how one's hypothesis and understanding increases. (I am also probably biased towards higher protein because Im interested in body composition and I think its an important part of successful aging. :))

 

I must say, also, that some times the simplicity of the arguments I see for some things (like mTOR) baffles me. It kind of goes with the concept of good-bad, a false dichotomy in biology (for example, insulin sensitivity = good, insulin resistance = bad).



#22 LucasT

  • Guest
  • 17 posts
  • 7 â‚®
  • Location:Germany
  • NO

Posted 05 June 2017 - 10:32 AM



I agree that view is sure simplified. And sure mTOr is necessary, only at death it becomes totally inactive and high doses of rapamycin suppress the immune system dowregulating mTOR too much. here are 2 possible scenarios.

 


  1. Low-protein, hi-carb scenario: AMPK is high, insulin may be high but actually is moderate in pre-diabetics. IGF-1 is lowish. The leucine signal is low. This means that few molecules of the mTOR complex are attracted to the lysosome surface and can be phsophorylated(activated). Hence, this is a condition where mTOR activity si low (phosphorylation ratio = phosporylated/unphosphorylated mtOR is low)

  2. Hi-protein, low-carb scenario: AMPK may be low but may not be so low because of gluconeogenesis-derived glucose. Insulin is high because of hi protein. IGF-1 is very high. The leucine signal is high. A moderate AMPK is overwhelmed by a huge IGF-1+Insulin signal and PIPK3-Akt signal. Overall result is an amplified mTOr activity.

 

This kind of answer part of your scenarios:

 

A 7-day high protein hypocaloric diet promotes cellular metabolic adaptations and attenuates lean mass loss in healthy males

 

PRO-ER: High protein-Energy restricted

CHO-ER: Carbohydrate-Energy restricted

 

Within the PRO-ER group significant pre-post intervention time point difference was observed in PGC-1α (fold increase = 1.27, p = 0.0402), AMPK (fold increase = 2.09, p = 344 0.027), SIRT1 (fold increase = 1.50, p = 0.026) and SIRT3 (fold increase = 1.19, p = 345 0.010) mRNA expression). No time point gene expression changes were observed in any other dietary group (Figure 2 A-E), or in the expression of PPAR mRNA. 

 

figure2.png

These results are corroborated by similar studies investigating the impact of high fat feedings on mitochondrial biogenesis [15, 25]. It was shown that five days on a hypocaloric HF/LC diet positively increased phosphorylation of AMPK and deacetylation of PGC-1α, where as the hypocaloric LF/HC diet negatively reduced the phosphorylation of AMPK and deacetylation of PGC-1α [15]. These results, along with the findings from the current study suggest that high carbohydrate intake prevents the activation of the AMPK-SIRT1 axis that is otherwise observed in a hypocaloric state. Furthermore, and importantly the method of carbohydrate restriction does not seem important, increasing both dietary fat and/or protein result in similar up-regulation of metabolic markers of mitochondrial biogenesis.



#23 mccoy

  • Guest
  • 162 posts
  • 33 â‚®
  • Location:Italy

Posted 05 June 2017 - 07:10 PM

Lucas, 7 days is a pretty short time, which tells us nothing about the long terms effect (sustainability) of high protein and high fats.

 

 

it also remains the fact that Okinawans, who ate 90% carbs in energy, are part of the blue zone populations whereas others who ate almost no carbs (the eskimos) are not. MNaybe I'm speaking of extremes here which are really not applicable to real life.

 

The articles from Solon biot et al. and simpson et al. (on lab mice) suggest a greater longevity with very high carbs and low protein, and the same authors hint at the Okinawans (in another reference) as a real life example.

I see some problems with such a thesis (1:10 protein:carbs ratio seems not practically possible) but they showed in detail that longevity is enhanced by hi carbs and decreased by high protein. In lab rats. None showed the opposite, not in lab rats nor in humans.

 

 
The Ratio of Macronutrients, Not Caloric Intake, Dictates Cardiometabolic Health, Aging, and Longevity in Ad Libitum-Fed Mice
 
  https://doi.org/10.1...met.2014.02.009

 

 

Ageing Res Rev. 2017 Mar 6. pii: S1568-1637(17)30046-6. doi: 10.1016/j.arr.2017.03.001. [Epub ahead of print]

Dietary protein, aging and nutritional geometry.

 

 

 





Also tagged with one or more of these keywords: diet, longevity, monounsaturated fat, carbs, low protein, starch, health

1 user(s) are reading this topic

0 members, 1 guests, 0 anonymous users