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Todd Allen

carbohydrate restriction for type 2 diabetes

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Interesting study, although proteins were not so moderate, they were rather high compared to the accepted standards(almost twice the 0.8 RDA g kg-1). The short term results were good, what about the long term sustainability though? Hi proteins and hi fats for years, any potential side effects? Kidneys, IGF-1, atherosclerosis? Degenerative disease?

 

Ron Rosedale and Jason Fung are more balanced in that they recommend moderate proteins in the region of 0.6-0.8 g kg-1, eschewing potential problems from protein excess. Phinney and Volek are consultants of the Atkins organization, which we all know is a champion of the (low carb) high protein regime

 

 

 

Daily protein intake was targeted to a level of 1.5 g·kg−1 of reference (ie, medium-frame “ideal”) body weight and participants were coached to incorporate dietary fats to satiety. Other aspects of the diet were individually prescribed to ensure safety, effectiveness, and satisfaction, including consumption of 3-5 servings of nonstarchy vegetables and adequate mineral and fluid intake for the ketogenic state.

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I suspect you are right that lowering protein would likely be better though in the context of carbohydrate restriction that means even more fat.

 

As far as your suggested possibilities for long term issues, my guess is that those which might stem from elevated IGF1 are most likely, especially at this level of protein intake.  Kidney issues, atherosclerosis and degenerative problems are all highly correlated to type 2 diabetes and reducing diabetes could be a potent factor in improving them too.

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I suspect you are right that lowering protein would likely be better though in the context of carbohydrate restriction that means even more fat.

 

As far as your suggested possibilities for long term issues, my guess is that those which might stem from elevated IGF1 are most likely, especially at this level of protein intake.  Kidney issues, atherosclerosis and degenerative problems are all highly correlated to type 2 diabetes and reducing diabetes could be a potent factor in improving them too.

 

I agree, it sounds like a Faustian bargain: higher mortality risk because of diabetis or higher mortality risk because of high proteins or fats.

 

Rosedale's opinion is that fats are not at all negative and in his book he gives some high thresholds for blood cholesterol. His main experience stems from curing diabetic patients and he has been apparently successfull in many cases. But his strategy entails very little protein, down to 0.5 g kg-1 for T2 diabetes. And he advises lots of vegetables, lots of fish and  little saturated fats.

 

It is astounding how it is possible to heal people of the same malady by two apparently opposite dietary approaches:

 

  1. Low carbs, hi fats
  2. Low fats, hi carbs

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Why do you think they are opposite, mccoy? They are both low on protein, which may be the real culprit after all. I still could not figure it out why protein ingestion causes insulin secretion in which protein has nothing to do with glucose levels in the bloodstream. If someone knows the answer, please let me know. I am really curious.

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Burak yes, the Rosedale diet is  low-protein, but we should specify that because many low-carb variations are hi in protein.

 

As a matter of fact, many low-carbers cringe when they hear about low protein, because that's pretty satiating and eating fat to achieve satiety is not so effective. Many are not able to restrict protein intake but many others are accepting the sensible reasonings of Dr. Rosedale focused on longevity.

 

Rosedale recognizes the role of mTOR activation by abundance of dietary amminoacids. He also recognizes the gluconeogenesis mechanism which would add up to the carbs ingested.

 

He has treated so many diabetics and knows that insulin is released by proteins as well.

 

Insulin seems to be both a glucose and amminoacid sensor, apparently insulin regulates protein metabolism, specifically prevents excessive protein breakdown, for example in muscles after exercise (hence the suggestion to ingest either carbs and protein after a workout if MPS synthesis is desired).  

 

Baillieres Clin Endocrinol Metab. 1993 Oct;7(4):989-1005.
Insulin action on protein metabolism.

 

The common denominator of so different diets seems to be low protein, as you say, and very low amounts of either dietary components: fats or carbs.

 

No one has devised a mechanistic explanation for that  AFAIK.

 

The rationale behind the Rosedale diet is clear though: lowering both the amminos signal and the insulin signal he eliminates both the triggering factors of mTOR. The body goes in autophagy-regeneration mode and some degenerative and metabolic illnesses may be cured. A possible hypothesis.

Edited by mccoy

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I suspect you are right that lowering protein would likely be better though in the context of carbohydrate restriction that means even more fat.

 

As far as your suggested possibilities for long term issues, my guess is that those which might stem from elevated IGF1 are most likely, especially at this level of protein intake....

 

IGF-1 and mTOR, which does not transfer on the lysosome body without an 'abundance' of amminoacids. IGF-1 and insulin also trigger akt which swittches on mTOR.

 

 

A chronic amplification in mTOR activity, which may ensue due to the chronically high amounts of dietary amminoacids and blood insulin+IGF-1 released by the same amminos, is known to increase degenerative diseaseas and neoplastic diseases.

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Thanks for the input mccoy, that seems reasonable. I think, especially after reading CE topic, the number one reason why protein restriction (or rather AA restriction-or moderation-) improves glucose metabolism is through increasing metabolism (glucose burning for heat regardless of whether we need the heat or not since it is relatively clean process so why not burn the excess glucose and remove it from bloodstream) by activating BAT. The most contribution comes from methionine restriction it seems. After going mostly plant based (reducing AA but not total protein), I lost 5-6 kg despite increasing calories. Fiber content and calorie bioavailibility could also be a culprit. I am having a hard time gaining them back now that I also implement a little bit of CE. 

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My thoughts on this...

 

Type 2 diabetes is provoked by chronically elevated insulin.  Two factors are at play, the total sum of insulin sometimes referred to as area under the curve (AUC) and the baseline of the lowest level it drops to on the average daily cycle .  The ratio of the insulin level to it's baseline level has a big impact on the strength of response or ones insulin sensitivity.  Both carbs and protein are insulinogenic and restricting either can have a beneficial impact on type 2 diabetes or the precursor of insulin resistance/metabolic syndrome.

 

With carbs, I expect most of the value comes from restricting high glycemic load sugars and fast digesting simple starches.  The healthy high carb whole plants heavy diets tend to do this with a high ratio of indigestible fiber and slow resistant starches with respect to the load of simple sugars and fast starches.

 

Protein has a multiplier effect on this as a big factor in keeping the baseline of insulin elevated.  Restricting total protein or the most insulinogenic amino acids helps lower the baseline and fasting. intermittent fasting and longer periods of mimicking fasting with aggressive protein restriction all appear beneficial.

 

As for the fats, they aren't insulinogenic but are most harmful in the presence of insulin which suppresses their metabolism.

 

A classic CR diet works by keeping the insulin baseline low by restricting protein, keeps the AUC low by restricting high glycemic carbs and even with periods of moderately elevated insulin through high carbohydrate intake the modest intake of saturated fat and total calories means the fat still gets metabolized before it has much impact.

 

The opposite approach of a calorically richer high fat diet with a significant amount of protein and perhaps a worse ratio of fiber to fast carbs works because an extreme restriction of the total carb load keeps the AUC reasonably low despite the higher protein.  The higher insulin baseline due to the protein keeps blood glucose low spurring the metabolism of fats to a degree that even with a high intake of saturated fats, they are preferentially burned and their harm is minimized.

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Mccoy, thanks!  Fantastic article.  So much to absorb.  Particularly interesting to me were the parts on heat shock proteins and endoplasmic reticulum stress.  In the bit on ER stress it mentions the role of TMAO as a chaperone that assists with badly behaving proteins.  Dean gave me a bit of a scare about the eggs I was eating as they have been shown able to elevate TMAO levels and a study by Stanley Hazen in the NEJM showed a correlation between elevated TMAO and CVD.  People like Dr Greger piled on with an assumption of causation and started demonizing foods previously believed healthy such as eggs, liver and even fish.

 

But after some consideration I rejected that assumption and bet my life that the elevated TMAO was not causing CVD but is a response to the metabolic derangement causing CVD.  And I greatly upped my intake of eggs (currently 4/day contemplating going to 6/day) and fish, especially sardines, and started eating liver - I now regularly eat carefully sourced chicken, beef, pork and lamb liver.  People with my disease frequently die young from CVD and I was ahead of the game with biomarkers indicating severe trouble.  If I have bet wrong I should be dying soon but for the moment my health and fitness seem to be improving with dramatic speed.  The only biomarker getting "worse" has  been total cholesterol.  However, I think the evidence high TC causes CVD is as weak as that for TMAO.  Dr. Joseph Kraft's work suggests CVD is largely the result of hyperinsulinemia and this paper suggests why elevated TMAO is a beneficial response.

 

I now believe much of the damage of my disease is caused by hyperinsulinemia brought on by a loss of GLUT4 in skeletal muscle because the mutant androgen receptor protein accumulates in the nucleus and interferes with the transcription of the GLUT4 gene.  I have been taking just shy of scalding hot baths nightly until I feel like I'm going to pass out or puke, increasing temp and time as my tolerance has grown, trying to increase heat shock protein expression to reduce the accumulation of mutant AR protein.  I have no idea to what degree I've achieved it, but I do  believe it has improved circulation and perfusion into muscle and it appears there has been a dose/response type action with respect to muscle performance and growth.   And from this paper I see that heat shock proteins may also be helping with the insulin resistance/hyperinsulinemia too.

Edited by Todd Allen

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