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JesseLawler

Ketotic CR Diet - anyone doing this?

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I'm interested in cognition-enhancement as well as life-extension and there's a lot of anecdotal claims of increased mental sharpness on a ketotic diet, where the brain and body are powered largely from "ketone bodies" derived from fats, rather than glucose/glycogen stores.

 

(The ketotic diet has some other health benefits as well, but many of those seem to be largely duplicative with CR.)

 

Is anyone in this community doing a "ketotic version" of CR?  (High fat, low/medium protein, extremely low carb.)

 

I'd be very interested to hear your experiences -- although admittedly, I hate the idea of giving up fruit.

 

Jesse

 

PS:  These forums seem oddly quiet.  I read somewhere that there are about 10,000 CR practicioners -- is there someplace other than this website where people are hanging out online?

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Try this: http://arc.crsociety.org/index.php

 

It's the old CR Society email lists.  They are active with daily posts.  Some CR followers are slow to move over to the newer formats.  We figure that eventually everyone will be on this forum instead.

 

There may be 10,000 world wide CR followers, but they don't all post here. Really there's only about a couple of hundred who post and 2 dozen that post anything regularly.  That being said, the email list archives do contain some great threads on how to be healthy with a CRON diet and all the little aspects that go along with it.

 

Another favorite site for me is http://www.longecity.org/forum/forum/237-calorie-restriction/

I find there's a bit less science and more opinion in the postings there sometimes.

Edited by keithsct

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Thanks Keith!  

 

The first link in your message doesn't open for me -- just spins forever on a white screen.  However, I'll check out Longecity.

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There are lots of CR practitioners following some version of -- or at least what they take to be some version of -- a ketogenic diet. Most of us, though, are convinced by older studies showing high-fat diets (though individuals vary greatly in their response to dietary fats, in part based on APOE-status) are not such a great idea. Ketosis can be achieved more safely, many believe, via fasting.

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Guest Max

Hi,

I was trying this for 8 weeks in 2013. I've crossed LCHF (staying under 20 g carbs a day) with ADF but this wasn't easy since I was doing quite a lot of exercise then. I'm on statins (heterozygous FH) and I was surprised to see those great LDL/HDL values after 4 and 8 weeks.

But it was hard to keep up and now I'm doing a more "livable" version - LCHF focussed on (poly) unsaturated oils under strict avoidance of grains, potato, rice and flour products (staying under 50 g carbs a day - about 10-15% of daily calories) with a low caloric approach every 2nd day (approx. 600 kcals). I feel quite good in keeping this up and lost 5 kg in 4 weeks. Sport is limited to 2 times a week, HIIT-like style (Doug McGuff-like exercise).

 

It's my goal to get rid of the ezetimibe first to reduce medications..life style change was much more effective than doubeling the statin dosage!

 

Max

 

 

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Hi there David -- I'm forging ahead (well, slowly, but still forging) with finding info on this.


 


I'm about to switch to a ketogenic diet at the end of the month, following a one-week water fast (details here:http://smartdrugsmar...water-fast-week).  The basic plan is that the fast will get me into ketosis, and then I'm going to try it out a ketogenic diet for at least a couple of months to see how it feels.


 


The anecdotal stories about people feeling clearer-headed while in ketosis has me curious.  I'm a sucker for mental clarity.    ;)


 


Other than reading about CR in late December, I haven't actually started reducing my calories yet, but I'll be doing more research into this -- and likely a podcast episode or two -- in the coming months.


 


Jesse


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Is anyone in this community doing a "ketotic version" of CR?  (High fat, low/medium protein, extremely low carb.)

 

Low calorie diets are ketogenic even if they are high carb, low fat.

 

There was a study published in *Nutrition and Metabolism*  that compared three diets (in rodents).

1. Full calorie low carb high fat

2. Low calorie high carb low fat

3. Low calorie low carb high fat

 

Highest ketones were produce in diet 3, then 2 and finally 1.

 

But - I don't (?) think there is any indications that a high fat/low carb Low calorie diet is more effective than a low fat/high carb diet.

 

Regards

Randy

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Thanks Randy -- Any details on this study?  (Name?  Month it appeared?)

 

I'm not quite clear on why diet #2 above would result in ketosis if someone is a long-time CR practicioner, as they wouldn't have enough body fat stores to be consistently tapping for energy, so where would the ketone bodies be coming from?  (Besides a small amount from the diet.)

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Thanks Randy -- Any details on this study?  (Name?  Month it appeared?)

I looked and have not been able to find it. I know it was in *Nutrition and Metabolism* and I think it's > 4 years out.

I know it there cause I reread it cause the results were just as unexpected as you noted. I'll keep looking.

 

Even skinny CR folk have plenty of fat to burn - via beta oxidation or ketosis. 

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Guest Alan Pater

Epilepsia. 2008 Nov;49 Suppl 8:114-6. doi: 10.1111/j.1528-1167.2008.01853.x.
Targeting energy metabolism in brain cancer with calorically restricted ketogenic diets.
Seyfried TN1, Kiebish M, Mukherjee P, Marsh J.
PMID:19049606
http://onlinelibrary.wiley.com/doi/10.1111/j.1528-1167.2008.01853.x/full
http://onlinelibrary.wiley.com/doi/10.1111/j.1528-1167.2008.01853.x/pdf

Abstract

Information is presented on the calorically restricted ketogenic diet (CRKD) as an alternative therapy for brain cancer. In contrast to normal neurons and glia, which evolved to metabolize ketone bodies as an alternative fuel to glucose under energy-restricted conditions, brain tumor cells are largely glycolytic due to mitochondrial defects and have a reduced ability to metabolize ketone bodies. The CRKD is effective in managing brain tumor growth in animal models and in patients, and appears to act through antiangiogenic, anti-inflammatory, and proapoptotic mechanisms.

Nutr Metab (Lond). 2007 Feb 21;4:5.
The calorically restricted ketogenic diet, an effective alternative therapy for malignant brain cancer.
Zhou W1, Mukherjee P, Kiebish MA, Markis WT, Mantis JG, Seyfried TN.
PMID:17313687[PubMed] PMCID:PMC1819381Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1819381/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1819381/pdf/1743-7075-4-5.pdf

Abstract

BACKGROUND: Malignant brain cancer persists as a major disease of morbidity and mortality in adults and is the second leading cause of cancer death in children. Many current therapies for malignant brain tumors fail to provide long-term management because they ineffectively target tumor cells while negatively impacting the health and vitality of normal brain cells. In contrast to brain tumor cells, which lack metabolic flexibility and are largely dependent on glucose for growth and survival, normal brain cells can metabolize both glucose and ketone bodies for energy. This study evaluated the efficacy of KetoCal, a new nutritionally balanced high fat/low carbohydrate ketogenic diet for children with epilepsy, on the growth and vascularity of a malignant mouse astrocytoma (CT-2A) and a human malignant glioma (U87-MG).

METHODS: Adult mice were implanted orthotopically with the malignant brain tumors and KetoCal was administered to the mice in either unrestricted amounts or in restricted amounts to reduce total caloric intake according to the manufacturers recommendation for children with refractory epilepsy. The effects KetoCal on tumor growth, vascularity, and mouse survival were compared with that of an unrestricted high carbohydrate standard diet.

RESULTS: KetoCal administered in restricted amounts significantly decreased the intracerebral growth of the CT-2A and U87-MG tumors by about 65% and 35%, respectively, and significantly enhanced health and survival relative to that of the control groups receiving the standard low fat/high carbohydrate diet. The restricted KetoCal diet reduced plasma glucose levels while elevating plasma ketone body (beta-hydroxybutyrate) levels. Tumor microvessel density was less in the calorically restricted KetoCal groups than in the calorically unrestricted control groups. Moreover, gene expression for the mitochondrial enzymes, beta-hydroxybutyrate dehydrogenase and succinyl-CoA: 3-ketoacid CoA transferase, was lower in the tumors than in the contralateral normal brain suggesting that these brain tumors have reduced ability to metabolize ketone bodies for energy.

CONCLUSION: The results indicate that KetoCal has anti-tumor and anti-angiogenic effects in experimental mouse and human brain tumors when administered in restricted amounts. The therapeutic effect of KetoCal for brain cancer management was due largely to the reduction of total caloric content, which reduces circulating glucose required for rapid tumor growth. A dependency on glucose for energy together with defects in ketone body metabolism largely account for why the brain tumors grow minimally on either a ketogenic-restricted diet or on a standard-restricted diet. Genes for ketone body metabolism should be useful for screening brain tumors that could be targeted with calorically restricted high fat/low carbohydrate ketogenic diets. This preclinical study indicates that restricted KetoCal is a safe and effective diet therapy and should be considered as an alternative therapeutic option for malignant brain cancer.

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Thanks Al. The thing is, KetoCal is a high fat/low carbohydrate supplement, so it really doesn't document Randy's recollection. The first paper, a review, also doesn't seem to have any studies that address the point.
 
James Cain first brought (1) to our attention last September (and you (Al) were helpful enough to provide additional resources (see link in reference citation below). It looked at the effect of CR  on epileptic seizures in mic, finding that the effect is not due to the generation of ketone bodies, but to the reduction in glucose availability;  on the main point (that a moderate-carb diet is sufficient to trigger the production of ketone bodies) roughly does the job, through it is not exactly the one Randy remembers;
 

After the 7-week pretrial period, the mice were arranged into five groups (n= 13–15 mice/group). All mice were then fasted for 16 h to establish a similar metabolic state at the start of the experiment. The mice in each group were assigned to one of five dietary conditions:
 
1) Standard diet (SD) fed ad libitum with water alone prior to seizure testing (SD-UR),
 
2) Standard diet restricted to achieve a 20–23% body weight reduction with water alone prior to seizure testing (SD-R),
 
3) Standard diet restricted to achieve a 20–23% body weight reduction with water plus 25-mMglucose prior to seizure testing (SD-R[Glu]),
 
4) Standard diet restricted to achieve a 20–23% body weight reduction with water plus 25-mM glucose and 8-mM 2-DG [2-depxuglucose, which blocks cellular glucose metabolism] prior to seizure testing (SD-R[Glu][2-DG]), and
 
5) Standard diet restricted to achieve a 20–23% body weight reduction with water plus 25-mM glucose and 50-mM bOHB prior to seizure testing (SD-R[Glu][bOHB]).

 

gallery_727_15_65693.jpg

 

P.S. Al: please do me and you and everyone on the Forum a favor: register on the Forums and log in each time before you post! This will ensure that you can't be impersonated, and will make it easier to keep track of your questions, input, and progress).

 

Reference
1: Meidenbauer JJ, Roberts MF. Reduced glucose utilization underlies seizure protection with dietary therapy in epileptic EL mice. Epilepsy Behav. 2014 Oct;39:48-54. doi: 10.1016/j.yebeh.2014.08.007. Epub 2014 Sep 7. PubMed PMID: 25200525; PubMed Central PMCID: PMC4252783.

Edited by Michael R

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Thanks Al. The thing is, KetoCal is a high fat/low carbohydrate supplement, so it really doesn't document Randy's recollection. The first paper, a review, also doesn't seem to have any studies that address the point.

 

James Cain first brought (1) to our attention last September (and you (Al) were helpful enough to provide additional resources (see link in reference citation below). It looked at the effect of CR  on epileptic seizures in mic, finding that the effect is not due to the generation of ketone bodies, but to the reduction in glucose availability;  on the main point (that a moderate-carb diet is sufficient to trigger the production of ketone bodies) roughly does the job, through it is not exactly the one Randy remembers;

 

 

Thanks and I don't think that was the study I mentioned. I'll keep looking.

 

Regards

Randy

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Here's the paper that reported hydroxybutyrate levels were reduce more in a restricted high carb/lowfat diet than a unrestricted  low carb/high fat diet.

Management of multifactorial idiopathic epilepsy in EL mice with caloric restriction and the ketogenic diet: role of glucose and ketone 
http://www.nutritionandmetabolism.com/content/1/1/11

See figure 4 below. Four diets were compared:

  1. Standard diet - calorie unrestricted
     
  2. Standard diet - calorie restricted
     
  3. Ketogenic diet - calorie unrestricted
     
  4. Ketogenic diet - calorie restricted

Note that the Standard diet (high carb/low fat) with Restricted calories produced More hydroxybutyrate than the Ketogenic (low carb/high fat) Unrestricted calorie diet.

 
 
Figure 4
1743-7075-1-11-4.jpg

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Here's the paper that reported hydroxybutyrate levels were reduce more in a restricted high carb/lowfat diet than a unrestricted  low carb/high fat diet.

Sorry what I meant to say:

 hydroxybutyrate levels were INCREASED more in a restricted high carb/lowfat diet than a unrestricted  low carb/high fat diet.

 

Randy

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Good digging, Randy -- thanks!

 

A couple of caveats worth noting. First, in the two CR diets "the daily amount of food given to each R mouse was reduced gradually until it reached 77–80% of its initial (pre-trial) body weight." This is only moderate CR in rodent studies, but (assuming CR proper -- ie, starting from a normal body composition) is about as high a level of CR as any human CR practitioner ever manages. It's not clear to me what the threshold is for CR at levels of carb intake that are not ketogenic in most people to become ketotic, and especially ketotic at levels typical of classic keto diets in humans or rodents. Paul McGlothin eats a quite high-carb diet, albeit with very low-GI and somewhat low-absorptive carb sources, and spends much of his day in ketosis. In a largeish, fairly long-term study pitting a low-fat/high-carb reduced-energy diet to a Calorie unrestricted (but de facto energy-restricted) diet for weight loss in obese individuals,(1)

 

 

“The percentage of participants who had positive test results for urinary ketones was greater in the lowcarbohydrate than in the low-fat group at 3 months (63% vs. 20%; P < 0.001) and 6 months (28% vs. 9%; P < 0.01). We found no statistically significant differences between groups after 6 months. The decrease from 3 to 24 months is consistent with liberalization of carbohydrate intake over time, as part of the study protocol [ie, Atkins model of Induction, Ongoing Weight Loss (OWL), Pre-Maintenance and Lifetime Maintenance].”  (1)

 

Unfortunately, they only say the % with a positive test (ie, > 5 mg/dL) — no dose-response data are given. There was a similar result, with a similar lack of granularity of reporting, in (2).

 

However, it's notable that at least in (2), the level of carb restriction terribly severe: the P:F:C in the low-carb group in (2) were at different points in the ballpark of 25:43:[29-34]% — more like The Zone than Atkins. And the level of de facto energy restriction was also greater, tho' not by a huge amount: ≈150 Cal/d during the first 3 mo (when the big drop in weight occurred), but then only ~80 Cal/d thereafter. Actual (as vs. prescribed) macronutrient intake were not reported in (1).

 

IAC, it's not at all clear why one would actively want to put oneself into ketosis, whether for epilepsy or anything else: as Jesse says, the actual benefits of a ketogenic diet evidently arise from the concomitant CR, not the production of ketone bodies.

 

PS: Randy, and all: note that when you're logged in, you can always edit your own posts for errors like the above using the "Edit" button that's right next to "Quote" and "MultiQuote."

 

Reference

1: Foster GD, Wyatt HR, Hill JO, Makris AP, Rosenbaum DL, Brill C, Stein RI, Mohammed BS, Miller B, Rader DJ, Zemel B, Wadden TA, Tenhave T, Newcomb CW, Klein S. Weight and metabolic outcomes after 2 years on a low-carbohydrate versus low-fat diet: a randomized trial. Ann Intern Med. 2010 Aug 3;153(3):147-57. doi: 10.7326/0003-4819-153-3-201008030-00005. PubMed PMID: 20679559; PubMed Central PMCID: PMC2949959.

 

2: Bazzano LA, Hu T, Reynolds K, Yao L, Bunol C, Liu Y, Chen CS, Klag MJ, Whelton PK, He J. Effects of low-carbohydrate and low-fat diets: a randomized trial. Ann Intern Med. 2014 Sep 2;161(5):309-18. doi: 10.7326/M14-0180. PubMed PMID: 25178568.

Edited by Michael R

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I'm on a ketogenic diet for 2 months now with the main purpose of weight reduction.

 

It's was remarkably that after 4 weeks weight loss stalled with fasting every 2nd day (600-800 kcal daily uptake) fpr more than 2 weeks.

It starteted again after I cancelled those CR days.

So I don't restrict calories anymore but track my food and it's interesting to learn that there's an unintended small daily caloric deficit of 130 kcal and still a good weight loss...even without endurance exercise but muscle training once a week (following Doug McGuff "Body by Science").

 

Ketosis is stable showing 4-8 mmol/L each morning and my first blood testing gave great results - as heterozygous FH carrier (in company of ApoE3/4) I was surprised to learn how much better LDL/HDL are getting even if  fats (much of them saturated) make 80% of your daily input und carbs are reduced to 30 g!

Next time I'll let them check C-reactive protein...

 

Max

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Guest Rudolph

Max, Jesse, did you or are you planning to track the loss of your bodymass with regard to fat vs proteins? There seems to be a rather high turnover in lean bodymass (muscle proteins) to maintain blood glucose levels and this is my main problem with keto diets. Rather dangerous if your heart muscle is wasted. Sorry no refs now, only my memory.

 

Ruud

 

NB Jesse: the mental clarity issue WAS also for me a huge problem. For years I tried low GI, low carbs, slow carb metabolism diets (combine fats with carbs), etc.  Since i found out that it was actually the FAT content that was the culprit in [my] insuline sensitivity I have cut the fats out for as much as possible and feel better than ever before.

 

NB2: the BBC documentary Fat vs Sugar is a must watch when you are interested in keto.

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Thanks for the tip, Rudolph -- 

 

I'll check out that documentary.  Currently I'm about 2 weeks into eating ketogenic, and planning on doing 6-8 weeks then re-running my blood chemistry to see how my numbers move around.  I'm not doing anything to restrict calories as of yet... I'm sort of taking a staged approach to see how different diets feel to live with, before making any binding decisions.  :)

 

Jesse

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