60 replies to this topic

[MrHappy]

Banning on the sly, without notice nor indication in the status, is also a no-no on decent forums. What's going on here?

So guys, if you don't here from me anymore, you can appeal to MrHappy Good luck!

You received a temporary ban for ongoing personal attacks and harassment spanning 3 threads. I welcome intellectual discussion, but you've been warned before about personal attacks. Consider this a final warning.

[xEva]

Personal attacks? Where exactly? You confuse a ketogenic diet with a low-cal diet, to which you continue to refer as if they were synonyms, including in this thread -- that's what I objected to. I tried to alert you that what you called a ketogenic diet was in fact a low-carb, high protein diet. That's what you call the ad hominem and personal attack. You also flagged me as a spammer. Based on what of my actions did you do that?

[Godot]

xEva, you should really consider trying to be nicer to people. It seems every other post you're attacking someone, interpreting whatever people say the most negative possible way. You've been freely attacking MrHappy for no reason. If I were him I'd want to ban you too.

[xEva]

xEva, you should really consider trying to be nicer to people. It seems every other post you're attacking someone, interpreting whatever people say the most negative possible way. You've been freely attacking MrHappy for no reason. If I were him I'd want to ban you too.

Ha! Interpreting in most negative possible way? And being nicer to whom? Are you referring to this your post by any chance:

xEva - You make some very strong statements about ketosis that seem to be quite unique to you, such as the body taking a month to adapt to using ketones efficiently, and peripheral insulin resistance being induced by plasma FFAs irrespective of blood glucose. Could you please provide some sources for these claims?

A guy comes into the discussion faking knowledge with words like 'statements unique to you' as if you bothered to at least google in order to find out where the truth lies lol.. And then it turns out that this is the standard state of knowledge. Not some avangard or edge science, mind you, but what's been known for the last 50 years lol And then you bitched that I took offense at your pretenses. And how did MrHappyt handled this as a moderator? He upvoted your post and downvoted mine. That's how forums and made and lost. When ignorance is encouraged and knowledge is not.

Edited by xEva, 19 April 2013 - 01:37 AM.

[alecnevsky]

I've been pretty rigorous in my first 3 weeks in keeping the carbs below 30g. For my 4th week, I've probably averaged 40g (just b/c of flavored whey.) That however was combined with a strenuous HIIT session. As a result, I tend to show mod to heavy fat metabolism (perhaps not entirely a ketotic state but just state of some fat burning) via ketonuria. The heavy cream is literally the best idea ever. Thanks. Does anyone see any risks with literally drinking 1/3 to .5 liter of organic heavy cream/day ? Also, I read some studies on creatine and the sodium pump, does anyone know for sure that supplementing creatine(with sodium) in a ketotic state is not a waste of time?


Re: xEva vs Mr.Happy
As far as technical arguments go, I am not entirely sure they're helpful in this thread. While I think the differences between a fat burning and a ketotic state are important to understand(for me), most people in this thread assume that even a mild fat burning state (say, <100g carbs/day) may provide some marginal benefits. Seeing that I am mostly concerned with ketone metabolism in the brain (for which this distinction seems crucial), I would hate to see xEva banned from participation. I do believe that both, MrHappy and xEva, are knowledgeable users with thorough understanding of both practical and clinical properties of this metabolic state., and, it would be to our common disadvantage to see anyone banned. Nevertheless, some of these disagreements may not be relevant to other people who are largely concerned with a general fat-burning state. I may even be wrong about the nature of the argument b/c I've been ignoring it. Goes to show how relevant it is to me.

[Godot]

xEva - Yes, you give a good example. You interpreted what I said in an unnecessarily negative way. When someone says your statement seems unique, it means they haven't heard it from anyone else. I'm still not sold on your perspective, but I didn't feel like bickering with you about it because you reacted with such senseless hostility, as you have reacted to MrHappy in this thread. You seem to have a good level of knowledge and I appreciate that you want to share it, but you also seem to be openly hostile. Maybe you could just chill out a little?

Edited by Godot, 19 April 2013 - 01:26 AM.

[alecnevsky]

Ketosis puts you body in a unhealthy metabolic state. Ketosis promotes free-radical formation, lowers your cellular antioxidants and damages the circulatory system [1-3]!


[1] Free Radic Biol Med. 1998 Dec;25(9):1083-8. Ketosis (acetoacetate) can generate oxygen radicals and cause increased lipid peroxidation and growth inhibition in human endothelial cells. Jain SK, Kannan K, Lim G.


[2] Diabetes. 1999 Sep;48(9):1850-5. Hyperketonemia can increase lipid peroxidation and lower glutathione levels in human erythrocytes in vitro and in type 1 diabetic patients. Jain SK, McVie R.


[3] Diabetes Care. 1999 Jul;22(7):1171-5. Effect of hyperketonemia on plasma lipid peroxidation levels in diabetic patients. Jain SK, McVie R, Jackson R.

Also, can someone address the first study? Lipid peroxidation was one of my main concerns before induction. Isn't this due to PUFA mainly?

[misterE]

Also, can someone address the first study? Lipid peroxidation was one of my main concerns before induction. Isn't this due to PUFA mainly?

When you oxidize fatty acids for fuel, in creates lipid-peroxides as a by-product. The body is not designed to burn fat as fuel.


The first step to burning fat is lipolysis, which releases stored-fat as free-fatty-acids (FFA's) into the circulation. These fatty-acids accumulate in organs like the liver, muscles, pancreas, brain, etc, These FFA's then enter the cell mitochondria and become intramyocellular-lipids, which are then oxidized as energy.


Normally, when you eat a meal, the insulin you make in response inhibits lipolysis and temporarily inhibits fat-burning. This prevents a chronic release of FFA's into the liver, muscles and pancreas. In folks with type-2 diabetes, they eat and secrete insulin, but there insulin is unable to inhibit lipolysis because their adipose-tissue is insulin-resistant (from being overstuffed with fat you ate). This means people with type-2 diabetes are constantly in lipolysis and oxidizing fatty-acids instead of glucose. Diabetes is the bodies way of forcing you to burn fat (as a survival mechanism, to prevent you from growing out of proportion and so obese you can’t walk or defend yourself).


The underlying condition of type-2 diabetes is lipotoxicity, which is when the muscles become marbled and fatty and can't absorb glucose, when the liver becomes fatty and begins spewing out VLDL's instead of HDL's, and when the pancreas gets fatty and can't secrete much insulin into circulation.


All this fat is supposed to be stored away in the adipose-tissue, but instead it has accumulated in vital-organs. Stimulating insulin-secretion by eating lots of starches can help redistribute all this fat out of the organs and back into the adipose-tissue and promote a healthy amount of lipolysis, instead of a chronic amount like we see with people with insulin-resistance and diabetes.

Edited by misterE, 19 April 2013 - 02:19 AM.

[xEva]

[1] Free Radic Biol Med. 1998 Dec;25(9):1083-8. Ketosis (acetoacetate) can generate oxygen radicals and cause increased lipid peroxidation and growth inhibition in human endothelial cells. Jain SK, Kannan K, Lim G.


[2] Diabetes. 1999 Sep;48(9):1850-5. Hyperketonemia can increase lipid peroxidation and lower glutathione levels in human erythrocytes in vitro and in type 1 diabetic patients. Jain SK, McVie R.


[3] Diabetes Care. 1999 Jul;22(7):1171-5. Effect of hyperketonemia on plasma lipid peroxidation levels in diabetic patients. Jain SK, McVie R, Jackson R.

Also, can someone address the first study?

All of these studies refer to diabetic hyperketonemia, including the first, which was in fact an in vitro study and implicated acetoacetate and not 'the main' ketone beta-hydroxybutyrate. I did not read the full paper but from their abstract it looks like a mere conjecture, which is also implied in the heading: they state "Ketosis (acetoacetate) can generate oxygen radicals and cause increased lipid peroxidation...", not that it does:

http://www.ncbi.nlm..../pubmed/9870562

Elevated level of cellular lipid peroxidation can increase the incidence of vascular disease. The mechanism by which ketosis causes accelerated cellular damage and vascular disease in diabetes is not known. This study was undertaken to test the hypothesis that elevated levels of ketone bodies increase lipid peroxidation in endothelial cells. Human umbilical venous endothelial cells (HUVEC) were cultured for 24 h at 37 degrees C with ketone bodies (acetoacetate, beta-hydroxybutyrate). Acetoacetate, but not beta-hydroxybutyrate, caused an increase in lipid peroxidation and growth inhibition in cultured HUVEC. To determine whether ketone bodies generate oxygen radicals, studies using cell-free buffered solution were performed. They showed a significant superoxide dismutase (SOD) inhibitable reduction of cytochrome C by acetoacetate, but not by beta-hydroxybutyrate, suggesting the generation of superoxide anion radicals by acetoacetate. Additional studies show that Fe2+ potentiates oxygen radical generation by acetoacetate. Thus, elevated levels of ketone body acetoacetate can generate oxygen radicals and cause lipid peroxidation in endothelial cells, providing a possible mechanism for the increased incidence of vascular disease in diabetes.

Diabetic ketoacidosis is a very different state where the blood level of beta-hydroxybutyrate can reach 20 mMol/L and even higher (compare with 5-7 mMol/L during the fast and 2-3 during a ketogenic diet). Diabetic ketoacidosis also comes with super high glucose, which is minimal both during a fast and a ketogenic diet.

Ketones are actually touted as one of the best antioxidants. That's why I don't take antioxidants like vit E or C, etc. during my fasts.

Ketoacids? Good medicine? http://www.ncbi.nlm....les/PMC2194504/

Ketone Bodies, Potential Therapeutic Uses - Wiley Online Library http://onlinelibrary...01753311780/pdf

However, the benefits of ketones which were basically proven at this point based on starvation and therapeutic ketogenic diets, cannot be automatically translated to non-therapeutic keotgenic diets, less so, any carb diet, to which they may not apply. High fat diets do carry various risks. Same goes for high protein diets.

[xEva]

xEva - Yes, you give a good example. You interpreted what I said in an unnecessarily negative way. When someone says your statement seems unique, it means they haven't heard it from anyone else. I'm still not sold on your perspective, but I didn't feel like bickering with you about it because you reacted with such senseless hostility, as you have reacted to MrHappy in this thread. You seem to have a good level of knowledge and I appreciate that you want to share it, but you also seem to be openly hostile. Maybe you could just chill out a little?

lol When someone haven't heard it from anyone else, they say. 'Your statement seems unique among us ignoramuses'. Else they imply that they studied the subject and know it pretty well.

[alecnevsky]

xEva - Yes, you give a good example. You interpreted what I said in an unnecessarily negative way. When someone says your statement seems unique, it means they haven't heard it from anyone else. I'm still not sold on your perspective, but I didn't feel like bickering with you about it because you reacted with such senseless hostility, as you have reacted to MrHappy in this thread. You seem to have a good level of knowledge and I appreciate that you want to share it, but you also seem to be openly hostile. Maybe you could just chill out a little?

I may sound strange and kind of opportunistic here but I have no idea why you (or anyone else) is getting so offended as to make independent comments on the matters of xEva's writing. I asked xEva some stupid questions earlier in the cancer thread and was essentially made clear that I have been misinformed. Whatever, knowledge is paramount here and xEva's contribution is reflected above by yet another solid response with reference literature. (Thank you.) I cannot just prance into med school here and ask researchers about some random keto topic so I'll take whatever I can get however I can get it. It seems people are confusing a scientific debate with personal attacks. Being accused of not knowing a goddamn thing is what most scientific debates are all about. lol .

[Chupo]

Ketosis puts you body in a unhealthy metabolic state. Ketosis promotes free-radical formation, lowers your cellular antioxidants and damages the circulatory system [1-3]!


[1] Free Radic Biol Med. 1998 Dec;25(9):1083-8. Ketosis (acetoacetate) can generate oxygen radicals and cause increased lipid peroxidation and growth inhibition in human endothelial cells. Jain SK, Kannan K, Lim G.


[2] Diabetes. 1999 Sep;48(9):1850-5. Hyperketonemia can increase lipid peroxidation and lower glutathione levels in human erythrocytes in vitro and in type 1 diabetic patients. Jain SK, McVie R.


[3] Diabetes Care. 1999 Jul;22(7):1171-5. Effect of hyperketonemia on plasma lipid peroxidation levels in diabetic patients. Jain SK, McVie R, Jackson R.

Also, can someone address the first study? Lipid peroxidation was one of my main concerns before induction. Isn't this due to PUFA mainly?

Lipid peroxidation is not caused by burning lipids for fuel. It happens when free radicals oxidize lipids (mainly PUFA) in membranes. Glucose metabolism creates more ROS than either fat or ketone metabolism.

http://en.wikipedia....id_peroxidation



This study proves that ketones themselves protect against oxidative stress. It worked even when injecting the BHB into the mice.

Treatment of cells with βOHB increased histone acetylation at the Foxo3a and Mt2 promoters, and both genes were activated by selective depletion of HDAC1 and HDAC2. Consistent with increased FOXO3A and MT2 activity, treatment of mice with βOHB conferred substantial protection against oxidative stress.

http://www.ncbi.nlm....pubmed/23223453

I don't have the full text but there is more info about it here Note the control mice had three times the 4-HNE, which is produced by lipid peroxidation.

The researchers wanted to determine whether increased levels of βOHB actually reduced oxidative stress in vivo. To do this, they implanted mice with a subcutaneous βOHB pump, which supplied a steady release of βOHB. Researchers then injected a chemical, paraquat, which induces build up of reactive oxygen species. Compared to control mice (with no βOHB pump), βOHB mice had an impressive 54% reduction in reactive oxygen species.

Researchers also evaluated a maker of oxidative stress in these mice, 4-hydroxynonenal (4-HNE). 4-NHE is a product of polyunsaturated lipid degradation and accumulates in response to oxidative stress. The control mice had a three-fold increase in 4-NHE, indicating high levels of oxidative stress. This increase was completely suppressed in βOHB mice, indicating that high levels of βOHB protect against oxidative stress.

When you use fat for fuel you increase their turnover and reduce the accumulation of lipid peroxides.

Thus palmitate oxidation entails utilizing complex II at roughly twice the (FADH2-dependent) rate as glucose oxidation entails. Therefore shifting away from glucose utilization toward lipid and amino acid utilization would be expected to substantially reduce the production of reactive oxygen species, without necessarily reducing ATP production. As described below, other beneficial effects also occur as a result of this altered pattern of glucose fuel use, including a shift toward producing antioxidizing NADPH and increased protein and lipid turnover, which reduces the accumulation of oxidized protein and lipids.

http://www.ncbi.nlm....les/PMC2755292/

Another study that found ketogenic diets increase glutathione and reduce free radical production reducing mtDNA damage.

Isolated hippocampal mitochondria from KD-fed rats showed functional consequences consistent with the improvement of mitochondrial redox status i.e. decreased H2O2 production and mtDNA damage. Together, the results demonstrate that the KD up-regulates GSH biosynthesis, enhances mitochondrial antioxidant status, and protects mtDNA from oxidant-induced damage.

http://www.ncbi.nlm....pubmed/18466343

[DePaw]

I've been pretty rigorous in my first 3 weeks in keeping the carbs below 30g. For my 4th week, I've probably averaged 40g (just b/c of flavored whey.) That however was combined with a strenuous HIIT session. As a result, I tend to show mod to heavy fat metabolism (perhaps not entirely a ketotic state but just state of some fat burning) via ketonuria. The heavy cream is literally the best idea ever. Thanks. Does anyone see any risks with literally drinking 1/3 to .5 liter of organic heavy cream/day ? Also, I read some studies on creatine and the sodium pump, does anyone know for sure that supplementing creatine(with sodium) in a ketotic state is not a waste of time?

No risks to drinking lots of cream in my eyes, some people don't tolerate dairy though in whihc case drinking full-fat coconut milk is properly a good alternative.

[alecnevsky]

aa

embedding is a total pain in the dick on longecity.

This is a brilliant interview however.


The question is: how do these improvements in "aerobic" performance (i don't agree that keto is strictly for aerobic performance b/c aerobic metabolism is moved by anaerobic metabolism) but, regardless, the question is whether/how the advantages of keto translate into day-to-day living insofar as endurance and focus goes versus glucose metabolism. Would someone on keto do better in pulling all nighters than someone on glucose working on adderall? My observations so far are suggestive of a positive impact on endurance in both athletics(amazing recovery and endurance) and longer avg durations of coherent thought.

Edited by alecnevsky, 20 April 2013 - 09:50 AM.

[alecnevsky]

I think it's notable that Attia took 1.5 years to put himself into a ketogenic state and still experienced horrific symptoms upon keto-induction. This definitely reinforces my experience in being essentially bed-ridden (vomiting, severe dehydration, nausea, severe lightheadedness etc.) for a week on abrupt induction. I am not even talking about performance decline but complete debilitation. Soccer/Track/Cycling/Swimming athletes should be very careful about deciding to induce ketosis out of the blue, especially if you have school/work responsibilities. Like Attia, I was literally drinking 3 gatorades/day (maltodextrin). Had I been older, I probably would have observed weight gain in terms of fat stores as well.

I am still wondering why that is the case biochemically. That is, whether higher amount of glucose (active glucose-dominant metabolism) cycled through cells determines their composition (or affinity for glucose) to a greater extent than lower amount (sedentary glucose-dominant metabolism). I think it may have something to do with Insulin.

Also, it's interesting he says that he got sharper as the day progressed due to presumably increase in ketones. I actually see increased concentrations in urine in the morning, not at night.

Edited by alecnevsky, 20 April 2013 - 10:40 PM.

[alecnevsky]

I apologize for blowing up the general thread with seemingly trivial personal details. But, seeing that someone may be interested in identifying keto-symptoms on this forum, the severe acidic breath(metallic,) GI problems associated with MCT and general fatigue have abated in 4th week of adaptation. I imagine this is b/c my body is now using a greater proportion of either or all of acetone, acetoacetone, beta-hydroxybutyrate. Still b/c post workout I show heavy ketosis and moderate in the morning, I do not think I am in a fully adapted state yet (where ketonuria would be essentially low-trace as I understand.) One thing I do notice, is that ketostix only show full color(the entire square is colored) post workout and only partial color (1/4 white 3/4 purple) otherwise. I am not sure whether that means the results are under or over-representative of ketone bodies. Also, I was supplementing with creatine ethyl ester in the 3rd week which, apparently, may have broken down into creatine monohydrate and ethanol and may have been a variable.

Edited by alecnevsky, 21 April 2013 - 07:15 AM.

[xEva]

embedding is a total pain in the dick on longecity.

not really. You just supply the link and the sys does it for you

I liked this Peter Attia. Very cool. I especially liked his training in a fasted state, like after a 24h fast. That's what I've always done and it's nice to here that someone else does it too. The bodybuilding guys here used to gasp in horror upon hearing such travesties. He was the first I heard who talked about metabolic flexibility (and I thought I had invented the term years ago ..oh well..)


Not sure what you mean by this:

(i don't agree that keto is strictly for aerobic performance b/c aerobic metabolism is moved by anaerobic metabolism)

I hope this is not a variation on that 19th century stupid saying that 'fats burn in the flames of carbs'.

I am still wondering why that is the case biochemically.

This is adaptation to a different environment (food is part of the environment). This implies epigenetic changes, and the best and fastest way to accomplish this is via a fast. When we are born, we too go through a change in the environment. What does the body do? It fasts.

When we fast, the genes active in the previous metabolic state sort of close down the shop and the set of fasting genes pops up (that's a simplified version ). Then you fast for a while and go into the diet of your choice. Keto should be easy after a fast. But it could be a carb based diet, say, with some variation from what it was in the past. I believe the difficulty people have when changing diets is due to them having several, often conflicting, operating modes (= sets of genes) working simultaneously. I believe this is what is meant by hypomethylation which is associated with various pathologies of old age.

I believe that going through changes via a fast, the transition is made cleaner: the no-longer needed genes are methylated. Then, following the fast, an appropriate for the diet/environment set of genes is expressed. The net result is accomplished quicker and with less pain. And it is well known that any new adaptation = stress and that stress is best handled in a fasted state. That's my take on it, anyway.

... Still b/c post workout I show heavy ketosis and moderate in the morning, I do not think I am in a fully adapted state yet (where ketonuria would be essentially low-trace as I understand.) One thing I do notice, is that ketostix only show full color (the entire square is colored) post workout and only partial color (1/4 white 3/4 purple) otherwise. I am not sure whether that means the results are under or over-representative of ketone bodies.

There is a correlation between beta-hydroxybutyrate in the blood and acetoacetone in urine during the adaptation stages to a keto diet. But as you know, ketonuria gradually goes away while ketonemia may be growing. While still present, the level of ketonuria ruffly reflects the level of ketonemia several hours ago.

I would interpret your post workout results that during the workout your level of ketosis goes up.

I believe it is your protein intake what lowers your level of ketosis. You guys take too much of it. It supposed to be 1g per kg of lean body mass. What, all of you here have 120 kg of lean body mass? I don't think that even Arnold had that much muscle in his hay day.

Edited by xEva, 22 April 2013 - 01:54 AM.

[alecnevsky]

Thank you for the reply and suggestions.

I pretty much just subscribed to Doug McGuff's MD idea on the metabolic cycle of the cell.

In his book, Body by Science, he says, "The first problem is the belief that the aerobic metabolic pathway can in fact be isolated from the rest of metabolism. The reality is that metabolism is an uninterrupted whole that is intrinsically tied together. The aerobic machinery is fueled by the substrate pyruvate, which can be produced only through the anaerobic pathway. Even at this most fundamental level, the interrelatedness of what Cooper believed to be antipodal elements of metabolism is self-evident" (p 21-23).

As far as protein requirement, I was told lean body mass * activity coefficient (.5-.9) with 120 being considerably less than I actually need whcih is like 144 by this formula. I highly doubt I get close to 144g a day however. 6oz steak is like 46g, bacon is at most like 20g/day, 2 servings whey is like 40g/day, eggs are 7g/egg.

Edited by alecnevsky, 22 April 2013 - 02:46 AM.

[alecnevsky]

This is where I read about the protein requirement on a ketogenic diet. The Art and Science of Low Carbohydrate Living by JeffS. Volek, PhD, RD Stephen D. Phinney, MD, PhD

"Response: First of all, a well-formulated low carbohydrate diet like Atkins is not really that high in protein. We recommend protein between 1.5 and 2.0 grams per kilogram reference body weight (0.7 to 0.9 grams per pound reference weight). This translates to between 90 and 150 grams per day for a range of adults, which is about what the average adult in the US is already eating. This level is well tolerated and is not associated with adverse effects on bone, kidney or other health indictors. The reason that protein intakes higher than the mInImUm recommended (0 . 8 grams per kilogram) were thought to negatively impact bone is because they cause a small but measureable increase in urinary calcium excretion. On the surface, this could indicate a higher risk for bone loss over time and development of osteoporosis. However, we now know that increasing dietary protein above the minimum also causes greater intestinal absorption of dietary calcium, which balances the slightly greater calcium loss in the urine. In fact, recent research suggests that diets higher in protein are associated with healthier bones as people age.

Similar to the situation with bone health, the concern about kidney problems stems from a belief that high protein diets contribute to renal disease. This belief is based on studies of restricting protein in people who already have severely damaged kidneys. However, there is no data linking the moderate protein intake range listed above to damage in people with normal kidney function. In technical terms, despite some evidence that higher protein intakes can increase glomerular filtration rate, the evidence linking this normal physiologic response to progressive loss of kidney function in healthy people is completely lacking" (p 53-54).


So it looks like they're using body weight rather than lean mass which may be less accurate. But given that we know the lean mass/body weight we should be pretty close in estimating it. So I am probably in the upper range of that at the moment which may be slowing down my adaptation. I imagine 2 is athletic and anabolic, 1.9 is athletic 1.8 is active 1.7 is recreationally active 1.6 is mostly sedentary 1.5 is entirely sedentary but this is just a speculation.

Edited by alecnevsky, 22 April 2013 - 07:26 AM.

[xEva]

Thank you for the reply and suggestions.

I pretty much just subscribed to Doug McGuff's MD idea on the metabolic cycle of the cell.

In his book, Body by Science, he says, "The first problem is the belief that the aerobic metabolic pathway can in fact be isolated from the rest of metabolism. The reality is that metabolism is an uninterrupted whole that is intrinsically tied together. The aerobic machinery is fueled by the substrate pyruvate, which can be produced only through the anaerobic pathway. Even at this most fundamental level, the interrelatedness of what Cooper believed to be antipodal elements of metabolism is self-evident" (p 21-23).

Sorry but ti me this sounds like a collection of words, starting with 'the rest of metabolism' and ending with its 'antipodal elements'. I have not read the book but this quote does not invite me.

This is where I read about the protein requirement on a ketogenic diet. The Art and Science of Low Carbohydrate Living by JeffS. Volek, PhD, RD Stephen D. Phinney, MD, PhD

Yes, but how did they arrive at their numbers? The number I'd use comes from the studies of fasting obese men (in the 1960-70s fasting was thought of as a good therapy for obesity and it was studied extensively). Having found out how much lean mass a man would loose in a given fasting period, they followed up with the studies of how much protein to supply to prevent this from happening. That's how, roughly, 1g per kg of lean mass was arrived at.

In contrast, from the quote you give it appears that their sole criterion is that it 'is well tolerated and is not associated with adverse effects' (based largely on regular, carb-based diets, I assume).

The thing is, all protein the body cannot utilize at the moment is converted to glucose. For a carb-based diet, extra protein does not change things much, but for a keto diet that extra protein matters as much as carbs do, simply because the net effect from either one is the same. That's why, in a classical ketogenic diet, carbs and protein are grouped together and their sum is used to arrive at 4:1 ratio of fat to (carbs+protein).

Even if you're not interested in a classical ketogenic diet, in your place I'd try to follow their guidelines at least during the induction period. Otherwise, all you do is postpone your adaptation.

[alecnevsky]

He explains this here. I am interested in what people think of this theory.

[xEva]

He explains this here. I am interested in what people think of this theory.

Me too interested in what people think. The way he talks (or writes in the quote above) only sets off my BS detector. But maybe theory is not his forte? He looks like a good practitioner with biceps the size of his head lol

Edited by xEva, 23 April 2013 - 01:46 AM.

[Hebbeh]

The thing is, all protein the body cannot utilize at the moment is converted to glucose.

Source?

Glucongenesis is much more complex than this.

And this is assuming that gluconeogenesis is 100% efficient which it is not.

And this also assumes that all amino acids convert to glucose which we know is not the case.

[alecnevsky]

He explains this here. I am interested in what people think of this theory.

Me too interested in what people think. The way he talks (or writes in the quote above) only sets off my BS detector. But maybe theory is not his forte? He looks like a good practitioner with biceps the size of his head lol

As I understand, if what he says in his book is true, then the size of his biceps is achieved with little cost in terms of time which would naturally leave him some time to be a good practitioner.

I've been doing "cardio" most of my life though, so I do have some qualms about accepting a theory of global metabolism conditioning.

[Hebbeh]

He explains this here. I am interested in what people think of this theory.

Me too interested in what people think. The way he talks (or writes in the quote above) only sets off my BS detector. But maybe theory is not his forte? He looks like a good practitioner with biceps the size of his head lol

As I understand, if what he says in his book is true, then the size of his biceps is achieved with little cost in terms of time which would naturally leave him some time to be a good practitioner.

I've been doing "cardio" most of my life though, so I do have some qualms about accepting a theory of global metabolism conditioning.

If it was this simple, then all sports would train with the same results from the same protocols...but we know this isn't the case at all. Training protocols are very different for different sports. Marathoners certainly don't excel training like a sprinter.

[alecnevsky]

He explains this here. I am interested in what people think of this theory.

Me too interested in what people think. The way he talks (or writes in the quote above) only sets off my BS detector. But maybe theory is not his forte? He looks like a good practitioner with biceps the size of his head lol

As I understand, if what he says in his book is true, then the size of his biceps is achieved with little cost in terms of time which would naturally leave him some time to be a good practitioner.

I've been doing "cardio" most of my life though, so I do have some qualms about accepting a theory of global metabolism conditioning.

If it was this simple, then all sports would train with the same results from the same protocols...but we know this isn't the case at all. Training protocols are very different for different sports. Marathoners certainly don't excel training like a sprinter.

Right, but the goal of training, which is the goal, I think, of this book, is not to be a great marathoner or sprinter but to be in better health as measured by resting heart rate (with emphasis on variability,) body fat% and other metrics. I understand that training protocols are different. The question is whether one can achieve better health metrics by not training in ways that are deleterious to health (i.e., running marathons.)

Edited by alecnevsky, 23 April 2013 - 04:10 AM.

[Hebbeh]

He explains this here. I am interested in what people think of this theory.

Me too interested in what people think. The way he talks (or writes in the quote above) only sets off my BS detector. But maybe theory is not his forte? He looks like a good practitioner with biceps the size of his head lol

As I understand, if what he says in his book is true, then the size of his biceps is achieved with little cost in terms of time which would naturally leave him some time to be a good practitioner.

I've been doing "cardio" most of my life though, so I do have some qualms about accepting a theory of global metabolism conditioning.

If it was this simple, then all sports would train with the same results from the same protocols...but we know this isn't the case at all. Training protocols are very different for different sports. Marathoners certainly don't excel training like a sprinter.

Right, but the goal of training, which is the goal, I think, of this book, is not to be a great marathoner or sprinter but to be in better health as measured by resting heart rate (with emphasis on variability,) body fat% and other metrics. I understand that training protocols are different. The question is whether one can achieve better health metrics by not training in ways that are deleterious to health (i.e., running marathons.)

When it comes to health and longevity, all things in moderation is the key. Extreme fitness and longevity are mutually exclusive.

[alecnevsky]

He explains this here. I am interested in what people think of this theory.

Me too interested in what people think. The way he talks (or writes in the quote above) only sets off my BS detector. But maybe theory is not his forte? He looks like a good practitioner with biceps the size of his head lol

As I understand, if what he says in his book is true, then the size of his biceps is achieved with little cost in terms of time which would naturally leave him some time to be a good practitioner.

I've been doing "cardio" most of my life though, so I do have some qualms about accepting a theory of global metabolism conditioning.

If it was this simple, then all sports would train with the same results from the same protocols...but we know this isn't the case at all. Training protocols are very different for different sports. Marathoners certainly don't excel training like a sprinter.

Right, but the goal of training, which is the goal, I think, of this book, is not to be a great marathoner or sprinter but to be in better health as measured by resting heart rate (with emphasis on variability,) body fat% and other metrics. I understand that training protocols are different. The question is whether one can achieve better health metrics by not training in ways that are deleterious to health (i.e., running marathons.)

When it comes to health and longevity, all things in moderation is the key. Extreme fitness and longevity are mutually exclusive.

I do agree. But to clarify, extreme in terms of what? 12 min a week of HIT is not extreme in terms of time lost or wear and tear on the joints/metabolism. If we could lower the RHR with significant hr variability by doing controlled pushing/pulling exercises would that make us live less?

[xEva]

The thing is, all protein the body cannot utilize at the moment is converted to glucose.

Source?

Glucongenesis is much more complex than this.

And this is assuming that gluconeogenesis is 100% efficient which it is not.

And this also assumes that all amino acids convert to glucose which we know is not the case.

No one implied that 1 g of protein makes 1 g of glucose. The actual number is in the 0.5 - 0.6 range (-?) Still. Take cats. Their diet is nearly all protein, yet they run on glucose.

The question to you, what is the fate of the protein ingested in excess of body's needs for 'repairs and maintenance'?

[eddielang]

He explains this here. I am interested in what people think of this theory.

Me too interested in what people think. The way he talks (or writes in the quote above) only sets off my BS detector. But maybe theory is not his forte? He looks like a good practitioner with biceps the size of his head lol

As I understand, if what he says in his book is true, then the size of his biceps is achieved with little cost in terms of time which would naturally leave him some time to be a good practitioner.

I've been doing "cardio" most of my life though, so I do have some qualms about accepting a theory of global metabolism conditioning.

If it was this simple, then all sports would train with the same results from the same protocols...but we know this isn't the case at all. Training protocols are very different for different sports. Marathoners certainly don't excel training like a sprinter.

That's because there are specific adaptations to imposed demands. Of one isn't teaching the body how to skillfully sprint, swim, throw, the body won't adapt and learn that skill.

The whole HIT/Superslow can be a good strength/conditioning component for general athletic movements, as it trains MS-ROM in each plane of movement, but to run faster one must run faster.

Your heart doesn't care why it has to push more blood, only that it must. There is no 'cardio', only supply/demand.

He explains this here. I am interested in what people think of this theory.

Me too interested in what people think. The way he talks (or writes in the quote above) only sets off my BS detector. But maybe theory is not his forte? He looks like a good practitioner with biceps the size of his head lol

As I understand, if what he says in his book is true, then the size of his biceps is achieved with little cost in terms of time which would naturally leave him some time to be a good practitioner.

I've been doing "cardio" most of my life though, so I do have some qualms about accepting a theory of global metabolism conditioning.

If it was this simple, then all sports would train with the same results from the same protocols...but we know this isn't the case at all. Training protocols are very different for different sports. Marathoners certainly don't excel training like a sprinter.

That's because there are specific adaptations to imposed demands. Of one isn't teaching the body how to skillfully sprint, swim, throw, the body won't adapt and learn that skill.

HIT/Superslow can be a good strength/conditioning component for general athletic movements, as it trains MS-ROM in each plane of movement, but to run faster one must run faster.

Your heart doesn't care why it has to push more blood, only that it must. There is no 'cardio', only supply/demand.