126 replies to this topic

[stephen_b]

"...The median baseline seizure frequency per week at diet onset was 630 (range 1-1400)...."

That's 3.75 seizures per hour on average? yikes.

What mechanisms might explain kidney stones and fractures? Obviously there is some disregulation of calcium metabolism.

There are multiple ways of achieving ketosis. It may be that the study better supports the argument that achieving ketosis by the guidelines followed in the diet result in increased fracture risk, rather than ketosis in general.

[Skötkonung]

Lest anyone forget the hypothesis I proposed some time ago: Kidney stones in ketosis are promoted by a lack of IP6.

And I believe I showed you a study demonstrating that potassium supplementation solved the kidney stone problem -- it has now been implemented into the John Hopkins Ketogenic Diet Protocol. No need to chelate valuable minerals.

Kidney stones can be prevented in seizure patients on high-fat diet
"In their study of 301 children treated for epilepsy with the ketogenic diet, the researchers found that those who got potassium citrate twice daily were seven times less likely to develop kidney stones; one of 106 (0.9 percent) developed a kidney stone compared to 13 out of 195 (6.7 percent) who were given potassium citrate only after testing positive for elevated levels of blood calcium. Most children received one 30-milliequivalent packet (about 1,170 milligrams or 0.04 ounces) of potassium citrate twice daily."

Edited by Skotkonung, 22 October 2009 - 07:33 PM.

[Blue]

"...The median baseline seizure frequency per week at diet onset was 630 (range 1-1400)...."

That's 3.75 seizures per hour on average? yikes.

What mechanisms might explain kidney stones and fractures? Obviously there is some disregulation of calcium metabolism.

There are multiple ways of achieving ketosis. It may be that the study better supports the argument that achieving ketosis by the guidelines followed in the diet result in increased fracture risk, rather than ketosis in general.

Acidosis, very low IGF-1, poor micronutrient intake, something else? I would say that burden of evidence regarding safety rest on those advocating a long-term ketogenic diet for non-epileptics.

Another study:

BACKGROUND: The ketogenic diet (KD) is a high-fat, low-carbohydrate, and protein diet that effectively treats intractable epilepsy (IE). OBJECTIVE: The purpose of this study was to measure the change in bone mineral content (BMC) in children with IE treated with the KD for 15 mo. DESIGN: Prepubertal children >or=5 y of age with IE were eligible. A 4:1 ketogenic diet was maintained for 15 mo, and whole-body and spine BMCs were measured with dual-energy X-ray absorptiometry. Z scores were generated by comparing the children with IE with a cohort of 847 healthy children. Other measurements included demographics, anthropometry, serum 25-hydroxyvitamin D (25-OHD), intact parathyroid hormone, electrolytes, and dietary intake. All measurements were performed at baseline and at 3, 6, 12, and 15 mo. Longitudinal mixed effects models were used to analyze change in BMC over time. RESULTS: Twenty-five children (9 girls, 16 boys) with IE [age (x +/- SD): 7.3 +/- 1.9 y] participated. Growth and bone health status were suboptimal as were serum 25-OHD concentrations and dietary intake of calcium and vitamin D. Whole-body and spine BMC-for-age both declined by 0.6 z score/y and whole-body and spine BMC-for-height declined 0.7 z score/y and 0.4 z score/y, respectively. Height declined 0.5 z score/y. Body mass index (BMI; in kg/m(2)) z score, age, and ambulation were positive predictors of BMC, which declined sharply over 15 mo of KD treatment. CONCLUSION: Bone health in children with IE was poor, particularly for younger nonambulatory children with low BMI status. The KD resulted in progressive loss of BMC. The mechanism is unclear. Further studies are needed.
http://www.ncbi.nlm....pubmed/19064531

[Skötkonung]

As for bones:
Study: The effect of a low-carbohydrate diet on bone turnover
"Although the patients on the low-carbohydrate diet did lose significantly more weight than the controls did, the diet did not increase bone turnover markers compared with controls at any time point. Further, there was no significant change in the bone turnover ratio compared with controls."

Interestingly, one often not mentioned aspect of epileptics is that anticonvulsant drugs induce bone disease.

[Blue]

As for bones:
Study: The effect of a low-carbohydrate diet on bone turnover
"Although the patients on the low-carbohydrate diet did lose significantly more weight than the controls did, the diet did not increase bone turnover markers compared with controls at any time point. Further, there was no significant change in the bone turnover ratio compared with controls."

Interestingly, one often not mentioned aspect of epileptics is that anticonvulsant drugs induce bone disease.

A low-carboyhdrate diet is not necessarily ketogenic and ketones were not mentioned as being measured. The seond point is another possible explanation although one of the successes of the ketogenic diet for epileptics is reduced/eliminated medication.

Edited by Blue, 22 October 2009 - 07:45 PM.

[Shepard]

There is no such thing as long-term ketone production at the levels you'll see in induction phases (outside of dietary conversion). Ketones are an intermediate fuel, most tissues can adapt to using FFA after a relatively short period.

Edited by Shepard, 22 October 2009 - 08:02 PM.

[kismet]

And I believe I showed you a study demonstrating that potassium supplementation solved the kidney stone problem -- it has now been implemented into the John Hopkins Ketogenic Diet Protocol. No need to chelate valuable minerals

... and I believe I told you to stop perpetrating the lie of IP6 leading to meaningful chelation and thus mineral deficiency. The evidence to back this claim is still outstanding.

Acidosis (did any study measure blood pH?), low IGF-1, micros might be involved as Blue mentioned and IP6, but the latter is probably the strongest known risk factor for kidney stones. Quite difficult to deny it really.

Or maybe not? Blue where did you get acidosis from, is there data on blood pH (not just PRAL or other markers)?
From what I just found, it seems that the changes are at least similar to low fat. Both diets reduced blood pH somewhat but maybe it's just the reduced calorie intake?

Eur J Clin Nutr. 2007 Dec;61(12):1416-22. Epub 2007 Feb 14.
Acid-base analysis of individuals following two weight loss diets.
Yancy WS Jr, Olsen MK, Dudley T, Westman EC.

Edited by kismet, 22 October 2009 - 11:40 PM.

[Blue]

Blue where did you get acidosis from, is there data on blood pH (not just PRAL or other markers)?

Just a thought since the ketone bodies are acids that can cause severe acidosis (ketoacidosis).

[Skötkonung]

That protocol is certainly not followed by all studies claiming a "ketogenic diet". Here is one:

"At the first visit, participants were instructed how to fol-low the LCKD as individuals or in small groups, with aninitial goal of ≤20 g carbohydrate per day. Participantswere taught the specific types and amounts of foods theycould eat, as well as foods to avoid. Initially, participantswere allowed unlimited amounts of meats, poultry, fish,shellfish, and eggs; 2 cups of salad vegetables per day; 1cup of low-carbohydrate vegetables per day; 4 ounces ofhard cheese; and limited amounts of cream, avocado,olives, and lemon juice. Fats and oils were not restrictedexcept that intake of trans fats was to be minimized."

This study actually measured ketone bodies:
"The proportion ofparticipants with a urine ketone reading greater than tracewas 1 of 17 participants at baseline, 5 of 17 participants atweek 2, and similar frequencies at subsequent visits untilweek 14 when 2 of 18 participants had readings greaterthan trace and week 16 when 2 of 21 participants had readings greater than trace. During the study, only 27 of151 urine ketone measurements were greater than trace,with one participant accounting for all 7 occurrences ofthe highest urine ketone reading."

Despite this the title of the study proudly proclaims that it was a ketogenic diet: "A low-carbohydrate, ketogenic diet to treat type 2 diabetes""!!!
http://srv9.louhi.ne...3-7052-2-34.pdf

The study you have described does in fact feature a Ketogenic diet. I think you are confused about what constitutes ketogenesis.

Ketones are produced as a byproduct of gluconeogenesis, whereby the body is forced to make glucose from either exogenous or endogenous proteins. The body undergoes gluconeogenesis when carbohydrate is restricted below the level needed to satiate all glucose dependent tissues. Most people go into a state of gluconeogenesis at some point during the day. If prolonged gluconeogenesis occurs, the body begins to utilize ketones over glucose in order to spare protein (muscle in the case of starvation).

So, since most people need more than 200g of carbohydrate a day to satiate their glucose dependent tissues it would follow that people such as these...
"LCKD as individuals or in small groups, with aninitial goal of ≤20 g carbohydrate per day"
...Would be in a state if Ketosis. Their diet was Ketogenic.

Now you have indicated confusion about urine test. According to this study (An evaluation of Ketostix strips) urine ketone levels are not the most accurate way to judge the severity of ketosis. Some people excrete ketones through their breath or sweat, while others such as active individuals, will utilize all excess ketones thus having little in their urine. The only accurate way to measure direct levels of ketones is through the blood, but rest assured that anyone on a carbohydrate restricted diet for more than a few days will be in some degree ketosis.

Another paper: http://www.ncbi.nlm....f...&part=A4143

"Ketostix test is most accurate when urines are tested with a high specific gravity (between 1.010 and 1.020) and low-pH. Highly pigmented urine specimens may yield false positive readings. Levodopa will also cause a false positive result. Ketostix strips are less sensitive than Acetest tablets and have a high degree of variability between lots."

[Skötkonung]

And I believe I showed you a study demonstrating that potassium supplementation solved the kidney stone problem -- it has now been implemented into the John Hopkins Ketogenic Diet Protocol. No need to chelate valuable minerals

... and I believe I told you to stop perpetrating the lie of IP6 leading to meaningful chelation and thus mineral deficiency. The evidence to back this claim is still outstanding.

I'll stop bashing IP6 when you trash the notion that it is required to prevent kidney stones. Other potential benefits aside (such as with cancer and lower plasma cholesterol and triglyceride levels), I see no strong reason to endorse phytic acid as a required nutrient. If eaten in high amounts or if one has low access to essential minerals, it can be deleterious to health and cause malnutrition.

Seeds for a better future: ‘low phytate’ grains help to overcome malnutrition and reduce pollution
"Seed-derived dietary InsP₆ can contribute to iron and zinc deficiency in human populations. Excretion of ‘phytic acid phosphorus’ by non-ruminants such as poultry, swine and fish can contribute to water pollution."

[Blue]

That protocol is certainly not followed by all studies claiming a "ketogenic diet". Here is one:

"At the first visit, participants were instructed how to fol-low the LCKD as individuals or in small groups, with aninitial goal of ≤20 g carbohydrate per day. Participantswere taught the specific types and amounts of foods theycould eat, as well as foods to avoid. Initially, participantswere allowed unlimited amounts of meats, poultry, fish,shellfish, and eggs; 2 cups of salad vegetables per day; 1cup of low-carbohydrate vegetables per day; 4 ounces ofhard cheese; and limited amounts of cream, avocado,olives, and lemon juice. Fats and oils were not restrictedexcept that intake of trans fats was to be minimized."

This study actually measured ketone bodies:
"The proportion ofparticipants with a urine ketone reading greater than tracewas 1 of 17 participants at baseline, 5 of 17 participants atweek 2, and similar frequencies at subsequent visits untilweek 14 when 2 of 18 participants had readings greaterthan trace and week 16 when 2 of 21 participants had readings greater than trace. During the study, only 27 of151 urine ketone measurements were greater than trace,with one participant accounting for all 7 occurrences ofthe highest urine ketone reading."

Despite this the title of the study proudly proclaims that it was a ketogenic diet: "A low-carbohydrate, ketogenic diet to treat type 2 diabetes""!!!
http://srv9.louhi.ne...3-7052-2-34.pdf

The study you have described does in fact feature a Ketogenic diet. I think you are confused about what constitutes ketogenesis.

Ketones are produced as a byproduct of gluconeogenesis, whereby the body is forced to make glucose from either exogenous or endogenous proteins. The body undergoes gluconeogenesis when carbohydrate is restricted below the level needed to satiate all glucose dependent tissues. Most people go into a state of gluconeogenesis at some point during the day. If prolonged gluconeogenesis occurs, the body begins to utilize ketones over glucose in order to spare protein (muscle in the case of starvation).

So, since most people need more than 200g of carbohydrate a day to satiate their glucose dependent tissues it would follow that people such as these...
"LCKD as individuals or in small groups, with aninitial goal of ≤20 g carbohydrate per day"
...Would be in a state if Ketosis. Their diet was Ketogenic.

Now you have indicated confusion about urine test. According to this study (An evaluation of Ketostix strips) urine ketone levels are not the most accurate way to judge the severity of ketosis. Some people excrete ketones through their breath or sweat, while others such as active individuals, will utilize all excess ketones thus having little in their urine. The only accurate way to measure direct levels of ketones is through the blood, but rest assured that anyone on a carbohydrate restricted diet for more than a few days will be in some degree ketosis.

Another paper: http://www.ncbi.nlm....f...&part=A4143

"Ketostix test is most accurate when urines are tested with a high specific gravity (between 1.010 and 1.020) and low-pH. Highly pigmented urine specimens may yield false positive readings. Levodopa will also cause a false positive result. Ketostix strips are less sensitive than Acetest tablets and have a high degree of variability between lots."

Not sure that a 40 years old study says anything about current sticks.

A study ( http://www.imminst.o...t...ost&id=6910 ) you cited previously, regarding the ketogenic diet for children, states "The most common way to measure adherence to the ketogenic diet regimen is urine ketones (specifically, β-hydroxybutyrate, and acetoacetate), an easy and relatively cost-effective indicator of ketosis." The "ketogenic diet" study I cited previously failed this test of ketosis for almost all of those on the "ketogenic diet".

Regarding "rest assured that anyone on a carbohydrate restricted diet for more than a few days will be in some degree ketosis.", I am not assured. A normal western diet, not to mention an Atkins diet, diet gives plenty of not needed protein that can be degraded to glucose for the brain. If you want to make that claim, source please.

Edited by Blue, 23 October 2009 - 12:22 AM.

[Skötkonung]

Regarding "rest assured that anyone on a carbohydrate restricted diet for more than a few days will be in some degree ketosis.", I am not assured. A normal western diet, not to mention an Atkins diet, diet gives plenty of not needed protein that can be degraded to glucose for the brain. If you want to make that claim, source please.

So if the body is making glucose from protein, what will be the byproduct and what does the body do with that byproduct? You seem to be missing a few things.

Effects of a high-protein ketogenic diet on hunger, appetite, and weight loss in obese men feeding ad libitum 1,2,3
"Ad libitum energy intakes were lower with the LC diet than with the MC diet [P = 0.02; SE of the difference (SED): 0.27] at 7.25 and 7.95 MJ/d, respectively. Over the 4-wk period, hunger was significantly lower (P = 0.014; SED: 1.76) and weight loss was significantly greater (P = 0.006; SED: 0.62) with the LC diet (6.34 kg) than with the MC diet (4.35 kg). The LC diet induced ketosis with mean 3-hydroxybutyrate concentrations of 1.52 mmol/L in plasma (P = 0.036 from baseline; SED: 0.62) and 2.99 mmol/L in urine (P < 0.001 from baseline; SED: 0.36)."

These individuals had 30% of their diet consist of protein. That is double the American average.

Edited by Skotkonung, 23 October 2009 - 12:24 AM.

[Blue]

Regarding "rest assured that anyone on a carbohydrate restricted diet for more than a few days will be in some degree ketosis.", I am not assured. A normal western diet, not to mention an Atkins diet, diet gives plenty of not needed protein that can be degraded to glucose for the brain. If you want to make that claim, source please.

So if the body is making glucose from protein, what will be the byproduct and what does the body do with that byproduct? You seem to be missing a few things.

It is not my job to make your argument. If there is one, state it.

Effects of a high-protein ketogenic diet on hunger, appetite, and weight loss in obese men feeding ad libitum 1,2,3
"Ad libitum energy intakes were lower with the LC diet than with the MC diet [P = 0.02; SE of the difference (SED): 0.27] at 7.25 and 7.95 MJ/d, respectively. Over the 4-wk period, hunger was significantly lower (P = 0.014; SED: 1.76) and weight loss was significantly greater (P = 0.006; SED: 0.62) with the LC diet (6.34 kg) than with the MC diet (4.35 kg). The LC diet induced ketosis with mean 3-hydroxybutyrate concentrations of 1.52 mmol/L in plasma (P = 0.036 from baseline; SED: 0.62) and 2.99 mmol/L in urine (P < 0.001 from baseline; SED: 0.36)."

These individuals had 30% of their diet consist of protein. That is double the American average.

Both diets caused weight loss so they were CR diets. If energy intake is lower and percent protein is unchanged absolute protein intake will be lower. This still probably gives a protein intake higher than the average american. So yes, in this study low carbohydrates and high protein were ketogenic. But this was in a weight loss situation. The situation may well be different in a steady-state situation where fat tissue is not degraded. There is a likely a reason protein restriction is done in the ketogenic diet for children with epilepsy. If the protein restriction could be skipped the diet would be much less difficult for the children and parents.

Regardless, I showed a study that claimed a ketogenic diet in the title that was not ketogenic according to the measurement used in the golden standard, the ketogenic diet for children with epilepsy.

Edited by Blue, 23 October 2009 - 12:53 AM.

[Skötkonung]

It is not my job to make your argument. If there is one, state it.

It is your job to have a basic understanding of human metabolism before you go on arguing one point or another. If you don't think the process I described is accurate, please define an alternative.

[Skötkonung]

Both diets caused weight loss so they were CR diets. Energy intake looks to be about at least 1/4 lower than normal. If energy intake is lower and percent protein is unchanged absolute protein intake will be lower. This still probably gives a protein intake higher than the average american. So yes, in this study low carbohydrates and high protein were ketogenic. But this was in a weight loss situation. The situation may well be different in a steady-state situation where fat tissue is not degraded. There is a likely a reason protein restriction is done in the ketogenic diet for children with epilepsy. If the protein restriction could be skipped the diet would be much less difficult for the children and parents.

Average adult male intakes 2,500 calories daily. 1g protein is 4 calories. With that in mind, using your estimate that they were consuming 75% of normal caloric intake, these men were eating 1,875 calories daily. 30% of that is 562.5 calories from protein, or 140.625g of protein daily.

According to Trends in Intake of Energy and Macronutrients—United States, 1971-2000:
"In the current U.S. diet the average protein intake is 98.6 g/day (15.5 % of total energy) for men.."

So yes, even with a caloric deficit, these men were still consuming a high protein diet.

Regarding the children, I don't see why a low protein diet would be any different from a high protein diet in terms of ketosis? The body will utilize gluconeogenesis to provide glucose regardless of whether there is sufficient dietary protein. It will create glucose from the muscle if necessary.

Referring again to the JHU protocol for epilepsy treatment, they mention 1g of protein per 1 kg of weight (.5g to 1lb). That is about 15% of normal caloric intake, which makes it neither high nor low, but average.

Wikipedia refers to this in the article of Ketogenic diet:
"Wilder's colleague, paediatrician Mynie Peterman, later formulated the "classic" diet, with a ratio of one gram of protein per kilogram of body weight in children, 10–15 g of carbohydrate per day, and the remainder of calories from fat."

Edited by Skotkonung, 23 October 2009 - 01:11 AM.

[Blue]

Regarding the children, I don't see why a low protein diet would be any different from a high protein diet in terms of ketosis? The body will utilize gluconeogenesis to provide glucose regardless of whether there is sufficient dietary protein. It will create glucose from the muscle if necessary.

Referring again to the JHU protocol for epilepsy treatment, they mention 1g of protein per 1 kg of weight (.5g to 1lb). That is about 15% of normal caloric intake, which makes it neither high nor low, but average.

Wikipedia refers to this in the article of Ketogenic diet:
"Wilder's colleague, paediatrician Mynie Peterman, later formulated the "classic" diet, with a ratio of one gram of protein per kilogram of body weight in children, 10–15 g of carbohydrate per day, and the remainder of calories from fat."

One gram of protein per kilogram is restricted compared to the average american diet. The source regarding the ketogenic diet for children ( http://www.imminst.o...t...ost&id=6910 ) states that "The typical ratio of fats to carbohydrates and protein (in terms of grams) is 3:1 or 4:1" so protein and carbohydrates are considered equal as antagonists to ketone production.

If there is sufficient glucose from excess protein converted by gluconeogenesis there is no need to produce ketone bodies. Excess fat cannot be converted to glucose by gluconeogenesis and instead ketone bodies are made.

[Skötkonung]

If there is sufficient glucose from excess protein converted by gluconeogenesis there is no need to produce ketone bodies. Excess fat cannot be converted to glucose by gluconeogenesis and instead ketone bodies are made.

Ketone bodies are produced regardless of whether they are technically "needed" because they power gluconeogenesis. Gluconeogenesis and ketone production can be considered synonymous, as the two are more or less interdependent.

Described below is the metabolic pathway for Ketosis:
"Ketone bodies, from the breakdown of fatty acids to acetyl groups, are also produced during this state, and are burned throughout the body. Excess ketone bodies will slowly decarboxylate into acetone. That molecule is excreted in the breath and urine. When glycogen stores are not available in the cells (glycogen is primarily created when carbohydrates such as starch and sugar are consumed in the diet), fat (triacylglycerol) is cleaved to give 3 fatty acid chains and 1 glycerol molecule in a process called lipolysis."

So, to begin gluconeogenesis, first carbohydrate must be restricted. Initially, glycogen can be made into glucose, but the process does not work efficiently in reverse without the presence of insulin. Triacylglycerol produced during lipolysis will be used to power gluconeogenesis.

From the article on glycogen:
"As a meal containing carbohydrates is eaten and digested, blood glucose levels rise, and the pancreas secretes insulin. Glucose from the hepatic portal vein enters the liver cells' (hepatocytes). Insulin acts on the hepatocytes to stimulate the action of several enzymes, including glycogen synthase."

Because carbohydrate is restricted and thus insulin is not secreted, the body quickly runs low on glycogen and must seek an energy source for glucose dependent tissues. Gluconeogenesis cannot create more glycogen. Furthermore, if gluconeogenesis could create unlimited supplies of glucose without the presence of ketone bodies, then ketosis would never occur regardless of dietary protein levels - the body has plentiful protein reserves in the muscle and other structural tissues. The body has not evolved to let gluconeogenesis run rampant, as it would not be conducive to survival in fasted situations. Interestingly, lipolysis creates byproducts that are used to power gluconeogenesis, and that creates ketone bodies. Lipolysis also directly creates ketone bodies.

"When the liver engages in gluconeogenesis it burns fats (which are the energy for the gluconeogenic process), but is unable to fully metabolize them to carbon dioxide and water. These semi-metabolized fat products are then converted into ketone bodies. They are released into the blood, from where they are taken up and utilized by most tissues, where they are turned into carbon dioxide and water. The heart utilizes ketone bodies, so do the muscles, and also the brain which normally only burns glucose, although the brain cannot survive without glucose."

Ketogenesis:
"Ketone bodies are produced mainly in the mitochondria of liver cells. Its synthesis occurs in response to low glucose levels in the blood, and after exhaustion of cellular carbohydrate stores, such as glycogen. The production of ketone bodies is then initiated to make available energy that is stored as fatty acids."

About Lipolysis:
"Lipolysis is the breakdown of fat stored in fat cells. During this process, free fatty acids are released into the bloodstream and circulate throughout the body. Ketones are produced, and are found in large quantities in ketosis (a state in metabolism occurring when the liver converts fat into fatty acids and ketone bodies which can be used by the body for energy)."

To regulate catabolism, the body must reduce its need for glucose.

More about Ketosis:
Most of the body is able to utilize fatty acids as an alternative source of energy in a process where fatty acid chains are cleaved to form acetyl-CoA, which can then be fed into the Krebs Cycle. It is important to note that acetyl-CoA can only enter the Krebs Cycle bound to oxaloacetate. When carbohydrate supplies are inadequate, however, the liver naturally converts oxaloacetate to glucose via gluconeogenesis for use by the brain and other tissues. When acetyl CoA does not bind with oxaloacetate, the liver converts it to ketones (or ketone bodies), leading to a state of ketosis. During this process a high concentration of glucagon is present in the serum and this inactivates hexokinase and phosphofructokinase-1 (regulators of glycolysis) indirectly, causing most cells in the body to use fatty acids as their primary energy source. At the same time, glucose is synthesized in the liver from lactic acid, glucogenic amino acids, and glycerol, in a process called gluconeogenesis. This glucose is used exclusively for energy by cells such as neurons and red blood cells."

About acetyl-CoA:
"In animals, acetyl-CoA is central to the balance between carbohydrate metabolism and fat metabolism. In normal circumstances, acetyl-CoA from fatty acid metabolism feeds into the citric acid cycle, contributing to the cell's energy supply. In the liver, when levels of circulating fatty acids are high, the production of acetyl-CoA from fat breakdown exceeds the cellular energy requirements. To make use of the energy available from the excess acetyl-CoA, ketone bodies are produced which can then circulate in the blood. Therefore, when at rest, both the skeletal and cardiac muscles satisfy their energy requirement mainly through oxidation of ketone bodies."

Ketogenesis regulation:
"When the body has no free carbohydrates available, fat must be broken down into acetyl-CoA in order to get energy. Acetyl-CoA is not being recycled through the citric acid cycle because the citric acid cycle intermediates (mainly oxaloacetate) have been depleted to feed the gluconeogenesis pathway, and the resulting accumulation of acetyl-CoA activates ketogenesis."

In time, the body reduces its need for glucose to spare muscle and dietary protein:
"After the diet has been changed to lower blood glucose for 3 days, the brain gets 30% of its energy from ketone bodies. After about 40 days, this goes up to 70% (during the initial stages the brain does not burn ketones, since they are an important substrate for lipid synthesis in the brain). In time the brain reduces its glucose requirements from 120g to 40g per day."

Edited by Skotkonung, 23 October 2009 - 08:51 PM.

[Skötkonung]

One gram of protein per kilogram is restricted compared to the average american diet. The source regarding the ketogenic diet for children ( http://www.imminst.o...t...ost&id=6910 ) states that "The typical ratio of fats to carbohydrates and protein (in terms of grams) is 3:1 or 4:1" so protein and carbohydrates are considered equal as antagonists to ketone production.

4:1 is not a low protein diet. It is average. I looked at some ketogenic diets and I found one that is 4:1:1 for Fat, Protein, and Carbohydrate respectively.

1000 calories from fat would mean 250 calories coming form both carbohydrate and protein each. Scale that by a factor of 1.5 to achieve more realistic numbers for an adult male. 1,500 calories from fat and 375 from protein and carbohydrate each. At 4 calories per 1g of protein, that means an adult consuming a 2,250 calorie diet would be consuming 93.75g protein or over 16.67% dietary protein. Not high, but slightly above average compared to most Americans. Carbohydrates are maintained at the same 93.75g, which is enough to induce some level of ketone production, while also allowing for consumption of fruits and vegetables.

1:3 would yield higher results.

[Blue]

One gram of protein per kilogram is restricted compared to the average american diet. The source regarding the ketogenic diet for children ( http://www.imminst.o...t...ost&id=6910 ) states that "The typical ratio of fats to carbohydrates and protein (in terms of grams) is 3:1 or 4:1" so protein and carbohydrates are considered equal as antagonists to ketone production.

4:1 is not a low protein diet. It is average. I looked at some ketogenic diets and I found one that is 4:1:1 for Fat, Protein, and Carbohydrate respectively.

1000 calories from fat would mean 250 calories coming form both carbohydrate and protein each. Scale that by a factor of 1.5 to achieve more realistic numbers for an adult male. 1,500 calories from fat and 375 from protein and carbohydrate each. At 4 calories per 1g of protein, that means an adult consuming a 2,250 calorie diet would be consuming 93.75g protein or over 16.67% dietary protein. Not high, but slightly above average compared to most Americans. Carbohydrates are maintained at the same 93.75g, which is enough to induce some level of ketone production, while also allowing for consumption of fruits and vegetables.

1:3 would yield higher results.

Lots of assumptions and guesses. No need for that. Here is an exact description:

Energy distribution:
Fat

90%

LCT

100%

Carbohydrate

1.60 %

Protein

8.40 %

http://www.shsna.com/pages/ketocal.htm

So certainly a low protein diet.

Edited by Blue, 23 October 2009 - 11:37 PM.

[Blue]

If there is sufficient glucose from excess protein converted by gluconeogenesis there is no need to produce ketone bodies. Excess fat cannot be converted to glucose by gluconeogenesis and instead ketone bodies are made.

Ketone bodies are produced regardless of whether they are technically "needed" because they power gluconeogenesis. Gluconeogenesis and ketone production can be considered synonymous, as the two are more or less interdependent.

(lots of quotes)

Ketone bodies are not "needed" in order to do gluconeogenesis. For example, lactate after exercise is converted to glucose by gluconeogenesis.

None of your quotes states that excess dietary protein would not be converted to glucose during a glucose deficiency. Again, why would the ketogenic diet for children with epilepsy consider the carbohydrates + protein vs. fat ratio if excess protein intake would not inhibit ketone production? The diet would be enormously simpler if only carbohydrate restriction was needed.

Edited by Blue, 24 October 2009 - 12:48 AM.

[Saber]

If there is sufficient glucose from excess protein converted by gluconeogenesis there is no need to produce ketone bodies. Excess fat cannot be converted to glucose by gluconeogenesis and instead ketone bodies are made.

Ketone bodies are produced regardless of whether they are technically "needed" because they power gluconeogenesis. Gluconeogenesis and ketone production can be considered synonymous, as the two are more or less interdependent.

(lots of quotes)

Ketone bodies are not "needed" in order to do gluconeogenesis. For example, lactate after exercise is converted to glucose by gluconeogenesis.

None of your quotes states that excess dietary protein would not be converted to glucose during a glucose deficiency. Again, why would the ketogenic diet for children with epilepsy consider the carbohydrates + protein vs. fat ratio if excess protein intake would not inhibit ketone production? The diet would be enormously simpler if only carbohydrate restriction was needed.

From what I have read and Skotkonung's quotes, protein conversion into glucose via gluconeogenesis triggers ketosis through certain chemical pathways. Once the person is deep enough into ketosis, the body prefers ketone over glucose, so this keeps gluconeogenesis from going rampant. From then on, gluconeogenesis is only utilized to produce glucose for tissues that absolutely requires them and so it is important to consume enough fat otherwise you will go into rabbit starvation. Any glucogenesis will automatically trigger ketosis but it's important that you have enough fat to maintain the body once in ketosis or it will utilize glucose via gluconeogenesis for energy. I suspect this mechanism is evolution's way of preventing protein poisoning. It's all about how adapted your body is at this process. A person on a ketogenic diet long-term will be adapted and prefer fat over any protein.

If the person is consuming too much protein, we can logically assume that they are not consuming enough nearly enough fat to satisfy energy requirement, since if they were consuming enough fat to satisfy energy requirement and excess protein at the same time, they are severely over-eating or taking a lot of whey protein and not lifting any weight. Then we can assume that without enough fat, ketosis won't satisfy the body's energy requirement and gluconeogenesis will be the primary pathway for energy.

Excess protein causes protein poisoning and is often the misconception of the Atkins diet by many people and the "feels like I'm dying symptom".

So excess dietary proteins will be converted to glucose, but it is not a huge deal every once in a while. It happens when we are on a normal standard diet. When you put a person on it day after day, the high mortality is no surprise. I would expect to die after a month from protein poisoning. You will never consume enough protein for the body to satisfy it's glucose requirement via gluconeogenesis, not long-term. One of the symptom of rabbit starvation is an insatiable desire for fat or carbohydrate.
Try putting anyone on a high-protein diet and we will see, they will go into rabbit starvation, abandon the experiment and proceed to gorging on carbs and fat.

So in conclusion, there is no such thing as a high-protein diet. If a person can survive on a high-protein diet, then the protein ratio is not high enough and they're eating enough fat to stave off symptoms of rabbit starvation for the time being, although no doubt, it's stressing their body severely.

Of course, it is not absolute. We're playing with ratios here. We can assume that anyone consuming excess protein over long period will be a suspect of high mortality, this is obvious from what we seen of the danger of protein over-consumption.
A perfect ketogenic diet would be enough protein to maintain muscle and satisfy glucose-dependent tissues but no more, the rest should be fat.

A lot of us on the ketogenic diet probably doesn't have this ratio perfect but neither does normal people on a normal diet. A little protein metabolizing into glucose wouldn't necessarily be so bad as long as it isn't too much.
I fully admit I don't know what this ratio is and it's highly dependent on the person but I consume a normal recommended amount of protein with any accidental carbs and the rest is fat. It's probably best to keep protein at a normal level of a standard diet instead of gorging on meat everyday since we are using fat as an energy source over carbs, it doesn't make sense to raise protein consumption.

We should consider any excess protein greater than what is needed as poison and poison certainly increases mortality. Consuming excess protein on a ketogenic diet is a real danger and I think many people overconsume protein all along this process. Too much meat is eaten. I decrease my protein intake to only a few times per week. Unexpected, it has turned out to be almost like a vegetarian diet.

To the people who consume meat and fish everyday on a ketogenic diet, watch your protein intake. Hell, you may not even be in ketosis anymore.

Edited by Saber, 24 October 2009 - 03:26 AM.

[niner]

Nice post, Saber. What's rabbit starvation?

[Saber]

I don't think even the government has any idea exactly how much protein is need per day without the body metabolizing protein into glucose which we all see is detrimental. And it is because there is so much variable, but there is no reason whatsoever to double the RDA for protein even if you're weightlifting because the body never use all that protein in a day to form new muscle.
Of course, a lot of these guys take steroid and doesn't care about their health, so their logic is it's better to have more than you need.

For example, the protein RDA for a male my weight of 56kg is 45g. He should be eating a little bit more of protein on a keto diet, 45g on a high carb diet or other diet, assuming the Institute of Medicine is right. There is no reason whatsoever for him to consume more than this amount of protein unless he is very active or weight-lifting.

Let's plot out a random diet.

8oz of cream cheese -16g of protein and 800 calories
4 chicken eggs- 50.4 g of protein and 600 calories
4 tablespoon of peanut butter- 14g protein and 400 calories

Total 80.4g protein and 1800 calories.
This is just a wild-ass random diet. I don't know how much protein is need in order to satisfy the brain's glucose need, but it's safer to go overboard just a tad bit and put a little strain on the kidney instead of not having enough glucose for the brain.

If he just jumped in and eat a steak on top on this which I see many people do, just eat tons of meat, fish and poultry, he would probably go over the protein requirement and put great strain on the body long-term because he is obviously over-eating which goes back to my last point.
This is all assuming the RDA is correct and the person is rather sedentary.

Again, no absolutes because the body may just be switching in and out, using glucose or fat depending on how much protein and carbs you're consuming. This is just my theory.

I doubt you will ever consciously consume enough protein to put yourself into rabbit starvation, but depending on how much more protein than the RDA amount + however much it is your brain needs for glucose, you are probably out of ketosis at some point during the day and switching back to ketosis later. The thing is we don't know. There aren't a lot of studies on this and a person at home can't accurately know whether or not they are in ketosis.

The unknown is we don't know how much protein the body absolutely need and there are many variables, protein not being the exact amount that is labeled or getting lost somewhere in the process.

In the end, it's safer to eat just a bit more protein but all that meat, poultry and fish is going to strain you.

And to address my previous post saying that there is no such thing as a protein diet, we are arguing over semantic. I would only consider a diet high protein when it induces protein poisoning or straining you dangerously long-term.
Again, all a matter of degree. Unless a person has deliberately plot out their keto diet and thought about this, they're probably poisoning themselves with protein long-term, which was Blue's point.

Also edit: I meant I decrease my meat intake to only a few times per week.

Edited by Saber, 24 October 2009 - 04:17 AM.

[Shepard]

And we roll back around to Kwasniewski's Optimal Diet.

[Saber]

I think my two previous post may be a bit confusing.
Let me summarize this whole thing.

There is no such thing as a high-protein diet because it's like saying there's a high-poison diet.

If you're over-consuming protein, you're either:
A: Over-eating
B: Poisoning yourself by consuming too much protein and not enough fat at the same time, and this is not a safe keto diet.

And an alarming amount of people on the keto diet is in boat B. It's easy to go over that protein RDA if you're eating meat and at the same time over-estimating fat intake.

Just eat a lot of fat, a lot of fat or you're screwing yourself long-term.

As for the argument, does protein metabolizing into glucose temporarily halt ketosis? My theory is no, unless you're not eating enough fat. This is because the body prefers fat as an energy, but if you're not eating enough fat, it's going to start using protein, danger, danger, danger.

Protein metabolizing into glucose via gluconeogenesis happens concurrently in the body along with ketosis. Ketosis will not stop unless you give it a reason to by not eating enough fat.

And in theory, it is not possible to over-eat protein and eating enough fat at the same time and call this an optimal diet, because then you will be back in boat A. Those excess calories from protein over-consumption means you are over-eating and anytime someone is over-eating, they got worse things to worry about.

Then we got someone in the crowd asking, won't all that saturated fat make me stupid? [lol]

The argument never ends. Just browsing around the low-carb forums and looking at people's diet plan, they're slowly poisoning themselves with protein.

Edited by Saber, 24 October 2009 - 04:39 AM.

[rwac]

Just eat a lot of fat, a lot of fat or you're screwing yourself long-term.

But short term, a high protein diet might be good for fat loss.

[Saber]

Just eat a lot of fat, a lot of fat or you're screwing yourself long-term.

But short term, a high protein diet might be good for fat loss.

Not really. See, we are arguing over semantic once again. Ask ourselves what is a "high protein" diet?

If you're are eating more protein than you need, that is more than the amount needed for glucose-dependent tissues (which is not fixed depending on how adapted the brain is at utilizing ketones, the complexitiy [lol]) and assuming you're eating exactly the body calories requirement, then you're are not eating enough fat for it to be considered an optimal keto diet. And we know that if you don't have enough fat, you go into rabbit starvation and subsequent protein poisoning. Although it is minor and you won't get the huge symptoms unless stretched over a long period.

If you are eating enough fat to satisfy caloric spending and more protein then you need, which happens fairly often on a normal diet, then you are over-eating and all argument ends when you are over-eating.

It's so complex. This is my theory from just organic chemistry knowledge and logic since I haven't found a lot of studies going into exact details of what exactly happens during this process, what if this, what if that.

Shepard claims that the body will start using FFA. I don't even know what that is about. All the studies I have looked at feed people or rats a certain proportion of macronutrients and proceed to make a big sensational claim.
There's probably a lot going on that we don't know yet in terms of exact biochemistry. Glucose tablets has been shown to temporarily halt ketosis. Then can we truly assume that excess protein will also halt ketosis? Not really, for one, protein is not glucose and their metabolism into glucose is directly suppressed in the presence of ketosis. Ketosis can only sustained with high fat intake so if you're not eating enough fat and carbs, the body is eating away dietary protein and muscle and at the same time creating toxic byproducts. So you may lose weight by restricting fat, but it will be muscle that you're losing.

Remember, medical science in general still consider ketogenic diet to be bad. We don't know anything yet.

Edited by Saber, 24 October 2009 - 05:13 AM.

[rwac]

Not really. See, we are arguing over semantic once again. Ask ourselves what is a "high protein" diet?

So normal protein, less fat, near-zero carbs.
High percentage of protein might be useful for fat loss.

[Blue]

More nasty things from the ketogenic diet for children with epilepsy:

"Cardiac complications of the ketogenic diet, in the absence of selenium deficiency, have not been reported. Twenty patients on the ketogenic diet at one institution were investigated. Prolonged QT interval (QTc) was found in 3 patients (15%). There was a significant correlation between prolonged QTc and both low serum bicarbonate and high beta-hydroxybutyrate. In addition, three patients had evidence of cardiac chamber enlargement. One patient with severe dilated cardiomyopathy and prolonged QTc normalized when the diet was discontinued."
http://www.neurology...ract/54/12/2328

[Skötkonung]

More nasty things from the ketogenic diet for children with epilepsy:

"Cardiac complications of the ketogenic diet, in the absence of selenium deficiency, have not been reported. Twenty patients on the ketogenic diet at one institution were investigated. Prolonged QT interval (QTc) was found in 3 patients (15%). There was a significant correlation between prolonged QTc and both low serum bicarbonate and high beta-hydroxybutyrate. In addition, three patients had evidence of cardiac chamber enlargement. One patient with severe dilated cardiomyopathy and prolonged QTc normalized when the diet was discontinued."
http://www.neurology...ract/54/12/2328

QTc, which relates to timing and beat of the heart, is typically abnormal in seizure patients regardless of diet.

The QT interval in epilepsy patients compared to controls
http://neurologyasia...s/20073_068.pdf


Long QT syndrome presenting as epileptic seizures in an adult
"A 50 year old woman with a previous diagnosis of epilepsy presented to the emergency department with a generalised seizure. Her admission ECG showed QT prolongation secondary to bradycardia and a subsequent seizure in the department demonstrated that these events were secondary to cerebral hypoperfusion during episodes of torsades de pointes. This case illustrates how long QT syndrome can masquerade convincingly as epilepsy, delaying treatment and exposing the patient to a high risk of sudden cardiac death. Careful ECG analysis is recommended for all patients presenting with seizures."

The researchers are ignoring the fact that the Inuit lived free of cardiac problems.
http://www.cbc.ca/he...diet010921.html