410 replies to this topic

[DukeNukem]

Not sure if someone has posted this yet:

A brief critical overview of the biological effects of methylglyoxal and further evaluation of a methylglyoxal-based anticancer formulation in treating cancer patients.
Talukdar D, Ray S, Ray M, Das S.

Department of Biological Chemistry, Indian Association for the Cultivation of Science, Kolkata, India.

A historical perspective on methylglyoxal research is briefly presented, mentioning the documented anticancer and antiviral effects of methylglyoxal. The idea and the supporting experimental evidence of Albert Szent-Györgyi et al. that methylglyoxal is a natural growth regulator and can act as an anticancer agent are mentioned. Previously a few in vivo studies suggested safe administration of methylglyoxal. However, recent literature abounds with the toxic effects of methylglyoxal. The authors present a brief critical overview of studies indicating both toxic and beneficial effects of methylglyoxal and suggest that the beneficial effects of methylglyoxal outweigh its toxic effects. Encouraged by the studies of Szent-Györgyi et al., the present authors undertook systematic investigations to understand the mechanism of the anticancer effect of methylglyoxal. The results of these investigations led to the proposal that the fundamental changes in malignant cells are critical alterations of glyceraldehyde-3-phosphate dehydrogenase and mitochondrial complex I, and methylglyoxal's anticancer effect might be mediated by acting on these altered sites. Moreover, a new hypothesis on cancer has been proposed, suggesting that excessive ATP formation in cells may lead to malignancy. Toxicity and pharmacokinetic studies were performed on animals and it was observed that methylglyoxal is potentially safe for humans. A methylglyoxal-based anticancer formulation was developed and a three-phase study of treating a total number of 86 cancer patients was carried out. The results appear to be promising. Most of the cancer patients benefited greatly and a significant number of patients became free of the disease. Contrary to the effect of existing anticancer drugs, this methylglyoxal-based formulation is devoid of any toxic effect and reasonably effective against a wide variety of cancers. The symptomatic improvements of the many patients who died of progressive disease suggest that the formulation could also be used for palliation. The authors urge the scientific community to test the formulation and if found effective then to improve it further.
http://www.ncbi.nlm....pubmed/18533369

[Skötkonung]

If they have no evidence of ketone bodies being produced, then they are incorrect in calling their diet ketogenic. The golden standard regarding ketogenic diet, the research on ketogenic diet for chlidren with epilepsy, 1) do use ketone sticks to measure compliance and effect, 2) also take protein into account when formulating the diet.

Are you talking about yourself considering your displayed knowledge about hyman metabolism in other threads?

Here is the study I was talking about:

"At the first visit, participants were instructed how to fol-low the LCKD as individuals or in small groups, with an initial goal of ≤20 g carbohydrate per day. Participants were taught the specific types and amounts of foods theycould eat, as well as foods to avoid. Initially, participants were 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 of hard cheese; and limited amounts of cream, avocado,olives, and lemon juice. Fats and oils were not restricted except that intake of trans fats was to be minimized."

This study actually measured ketone bodies:
"The proportion of participants with a urine ketone reading greater than tracewas 1 of 17 participants at baseline, 5 of 17 participants at week 2, and similar frequencies at subsequent visits until week 14 when 2 of 18 participants had readings greater than trace and week 16 when 2 of 21 participants had readings greater than trace. During the study, only 27 of 151 urine ketone measurements were greater than trace, with one participant accounting for all 7 occurrences of the 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

I'm not the one objecting to the terminology used in these studies. This is not a once off occurrence, many researchers refer to very low carbohydrate diets as ketogenic yet according to you they are all wrong because they either didn't test for ketones or very little ketones were accounted for during testing. I doubt that such an obvious oversight would 1.) make it into a major peer reviewed journal on multiple occasions 2.) be overlooked repeatedly by multiple teams of phds who are conducting these studies.

A Low-Carbohydrate, Ketogenic Diet versus a Low-Fat Diet To Treat Obesity and Hyperlipidemia
"Ketonuria
Restriction of dietary intake of carbohydrates to less than 40 g/d typically results in ketonuria that is detectable by dipstick analysis, which can be used to monitor adherence to the low-carbohydrate diet (14, 15). At each return visit, participants provided a fresh urine specimen for analysis. The following semi-quantitative scale was used to categorize ketone content: none, trace (up to 0.9 mmol/L [5 mg/dL]), small (0.9 to 6.9 mmol/L [5 to 40 mg/dL]), moderate (6.9 to 13.8 mmol/L [40 to 80 mg/dL]), large80 (13.8 to 27.5 mmol/L [80 to 160 mg/dL]), and large160 (>27.5 mmol/L [>160 mg/dL])."

and..

"Diet Composition
Diet composition was measured on the basis of food records collected at each visit from a subsample of participants (13 from the low-carbohydrate diet group and 7 from the low-fat diet group.) The low-carbohydrate diet group consumed a mean (±SD) of 29.5 ± 11.1 g of carbohydrates (8% of daily energy intake), 97.9 ± 24.3 g of protein (26% of daily energy intake), and 110.6 ± 27.3 g of fat (68% of daily energy intake) daily. The low-fat diet group consumed 197.6 ± 34.2 g of carbohydrates (52% of daily energy intake), 70.5 ± 9.7 g of protein (19% of daily energy intake), and 48.9 ± 12.0 g of fat (29% of daily energy intake) daily. The estimated daily energy intake was 6.14 ± 1.37 MJ (1461.0 ± 325.7 kcal) in the low-carbohydrate diet group and 6.31 ± 0.68 MJ (1502.0 ± 162.1 kcal) in the low-fat diet group"

and..

"The proportion of participants in the low-carbohydrate diet group whose level of urinary ketones was classified as trace or greater was 86% (47 of 55) at 2 weeks and decreased to 42% (19 of 45) at 24 weeks. The proportion of participants in this group who had urinary ketone levels classified as moderate or greater was 64% (35 of 55) at 2 weeks and decreased to 18% (8 of 45) at 24 weeks."

and...

"Other possible explanations for the discrepancy in weight loss between groups include loss of energy through ketonuria and the increased thermic effect of a high-protein diet (23)."

Edited by Skotkonung, 13 November 2009 - 08:26 PM.

[Blue]

Not sure if someone has posted this yet:

A brief critical overview of the biological effects of methylglyoxal and further evaluation of a methylglyoxal-based anticancer formulation in treating cancer patients.
Talukdar D, Ray S, Ray M, Das S.

Department of Biological Chemistry, Indian Association for the Cultivation of Science, Kolkata, India.

A historical perspective on methylglyoxal research is briefly presented, mentioning the documented anticancer and antiviral effects of methylglyoxal. The idea and the supporting experimental evidence of Albert Szent-Györgyi et al. that methylglyoxal is a natural growth regulator and can act as an anticancer agent are mentioned. Previously a few in vivo studies suggested safe administration of methylglyoxal. However, recent literature abounds with the toxic effects of methylglyoxal. The authors present a brief critical overview of studies indicating both toxic and beneficial effects of methylglyoxal and suggest that the beneficial effects of methylglyoxal outweigh its toxic effects. Encouraged by the studies of Szent-Györgyi et al., the present authors undertook systematic investigations to understand the mechanism of the anticancer effect of methylglyoxal. The results of these investigations led to the proposal that the fundamental changes in malignant cells are critical alterations of glyceraldehyde-3-phosphate dehydrogenase and mitochondrial complex I, and methylglyoxal's anticancer effect might be mediated by acting on these altered sites. Moreover, a new hypothesis on cancer has been proposed, suggesting that excessive ATP formation in cells may lead to malignancy. Toxicity and pharmacokinetic studies were performed on animals and it was observed that methylglyoxal is potentially safe for humans. A methylglyoxal-based anticancer formulation was developed and a three-phase study of treating a total number of 86 cancer patients was carried out. The results appear to be promising. Most of the cancer patients benefited greatly and a significant number of patients became free of the disease. Contrary to the effect of existing anticancer drugs, this methylglyoxal-based formulation is devoid of any toxic effect and reasonably effective against a wide variety of cancers. The symptomatic improvements of the many patients who died of progressive disease suggest that the formulation could also be used for palliation. The authors urge the scientific community to test the formulation and if found effective then to improve it further.
http://www.ncbi.nlm....pubmed/18533369

Interesting. But what is good against cancer in cancer patients is not necessarily good for healthy persons. Like many cytostatic chemotherapy agents which do kill cancer cells but also kills or damages healthy cells and may increase the long-term risk for new cancers.

[Blue]

I'm not the one objecting to the terminology used in these studies. This is not a once off occurrence, many researchers refer to very low carbohydrate diets as ketogenic yet according to you they are all wrong because they either didn't test for ketones or very little ketones were accounted for during testing. I doubt that such an obvious oversight would 1.) make it into a major peer reviewed journal on multiple occasions 2.) be overlooked repeatedly by multiple teams of phds who are conducting these studies.

Well, if we are talking about just low-carbohydrate diets without significant ketone body production, then obviously the side effects of true ketogenic diet for children hardly applies, but neither do effects from ketone bodies seen in cell or animal studies.

[Skötkonung]

Not sure if someone has posted this yet:

A brief critical overview of the biological effects of methylglyoxal and further evaluation of a methylglyoxal-based anticancer formulation in treating cancer patients.
Talukdar D, Ray S, Ray M, Das S.

Department of Biological Chemistry, Indian Association for the Cultivation of Science, Kolkata, India.

A historical perspective on methylglyoxal research is briefly presented, mentioning the documented anticancer and antiviral effects of methylglyoxal. The idea and the supporting experimental evidence of Albert Szent-Györgyi et al. that methylglyoxal is a natural growth regulator and can act as an anticancer agent are mentioned. Previously a few in vivo studies suggested safe administration of methylglyoxal. However, recent literature abounds with the toxic effects of methylglyoxal. The authors present a brief critical overview of studies indicating both toxic and beneficial effects of methylglyoxal and suggest that the beneficial effects of methylglyoxal outweigh its toxic effects. Encouraged by the studies of Szent-Györgyi et al., the present authors undertook systematic investigations to understand the mechanism of the anticancer effect of methylglyoxal. The results of these investigations led to the proposal that the fundamental changes in malignant cells are critical alterations of glyceraldehyde-3-phosphate dehydrogenase and mitochondrial complex I, and methylglyoxal's anticancer effect might be mediated by acting on these altered sites. Moreover, a new hypothesis on cancer has been proposed, suggesting that excessive ATP formation in cells may lead to malignancy. Toxicity and pharmacokinetic studies were performed on animals and it was observed that methylglyoxal is potentially safe for humans. A methylglyoxal-based anticancer formulation was developed and a three-phase study of treating a total number of 86 cancer patients was carried out. The results appear to be promising. Most of the cancer patients benefited greatly and a significant number of patients became free of the disease. Contrary to the effect of existing anticancer drugs, this methylglyoxal-based formulation is devoid of any toxic effect and reasonably effective against a wide variety of cancers. The symptomatic improvements of the many patients who died of progressive disease suggest that the formulation could also be used for palliation. The authors urge the scientific community to test the formulation and if found effective then to improve it further.
http://www.ncbi.nlm....pubmed/18533369

Interesting. But what is good against cancer in cancer patients is not necessarily good for healthy persons. Like many cytostatic chemotherapy agents which do kill cancer cells but also kills or damages healthy cells and may increase the long-term risk for new cancers.

Yah, I was talking to Peter at HyperLipid about this earlier in the week. He has since made a post on his blog regarding methylglyoxal. I'm not convinced that methylglyoxal is indeed raised in ketonic individuals, but I do think methylglyoxal is harmful. I have since emailed the author of the Atkins study with some questions about his results.

[Blue]

A Low-Carbohydrate, Ketogenic Diet versus a Low-Fat Diet To Treat Obesity and Hyperlipidemia
"Ketonuria
Restriction of dietary intake of carbohydrates to less than 40 g/d typically results in ketonuria that is detectable by dipstick analysis, which can be used to monitor adherence to the low-carbohydrate diet (14, 15). At each return visit, participants provided a fresh urine specimen for analysis. The following semi-quantitative scale was used to categorize ketone content: none, trace (up to 0.9 mmol/L [5 mg/dL]), small (0.9 to 6.9 mmol/L [5 to 40 mg/dL]), moderate (6.9 to 13.8 mmol/L [40 to 80 mg/dL]), large80 (13.8 to 27.5 mmol/L [80 to 160 mg/dL]), and large160 (>27.5 mmol/L [>160 mg/dL])."

and..

"Diet Composition
Diet composition was measured on the basis of food records collected at each visit from a subsample of participants (13 from the low-carbohydrate diet group and 7 from the low-fat diet group.) The low-carbohydrate diet group consumed a mean (±SD) of 29.5 ± 11.1 g of carbohydrates (8% of daily energy intake), 97.9 ± 24.3 g of protein (26% of daily energy intake), and 110.6 ± 27.3 g of fat (68% of daily energy intake) daily. The low-fat diet group consumed 197.6 ± 34.2 g of carbohydrates (52% of daily energy intake), 70.5 ± 9.7 g of protein (19% of daily energy intake), and 48.9 ± 12.0 g of fat (29% of daily energy intake) daily. The estimated daily energy intake was 6.14 ± 1.37 MJ (1461.0 ± 325.7 kcal) in the low-carbohydrate diet group and 6.31 ± 0.68 MJ (1502.0 ± 162.1 kcal) in the low-fat diet group"

and..

"The proportion of participants in the low-carbohydrate diet group whose level of urinary ketones was classified as trace or greater was 86% (47 of 55) at 2 weeks and decreased to 42% (19 of 45) at 24 weeks. The proportion of participants in this group who had urinary ketone levels classified as moderate or greater was 64% (35 of 55) at 2 weeks and decreased to 18% (8 of 45) at 24 weeks."

and...

"Other possible explanations for the discrepancy in weight loss between groups include loss of energy through ketonuria and the increased thermic effect of a high-protein diet (23)."

Hm, that study hardly supports your view. Only 18% had moderate or greater ketone levels at 24 weeks. So obviously just carbohydrate restriction is not enough. One must also do protein restriction in order to get long-term, strong ketone body production as they do in the ketogenic diet for children with epilepsy.

Edited by Blue, 13 November 2009 - 08:46 PM.

[frederickson]

I think there has been quite a few good discussions on the merits of such a diet. Perhaps you have been avoiding those threads?

I cant' remember reading much of this thread, no. But IAC it must have been helluva study to convince rabagley so deeply of this idea that - one wonders - I should have seen it, it should have been really in your face, in one of the (dozens? or at least several) keto threads I did read. Does not at all sound like the conflicting evidence I've read over the course of the last month in those threads.

What are you implying? That we should all be agnostic until definitive scientific evidence illuminates the correct dietary regimen? I agree that it is important to remain agnostic without clear evidence. However, it is not as if we can't possibly apply probability to our agnosticism. People do this with religion all the time. I, for instance, don't know if God exists or not -therefor I am agnostic. However, based on the lack of available scientific evidence supporting God's existence, I think it is probable that he doesn't. The same goes for a high-fat, carbohydrate restricted diet. There is certainly no definitive evidence proving it superior to all other diets. However, based on the available scientific research, I believe probability is weighted in it's favor.

Since I started posting here, I have accumulated a list of over 65 studies demonstrating positive features of a carbohydrate restricted or ketogenic diet. I keep this list in a Word document. If you would like to see this list, to understand why I and others believe as we do, I would be more than happy to send it to you.

you make some good points skotkonung. relying exclusively upon what has been discovered in the scientific evidence is foolish, especially as it pertains to diet. there are too many political factors involved with funding of nutritional research to use scientific evidence as the sole basis for what constitutes a healthy diet.

put very bluntly... the nih is not interested in funding large-population based studies of low-carbohydrate diets, ketogenic diets, paleolithic diets, and many of the other nutritional approaches that people have found to be tremendously beneficial. the usda/nih is beholden to the corn and grain industry, and does not want to fund studies that may cast grains in a negative light.

it is a well-known fact amongst those that write grants that if you want funding, propose a study to establish the benefits of whole-grains. many of us realize it is bullshit, but that is how you get the funding. so please do not let a purported lack of population-based evidence on ketogenic/low-carb/paleo studies lead you to believe there is a lack of effect.

[Skötkonung]

This is what Petro wrote to me following my first email:

Not sure when I'll get time for this drivel but I ought to really! It's a pity it's a Wiley paper, I can't get the full text. But the crucial words are "potential precursors", "Atkins", "implies" and "potential" again. The net result is that these people measured the products of ketosis in people on a ketogenic diet and, lo and behold, ketones are there if there was compliance! The methylgloxal is described as a glycotoxin but is in fact an inhibitor of Glyceraldehyde-3-Phosphate Dehydrogenase, a step in glycolysis. I certainly don't find this surprising. Physiology fits together. You want to stop glycolysis, make and inhibitor of a key step in the process! Ketosis needs this. Don't be afraid of it. You are aware perhaps that methylgloxal is a promising chemotherapy agent (inhibiting cancer cell glycolysis) and that acetone is suspected of being the active agent in the ketogenic diet for epilepsy control?

You could just ask where there is any sort of evidence base for their hypothesis that ketosis ramps up vascular damage! Everyone having to fast for more than two days would be in trouble, so hunger would be a major risk factor for CHD!

If you go to the worms and free radicals paper on the blog and imagine these clowns had written it. They would simply have said that restricting glucose increases respiration which markedly increases the generation of free radicals, but then forgot to mention that this "catastrophe" which "might" cause "potential tissue and vascular damage" was markedly beneficial in extending life span! Oh and by the way their only advice would be to eat more sugar...

Idiots. I'll see what I can do! Pity my shifts are difficult until next week...

Ta for the heads up

Peter

This is my follow-up:

I agree, that study is only one, unverified data point (although it is still interesting to me). I also wondered about the starvation aspect. It appears that methylglyoxal production only ramped up to a dangerous level between week 2 and 4 of the study. This means that vascular damage may only occur in situations involving frequent, prolonged starvation.. a rather rare, and unobserved occurrence. Perhaps I'm not properly understanding something here?

About your assertion that methylgloxal is an inhibitor of glyceraldehyde-3-phosphate dehydrogenase -- From what I have read, glyceraldehyde-3-phosphate and dihydroxyacetone-phosphate are actually precursors to methylglyoxal.

Study: Energy metabolism, altered proteins, sirtuins and ageing: converging mechanisms?
"It is suggested that ad libitum feeding conditions decrease NAD availability which also decreases metabolism of the triose phosphate glycolytic intermediates, glyceraldehyde-3-phosphate and dihydroxyacetone-phosphate, which can spontaneously decompose into methylglyoxal (MG). MG is a highly toxic glycating agent and a major source of protein advanced-glycosylation end-products (AGEs). MG and AGEs can induce mitochondrial dysfunction and formation of reactive oxygen species (ROS), as well as affect gene expression and intracellular signalling."

Interestingly, the same study goes on to indicate:
"In dietary restriction-induced fasting, NADH would be oxidised and NAD regenerated via mitochondrial action. This would not only activate sirtuins and extend lifespan but also suppress MG formation. This proposal can also explain the apparent paradox whereby increased aerobic activity suppresses formation of glycoxidized proteins and extends lifespan. Variation in mitochondrial DNA composition and consequent mutation rate, arising from dietary-controlled differences in DNA precursor ratios, could also contribute to tissue differences in age-related mitochondrial dysfunction."

Unfortunately in the Ketogenic state, at least according to BEISSWENGER et al, methylglyoxal is not being reduced as would be expected in nutritional analogues such as caloric restriction and fasting:
"We found that by 14-28 days, methylghyoxal levels rose 1.67-fold ( P= 0.039 ) and acetol and acetone levels increased 2.7- and 6.12-fold, respectively ( P= 0.012 and 0.028)."

I also wondered if during the course of the BEISSWENGER et al study, the participants were taking in high concentrations of fried and grilled foods to meet their new dietary criteria? Methylghyoxal has been shown to increase when consuming fried or baked foods. If this were the case, a ketogenic diet could be augmented to include slow, low temperature, cooking methods and thus reduce methylghyoxal concentrations.

Take for instance this study on asparagine maillard reactions (commonly found it cooked animal products) and their correlation to methylghyoxal: Correlation of methylglyoxal with acrylamide formation in fructose/asparagine Maillard reaction model system.

"The results indicated that the formation of AA increased with the heating time, and nearly 75% of AA was formed through the participation of α-dicarbonyl compounds. The amounts of formation and consumption of MG increased with heating time, and from 12 min of reaction, the consumed amounts of MG accounted for 62.1–90.3% on the basis of total amounts of MG formed in MR, suggesting that most of the MG took part in further reactions. Meanwhile, Asn concentration decreased with heating time in both models. The formation of AA and consumption of Asn were highly correlated with MG. Indeed, as MG concentration in MG/Asn model system decreased during heating at 150 °C, the concentration of AA significantly increased. The coefficient of correlation between consumed amounts of MG and the formed amounts of AA was 0.931, demonstrating that MG plays a role in AA formation."

At any rate, I am very excited to hear you may do a write-up on this issue. It would be great to learn more about the role of glycotoxins in a ketogenic diet. I still hold hope that I am not totally understanding the underlying processes surrounding methylghyoxal, and that it is not a intrinsic (dangerous) byproduct of prolonged ketosis.

I also realize that lipid peroxidation does lead to AGE formation, and that in some cases it appears to do so more rapidly than glycation. CML, a product of the oxidative degradation of glycated protein and a common measure of AGE levels, is actually formed through the oxidation of arachidonic acid in much higher quantities than from glycation (Link). Polyunsaturated fats also quite easily form other AGEs, such as malondialdehydelysine (MDA-lys) and carboxyethyllysine (CEL). However, it appears saturated fats are quite different and result in much less glycation related damage:

Study: Modification of the longevity-related degree of fatty acid unsaturation modulates oxidative damage to proteins and mitochondrial DNA in liver and brain

"These results, together with previous data from our laboratories, show that increasing the degree of fatty unsaturation of postmitotic tissues in vivo can raise not only lipid but also protein and mtDNA oxidative damage. This is mechanistically relevant in relation to the constitutively low tissue fatty acid unsaturation of long-lived animals."
Thanks again for writing me back.

[Skötkonung]

A Low-Carbohydrate, Ketogenic Diet versus a Low-Fat Diet To Treat Obesity and Hyperlipidemia
"Ketonuria
Restriction of dietary intake of carbohydrates to less than 40 g/d typically results in ketonuria that is detectable by dipstick analysis, which can be used to monitor adherence to the low-carbohydrate diet (14, 15). At each return visit, participants provided a fresh urine specimen for analysis. The following semi-quantitative scale was used to categorize ketone content: none, trace (up to 0.9 mmol/L [5 mg/dL]), small (0.9 to 6.9 mmol/L [5 to 40 mg/dL]), moderate (6.9 to 13.8 mmol/L [40 to 80 mg/dL]), large80 (13.8 to 27.5 mmol/L [80 to 160 mg/dL]), and large160 (>27.5 mmol/L [>160 mg/dL])."

and..

"Diet Composition
Diet composition was measured on the basis of food records collected at each visit from a subsample of participants (13 from the low-carbohydrate diet group and 7 from the low-fat diet group.) The low-carbohydrate diet group consumed a mean (±SD) of 29.5 ± 11.1 g of carbohydrates (8% of daily energy intake), 97.9 ± 24.3 g of protein (26% of daily energy intake), and 110.6 ± 27.3 g of fat (68% of daily energy intake) daily. The low-fat diet group consumed 197.6 ± 34.2 g of carbohydrates (52% of daily energy intake), 70.5 ± 9.7 g of protein (19% of daily energy intake), and 48.9 ± 12.0 g of fat (29% of daily energy intake) daily. The estimated daily energy intake was 6.14 ± 1.37 MJ (1461.0 ± 325.7 kcal) in the low-carbohydrate diet group and 6.31 ± 0.68 MJ (1502.0 ± 162.1 kcal) in the low-fat diet group"

and..

"The proportion of participants in the low-carbohydrate diet group whose level of urinary ketones was classified as trace or greater was 86% (47 of 55) at 2 weeks and decreased to 42% (19 of 45) at 24 weeks. The proportion of participants in this group who had urinary ketone levels classified as moderate or greater was 64% (35 of 55) at 2 weeks and decreased to 18% (8 of 45) at 24 weeks."

and...

"Other possible explanations for the discrepancy in weight loss between groups include loss of energy through ketonuria and the increased thermic effect of a high-protein diet (23)."

Hm, that study hardly supports your view. Only 18% had moderate or greater ketone levels at 24 weeks. So obviously just carbohydrate restriction is not enough. Just must also do protein restriction in order to get long-term, strong ketone body production as they do in the ketogenic diet for children with epilepsy.

Ketonuria pertains mostly to the level of acetone being excreted in the urine, not to the quantity of ketones being created and distributed in the body. Acetone is thought to be implicated in the anti-convulsive nature of the KD. It could be the seizure dietary protocol is structured to induce maximum production and excretion of acetone and other ketosis biproducts and is not simply limited to inducing the production of ketones. Reducing protein may increase acetone but not inhibit ketosis.

At any rate, the authors did not mention the lower levels of ketosis in the tailing end of the study. However, as each patient was self regulating their dietary intake of protein / fats / carbohydrate, it could be that they gradually increased their carbohydrate intake as time went on. Only the most diligent were able to maintain a very low carbohydrate intake throughout the duration of the study.

Edited by Skotkonung, 13 November 2009 - 08:53 PM.

[Blue]

A Low-Carbohydrate, Ketogenic Diet versus a Low-Fat Diet To Treat Obesity and Hyperlipidemia
"Ketonuria
Restriction of dietary intake of carbohydrates to less than 40 g/d typically results in ketonuria that is detectable by dipstick analysis, which can be used to monitor adherence to the low-carbohydrate diet (14, 15). At each return visit, participants provided a fresh urine specimen for analysis. The following semi-quantitative scale was used to categorize ketone content: none, trace (up to 0.9 mmol/L [5 mg/dL]), small (0.9 to 6.9 mmol/L [5 to 40 mg/dL]), moderate (6.9 to 13.8 mmol/L [40 to 80 mg/dL]), large80 (13.8 to 27.5 mmol/L [80 to 160 mg/dL]), and large160 (>27.5 mmol/L [>160 mg/dL])."

and..

"Diet Composition
Diet composition was measured on the basis of food records collected at each visit from a subsample of participants (13 from the low-carbohydrate diet group and 7 from the low-fat diet group.) The low-carbohydrate diet group consumed a mean (±SD) of 29.5 ± 11.1 g of carbohydrates (8% of daily energy intake), 97.9 ± 24.3 g of protein (26% of daily energy intake), and 110.6 ± 27.3 g of fat (68% of daily energy intake) daily. The low-fat diet group consumed 197.6 ± 34.2 g of carbohydrates (52% of daily energy intake), 70.5 ± 9.7 g of protein (19% of daily energy intake), and 48.9 ± 12.0 g of fat (29% of daily energy intake) daily. The estimated daily energy intake was 6.14 ± 1.37 MJ (1461.0 ± 325.7 kcal) in the low-carbohydrate diet group and 6.31 ± 0.68 MJ (1502.0 ± 162.1 kcal) in the low-fat diet group"

and..

"The proportion of participants in the low-carbohydrate diet group whose level of urinary ketones was classified as trace or greater was 86% (47 of 55) at 2 weeks and decreased to 42% (19 of 45) at 24 weeks. The proportion of participants in this group who had urinary ketone levels classified as moderate or greater was 64% (35 of 55) at 2 weeks and decreased to 18% (8 of 45) at 24 weeks."

and...

"Other possible explanations for the discrepancy in weight loss between groups include loss of energy through ketonuria and the increased thermic effect of a high-protein diet (23)."

Hm, that study hardly supports your view. Only 18% had moderate or greater ketone levels at 24 weeks. So obviously just carbohydrate restriction is not enough. Just must also do protein restriction in order to get long-term, strong ketone body production as they do in the ketogenic diet for children with epilepsy.

Ketonuria pertains mostly to the level of acetone being excreted in the urine, not to the quantity of ketones being created and distributed in the body. Acetone is thought to be implicated in the anti-convulsive nature of the KD. It could be the seizure dietary protocol is structured to induce maximum production and excretion of acetone and other ketosis biproducts and is not simply limited to inducing the production of ketones. Reducing protein may increase acetone but not inhibit ketosis.

At any rate, the authors did not mention the lower levels of ketosis in the tailing end of the study. However, as each patient was self regulating their dietary intake of protein / fats / carbohydrate, it could be that they gradually increased their carbohydrate intake as time went on. Only the most diligent were able to maintain a very low carbohydrate intake throughout the duration of the study.

Do you have any source for that protein restriction selectively affects acetone? Seems far more likely considering that protein can be converted to glucose that a high protein intake reduces ketone body need and proudction in general.

Regarding the initial ketone production this may be due to the initial changed metabolism and great weight reduction/"starvation mode" that later stabilized.
http://www.annals.or....expansion.html

[Skötkonung]

Do you have any source for that protein restriction selectively affects acetone? Seems far more likely considering that protein can be converted to glucose that a high protein intake reduces ketone body need and proudction in general.

Regarding the initial ketone production this may be due to the initial changed metabolism and great weight reduction/"starvation mode" that later stabilized.
http://www.annals.or....expansion.html

This is interesting, not sure if it is related, but...

Gluconeogenic precursors stimulate acetone metabolism in isolated murine hepatocytes
"It is concluded that acetone may play a role in maintenance of hepatic glucose output in ketonemia and may do so by using a wide range of substrates for NADPH + H⁺ generation which, as a cofactor, is needed for the cytochrome P450s to metabolize acetone."

I'm at work, but when I get home I will access studies on this topic.

Edited by Skotkonung, 13 November 2009 - 09:14 PM.

[JLL]

Purpose: Numerous dietary factors elevate serum levels of insulin and insulin-like growth factor I (IGF-I), both potent prostate cancer mitogens. We tested whether varying dietary carbohydrate and fat, without energy restriction relative to comparison diets, would slow tumor growth and reduce serum insulin, IGF-I, and other molecular mediators of prostate cancer in a xenograft model.

Experimental Design: Individually caged male severe combined immunodeficient mice (n = 130) were randomly assigned to one of three diets (described as percent total calories): very high-fat/no-carbohydrate ketogenic diet (NCKD: 83% fat, 0% carbohydrate, 17% protein), low-fat/high-carbohydrate diet (LFD: 12% fat, 71% carbohydrate, 17% protein), or high-fat/moderate-carbohydrate diet (MCD: 40% fat, 43% carbohydrate, 17% protein). Mice were fed to maintain similar average body weights among groups. Following a preliminary feeding period, mice were injected with 1 x 106 LNCaP cells (day 0) and sacrificed when tumors were ≥1,000 mm3.

Results: Two days before tumor injection, median NCKD body weight was 2.4 g (10%) and 2.1 g (8%) greater than the LFD and MCD groups, respectively (P < 0.0001). Diet was significantly associated with overall survival (log-rank P = 0.004). Relative to MCD, survival was significantly prolonged for the LFD (hazard ratio, 0.49; 95% confidence interval, 0.29-0.79; P = 0.004) and NCKD groups (hazard ratio, 0.59; 95% confidence interval, 0.37-0.93; P = 0.02). Median serum insulin, IGF-I, IGF-I/IGF binding protein-1 ratio, and IGF-I/IGF binding protein-3 ratio were significantly reduced in NCKD relative to MCD mice. Phospho-AKT/total AKT ratio and pathways associated with antiapoptosis, inflammation, insulin resistance, and obesity were also significantly reduced in NCKD relative to MCD tumors.

Conclusions: These results support further preclinical exploration of carbohydrate restriction in prostate cancer and possibly warrant pilot or feasibility testing in humans.

http://cancerprevent...bstract/2/6/557

[JLL]

BACKGROUND: Recent evidence suggests carbohydrate intake may influence prostate cancer biology. We tested whether a no-carbohydrate ketogenic diet (NCKD) would delay prostate cancer growth relative to Western and low-fat diets in a xenograft model. METHODS: Seventy-five male SCID mice were fed a NCKD (84% fat-0% carbohydrate-16% protein kcal), low-fat (12% fat-72% carbohydrate-16% protein kcal), or Western diet (40% fat-44% carbohydrate-16% protein kcal). Low-fat mice were fed ad libitum and the other arms fed via a modified-paired feeding protocol. After 24 days, all mice were injected with LAPC-4 cells and sacrificed when tumors approached 1,000 mm(3). RESULTS: Despite consuming equal calories, NCKD-fed mice lost weight (up to 15% body weight) relative to low-fat and Western diet-fed mice and required additional kcal to equalize body weight. Fifty-one days after injection, NCKD mice tumor volumes were 33% smaller than Western mice (rank-sum, P = 0.009). There were no differences in tumor volume between low-fat and NCKD mice. Dietary treatment was significantly associated with survival (log-rank, P = 0.006), with the longest survival among the NCKD mice, followed by the low-fat mice. Serum IGFBP-3 was highest and IGF-1:IGFBP-3 ratio was lowest among NCKD mice while serum insulin and IGF-1 levels were highest in Western mice. NCKD mice had significantly decreased hepatic fatty infiltration relative to the other arms. CONCLUSIONS: In this xenograft model, despite consuming more calories, NCKD-fed mice had significantly reduced tumor growth and prolonged survival relative to Western mice and was associated with favorable changes in serum insulin and IGF axis hormones relative to low-fat or Western diet.

http://www.ncbi.nlm....pubmed/17999389

[Blue]

Purpose: Numerous dietary factors elevate serum levels of insulin and insulin-like growth factor I (IGF-I), both potent prostate cancer mitogens. We tested whether varying dietary carbohydrate and fat, without energy restriction relative to comparison diets, would slow tumor growth and reduce serum insulin, IGF-I, and other molecular mediators of prostate cancer in a xenograft model.

Experimental Design: Individually caged male severe combined immunodeficient mice (n = 130) were randomly assigned to one of three diets (described as percent total calories): very high-fat/no-carbohydrate ketogenic diet (NCKD: 83% fat, 0% carbohydrate, 17% protein), low-fat/high-carbohydrate diet (LFD: 12% fat, 71% carbohydrate, 17% protein), or high-fat/moderate-carbohydrate diet (MCD: 40% fat, 43% carbohydrate, 17% protein). Mice were fed to maintain similar average body weights among groups. Following a preliminary feeding period, mice were injected with 1 x 106 LNCaP cells (day 0) and sacrificed when tumors were ≥1,000 mm3.

Results: Two days before tumor injection, median NCKD body weight was 2.4 g (10%) and 2.1 g (8%) greater than the LFD and MCD groups, respectively (P < 0.0001). Diet was significantly associated with overall survival (log-rank P = 0.004). Relative to MCD, survival was significantly prolonged for the LFD (hazard ratio, 0.49; 95% confidence interval, 0.29-0.79; P = 0.004) and NCKD groups (hazard ratio, 0.59; 95% confidence interval, 0.37-0.93; P = 0.02). Median serum insulin, IGF-I, IGF-I/IGF binding protein-1 ratio, and IGF-I/IGF binding protein-3 ratio were significantly reduced in NCKD relative to MCD mice. Phospho-AKT/total AKT ratio and pathways associated with antiapoptosis, inflammation, insulin resistance, and obesity were also significantly reduced in NCKD relative to MCD tumors.

Conclusions: These results support further preclinical exploration of carbohydrate restriction in prostate cancer and possibly warrant pilot or feasibility testing in humans.

http://cancerprevent...bstract/2/6/557

BACKGROUND: Recent evidence suggests carbohydrate intake may influence prostate cancer biology. We tested whether a no-carbohydrate ketogenic diet (NCKD) would delay prostate cancer growth relative to Western and low-fat diets in a xenograft model. METHODS: Seventy-five male SCID mice were fed a NCKD (84% fat-0% carbohydrate-16% protein kcal), low-fat (12% fat-72% carbohydrate-16% protein kcal), or Western diet (40% fat-44% carbohydrate-16% protein kcal). Low-fat mice were fed ad libitum and the other arms fed via a modified-paired feeding protocol. After 24 days, all mice were injected with LAPC-4 cells and sacrificed when tumors approached 1,000 mm(3). RESULTS: Despite consuming equal calories, NCKD-fed mice lost weight (up to 15% body weight) relative to low-fat and Western diet-fed mice and required additional kcal to equalize body weight. Fifty-one days after injection, NCKD mice tumor volumes were 33% smaller than Western mice (rank-sum, P = 0.009). There were no differences in tumor volume between low-fat and NCKD mice. Dietary treatment was significantly associated with survival (log-rank, P = 0.006), with the longest survival among the NCKD mice, followed by the low-fat mice. Serum IGFBP-3 was highest and IGF-1:IGFBP-3 ratio was lowest among NCKD mice while serum insulin and IGF-1 levels were highest in Western mice. NCKD mice had significantly decreased hepatic fatty infiltration relative to the other arms. CONCLUSIONS: In this xenograft model, despite consuming more calories, NCKD-fed mice had significantly reduced tumor growth and prolonged survival relative to Western mice and was associated with favorable changes in serum insulin and IGF axis hormones relative to low-fat or Western diet.

The conclusion of the first study is somewhat strange since the low-fat/high-carbohydrate diet produced the best survival. The high-fat/moderate-carbohydrate diet was the worst alternative. High-fat is bad regarding cancer unless you get a ketosis which produces various toxins which in addition to the bad effects seen in children on the ketogenic diet also kills cancer?

Edited by Blue, 23 November 2009 - 08:02 PM.

[Skötkonung]

The KD is primarily effective against cancer because of of the warburg effect.

http://en.wikipedia....burg_hypothesis

If in fact it does eventually raise methylglyoxal, it will also be raising glucose and IGF1 and that may counteract any benefit.

[oehaut]

That's a very interesting thread, as many others on this forum.

I'd like to ask a question.

I read a few posts ago someone saying "we don't know the long term effect of a keto diet".

But where are the studies showing the long-term effect of high-carbs diet? As far as i'm concern, I know none.

And if you look at the result of the Women's Health Initiative studies, it's really not so great. The women in the intervention group, ie low-sat, high vegetable and whole grain, had 3.1 more chance than baseline to get CVD. I guess it's a good place to say "DUH!"

I'm just wondering why high-carb diet are so much protected by everyone (well, not too much on this forum, thanks god).

From an outsider perspective it really looks like dogma.

I just wanted to point that this argument, ie "we don't know long term effect" isnt really relevant.

If you look at paper from Cordain or other on paleo, it seems pretty obvious that we have evolved for a long time on high animal diet and low plant diet. (65-35) in majority of case, at least.

Isn't that a long term evidence?

[JackChristopher]

But where are the studies showing the long-term effect of high-carbs diet? As far as i'm concern, I know none.

I'm just wondering why high-carb diet are so much protected by everyone (well, not too much on this forum, thanks god). From an outsider perspective it really looks like dogma. I just wanted to point that this argument, ie "we don't know long term effect" isnt really relevant.

If you look at paper from Cordain or other on paleo, it seems pretty obvious that we have evolved for a long time on high animal diet and low plant diet. (65-35) in majority of case, at least.

Isn't that a long term evidence?

This isn't directly on topic, but I wanted to address this:

The bulk of nutritional science (and studies) are done within a cultural milieu that assumes we adapted to high carb diets. And most humans have eaten high grain for over 10,000+ years. So, it's hard to find high-fat cultures to compare. Most comparisons studies are done with cultures who eat higher fat than others, but not as a majority of calorie.

From the eyes of the consensus today, anything that contradicts high grain diets is wild speculation, or pejoratively, a "fad" diet. To call it speculative is fair. But I personally think the idea that we're adapted to high-grain is also a speculative. Still, there's no doubt that high grain diets are the most heavily study diets.

I think the fundamental difference—and what ultimately causes the endless debating on the forums—is how much one is willing to infer away from the scientific consensus. Ultimately we all speculate here. But some stick much closer to it than others, but it depends on the issue. Certain people will only believe something if it's formally studied for years. Others will infer their own conclusions on much less hard data. Some people will dismiss anecdotes and informal historical evidence. I respect that, but I would never do that.

Believing humans evolved to eat high fat diets, infers pretty far away from the mainstream. There's very little hard data that explicitly tests that hypothesis.

[oehaut]

But where are the studies showing the long-term effect of high-carbs diet? As far as i'm concern, I know none.

I'm just wondering why high-carb diet are so much protected by everyone (well, not too much on this forum, thanks god). From an outsider perspective it really looks like dogma. I just wanted to point that this argument, ie "we don't know long term effect" isnt really relevant.

If you look at paper from Cordain or other on paleo, it seems pretty obvious that we have evolved for a long time on high animal diet and low plant diet. (65-35) in majority of case, at least.

Isn't that a long term evidence?

This isn't directly on topic, but I wanted to address this:

The bulk of nutritional science (and studies) are done within a cultural milieu that assumes we adapted to high carb diets. And most humans have eaten high grain for over 10,000+ years. So, it's hard to find high-fat cultures to compare. Most comparisons studies are done with cultures who eat higher fat than others, but not as a majority of calorie.

From the eyes of the consensus today, anything that contradicts high grain diets is wild speculation, or pejoratively, a "fad" diet. To call it speculative is fair. But I personally think the idea that we're adapted to high-grain is also a speculative. Still, there's no doubt that high grain diets are the most heavily study diets.

I think the fundamental difference—and what ultimately causes the endless debating on the forums—is how much one is willing to infer away from the scientific consensus. Ultimately we all speculate here. But some stick much closer to it than others, but it depends on the issue. Certain people will only believe something if it's formally studied for years. Others will infer their own conclusions on much less hard data. Some people will dismiss anecdotes and informal historical evidence. I respect that, but I would never do that.

Believing humans evolved to eat high fat diets, infers pretty far away from the mainstream. There's very little hard data that explicitly tests that hypothesis.

You're making good point.

I'd only like to ask : Is because the mainstream say something is true is most absolutly be? Everybody believes something so that thing is true? It's gonna take some better arguments than that to make me believe.

Also, as for hard data, there's many studies coming out these last years showing that low-carb do better than low-fat on many parameters of health (weight, dyslipidemia, metabolic syndrome, glucose control)

So that looks to me like some hard data showing we are not meant to eat that much of carbs.

So far we can for sure say that low-carb are at least as good as low-fat.

As you said, high-carb are the most studied one, and the most loved one. Researchers don't want to see their studies contradicting the mainstream thinking. And they won't get funding to study something that goes againsnt the mainstream too.

So it makes it even harder to get the data we need to get to know.

We all agree that refined carbs are pretty bad don't we? How many people eat whole unrefined grains, taking time to soak them to get rid of the anti-nutriment?

Most ppl eat cornflakes and white bread and white pasta. For me, it's just easier to avoid them. Why don't you eat vegetable instead or rice? What rice has that vegetables don't? What has pasta that vegetable don't? You'll get much less calories that way, and as many nutrients - if not much more.

Why would we need grains at all in our diet except for convenience and psychological need?

I'm really trying to find this answer, if you have any clue that might make me able to come to a good physiological reason i'll be happy to hear it.

[tunt01]

How many people eat whole unrefined grains, taking time to soak them to get rid of the anti-nutriment?

Most ppl eat cornflakes and white bread and white pasta. For me, it's just easier to avoid them. Why don't you eat vegetable instead or rice? What rice has that vegetables don't? What has pasta that vegetable don't? You'll get much less calories that way, and as many nutrients - if not much more.

Why would we need grains at all in our diet except for convenience and psychological need?

I'm really trying to find this answer, if you have any clue that might make me able to come to a good physiological reason i'll be happy to hear it.

i soak lentils. it's not complicated. i just leave containers of it sitting in water laying around and replace the water in the AM upon waking up. havent soaked rice yet, but i prob should. lot of my meals are a pile of veggies, olive oil, some nuts/seeds, lentils+rice, and spices (curcumin/garlic) splattered all over it. sometimes i put animal protein w/ it (fish typically).

this is what i eat 50% of the time (lunch/dinner). what i read about vegetarian dies is that it is best to mix rice w/ legumes for better amino acid balance. if you look around, you'll see veggie diets discussing what lacks lysine or methionine and that both are needed for complete nutrition. i dont' see anything wrong w/ rice. whats wrong is that people are inactive and dont burn off the caloric intake.

the other missing aspect is vitamin b12, which i take daily.

Edited by prophets, 25 November 2009 - 08:48 PM.

[tunt01]

fyi - best way to soak brown rice?

http://wholehealthso...brown-rice.html

[oehaut]

How many people eat whole unrefined grains, taking time to soak them to get rid of the anti-nutriment?

Most ppl eat cornflakes and white bread and white pasta. For me, it's just easier to avoid them. Why don't you eat vegetable instead or rice? What rice has that vegetables don't? What has pasta that vegetable don't? You'll get much less calories that way, and as many nutrients - if not much more.

Why would we need grains at all in our diet except for convenience and psychological need?

I'm really trying to find this answer, if you have any clue that might make me able to come to a good physiological reason i'll be happy to hear it.

i soak lentils. it's not complicated. i just leave containers of it sitting in water laying around and replace the water in the AM upon waking up. havent soaked rice yet, but i prob should. lot of my meals are a pile of veggies, olive oil, some nuts/seeds, lentils+rice, and spices (curcumin/garlic) splattered all over it. sometimes i put animal protein w/ it (fish typically).

this is what i eat 50% of the time (lunch/dinner). what i read about vegetarian dies is that it is best to mix rice w/ legumes for better amino acid balance. if you look around, you'll see veggie diets discussing what lacks lysine or methionine and that both are needed for complete nutrition. i dont' see anything wrong w/ rice. whats wrong is that people are inactive and dont burn off the caloric intake.

the other missing aspect is vitamin b12, which i take daily.

Not that rice is wrong per se. I just don't understand why grains are being pushed as so healthy. Most carbs should come from vegetables, legumes and potatos and a bit of grains here and there. But what's up with the food parymid telling us to eat at least 5 portions of grains a day?

A great way to cut on calorie is to trade grains for vegetable. You'll get as many nutrients, and way less calories.

I'm not pro low-carb or pro low-fat. I think people should first worry about moving more and eating less, as you said. Way before worrying about macronutriments profile. But I think grains are seriously over-hyped.

[TheFountain]

Not that rice is wrong per se. I just don't understand why grains are being pushed as so healthy. Most carbs should come from vegetables, legumes and potatos and a bit of grains here and there. But what's up with the food parymid telling us to eat at least 5 portions of grains a day?

It is their way of pushing cheap diets on the public because they know most people cannot afford to eat 5 portions of fresh vegetables a day. What's really ridiculous is why vegetables and fruits should be so expensive. It isn't like it's a scarce resource. All vegetable prices should be half what they currently are.

[Mind]

Not that rice is wrong per se. I just don't understand why grains are being pushed as so healthy. Most carbs should come from vegetables, legumes and potatos and a bit of grains here and there. But what's up with the food parymid telling us to eat at least 5 portions of grains a day?

It is their way of pushing cheap diets on the public because they know most people cannot afford to eat 5 portions of fresh vegetables a day. What's really ridiculous is why vegetables and fruits should be so expensive. It isn't like it's a scarce resource. All vegetable prices should be half what they currently are.

This is an interesting dilemma. Eating fresh fruit and vegetables is expensive. Even eating frozen fruits and vegetables is expensive. There are probably a million websites promoting the fact that producing 1 pound of meat takes 2,500 (even up to 6,000) gallons of water and takes 11 times more fossil fuels than non-meat foodstuffs. So why are vegetables so expensive?

On the topic of ketogenic diets, score another one for Gary Taubes: Children who drink full-fat milk have a lower BMI. Good, as far as lower BMI equates to better health.

[dubcomesaveme]

I'm thinking of doing a bit of Keto.
I'm thinking of basing it around Poached Eggs, homemade Greek Yogurt (whole milk), Avocado, and almonds.
-Should be a very high quality blend of protein
-Eggs and Yogurt will be cheap
-Minimal\infrequent cooking and food prep.


My hope is Greek Yogurt will boost l-tryptophan and serotonin enough to offset the dip caused by lack of carbs. I've heard negative opinions of dairy before, but I think the benefits associated with fermented foods/probiotics will outweigh them.

Perhaps sunflower seeds for extra vitamin E, oysters if I need to boost zinc. Organic Berries seem too expensive, I think I can get bulk rosehips from a co-op for cheap near me. That+romaine lettuce+veggies should provide enough vitamin C. Perhaps add in some nutritional yeast for extra B vitamins then see where I'm at.

Edited by dubcomesaveme, 07 November 2010 - 05:01 AM.

[motif]

I switched to paleo diet which is more or less same thing and I regret my parents didn't know about it.
They fed me with typical sick food menu like bread, dairy, processed meet etc etc. No wonder I was allergic
most of my life. Now I feel much better, more energy, no fatigue or being sleepy afternoon, skin like a baby,
pink tongue etc etc.

The only pseudo negative effects sometimes I have ketone breath, almost as my cat and shopping is really hard sometimes...
(I know, I should hunt) Wherever I look in the stores only grain and sugar products.. :(

[rwac]

The only pseudo negative effects sometimes I have ketone breath, almost as my cat and shopping is really hard sometimes...
(I know, I should hunt) Wherever I look in the stores only grain and sugar products.. :(

Congratulations!
I've been low carb for a while. The ketones in my urine stopped a while ago, now I only spill ketones after eating lots of carbs. I imagine that breath might be similar.

Sugar is my nemesis.

Edited by rwac, 09 November 2010 - 02:02 PM.

[motif]

Sugar is my nemesis.

it's mine too, very hard not to cheat sometimes...


Not sure though about one thing - looks like my anxiety level is much higher then it was on high carb diet...
I explain to myself this as natural since paleo people needed to fight fro life so igh adrenaline boost was necessary.
Problem is they had a way to discharge this negative energy and I usually don't have...

[rwac]

Not sure though about one thing - looks like my anxiety level is much higher then it was on high carb diet...
I explain to myself this as natural since paleo people needed to fight fro life so igh adrenaline boost was necessary.
Problem is they had a way to discharge this negative energy and I usually don't have...

Higher carb diets increase Serotonin levels, and you get used to the higher levels over time. You need to get used to the lower base levels of serotonin when you go low carb.
(Similar to insulin resistance perhaps ?)

Edited by rwac, 09 November 2010 - 03:23 PM.

[Dmitri]

But where are the studies showing the long-term effect of high-carbs diet? As far as i'm concern, I know none.

I'm just wondering why high-carb diet are so much protected by everyone (well, not too much on this forum, thanks god). From an outsider perspective it really looks like dogma. I just wanted to point that this argument, ie "we don't know long term effect" isnt really relevant.

If you look at paper from Cordain or other on paleo, it seems pretty obvious that we have evolved for a long time on high animal diet and low plant diet. (65-35) in majority of case, at least.

Isn't that a long term evidence?

This isn't directly on topic, but I wanted to address this:

The bulk of nutritional science (and studies) are done within a cultural milieu that assumes we adapted to high carb diets. And most humans have eaten high grain for over 10,000+ years. So, it's hard to find high-fat cultures to compare. Most comparisons studies are done with cultures who eat higher fat than others, but not as a majority of calorie.

From the eyes of the consensus today, anything that contradicts high grain diets is wild speculation, or pejoratively, a "fad" diet. To call it speculative is fair. But I personally think the idea that we're adapted to high-grain is also a speculative. Still, there's no doubt that high grain diets are the most heavily study diets.

I think the fundamental difference—and what ultimately causes the endless debating on the forums—is how much one is willing to infer away from the scientific consensus. Ultimately we all speculate here. But some stick much closer to it than others, but it depends on the issue. Certain people will only believe something if it's formally studied for years. Others will infer their own conclusions on much less hard data. Some people will dismiss anecdotes and informal historical evidence. I respect that, but I would never do that.

Believing humans evolved to eat high fat diets, infers pretty far away from the mainstream. There's very little hard data that explicitly tests that hypothesis.

You're making good point.

I'd only like to ask : Is because the mainstream say something is true is most absolutly be? Everybody believes something so that thing is true? It's gonna take some better arguments than that to make me believe.

Also, as for hard data, there's many studies coming out these last years showing that low-carb do better than low-fat on many parameters of health (weight, dyslipidemia, metabolic syndrome, glucose control)

So that looks to me like some hard data showing we are not meant to eat that much of carbs.

So far we can for sure say that low-carb are at least as good as low-fat.

As you said, high-carb are the most studied one, and the most loved one. Researchers don't want to see their studies contradicting the mainstream thinking. And they won't get funding to study something that goes againsnt the mainstream too.

So it makes it even harder to get the data we need to get to know.

We all agree that refined carbs are pretty bad don't we? How many people eat whole unrefined grains, taking time to soak them to get rid of the anti-nutriment?

Most ppl eat cornflakes and white bread and white pasta. For me, it's just easier to avoid them. Why don't you eat vegetable instead or rice? What rice has that vegetables don't? What has pasta that vegetable don't? You'll get much less calories that way, and as many nutrients - if not much more.

Why would we need grains at all in our diet except for convenience and psychological need?

I'm really trying to find this answer, if you have any clue that might make me able to come to a good physiological reason i'll be happy to hear it.

There are studies, but I would venture to guess the low carb diets are not as accepted because they don't know the long term effects. I believe I posted an article a few weeks ago mentioning how most of the studies ran for a few months and that the longest one comparing both low carb and low fat had been two years. That study did show low carb lowering cholesterol more, but those on low fat also lost weight, decreased sugar levels and cholesterol. Which completely contradicts what most people here say about carbs being evil and that it causes sugar and cholesterol to rise, but that two year study proved otherwise. I assume those on the low fat were actually given whole grains as opposed to the processed types and that's why there was a health benefit?

[Thorsten3]

Hi guys just wondering if any of you would be able to critique my 'dietery stack' if you like..

I have small knowledge of the ketogenic diet but have been reading quite a bit recently and I am also purchasing the recommended books by Edward, the OP.

I just need a bit of guidence really with regards to whether the foods below are going to fit the criteria.

I eat the following:

Pesto
Soya milk
Fish
Beef (organic)
Oats
Spiralina
Bee pollen
Algae
Cacao
Hemp seeds
Brazil nuts
Eggs (just the yolk)
Brocoli, sprouts, spinach (not too often)


I plan on eradicating fruits, although I love them. Avocado, humous have also been eradicated.

I plan on adding berries (what type? I dislike cherries - any ideas? Would goji be a good choice? Blueberries?), MCT oil, coconut oil.


What do you guys think? I suppose I am keen to experiment with this really. My books should be here soon and then I can get reading and have a better understanding of what this diet requires - but with my limited knowledge this is what I have come with so far.

I would aim to not eat carbs any higher than 15g/20g per day.. I copied that from Funk, sure that's what he said he was eating (well, in 2008, hope he doesn't mind lol) and that it was working for him. I am really keen on trying this. I am especially interested in the mood elevation which I have read is linked to increased levels of BHB in the brain.