Ketogenic Diet - Powerful Dietary Strategy for Certain Conditions

Approaching Infinity

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Re: Ketogenic Diet - Path To Transformation?

Ailén said:
We have been doing rough calculations to see what amount of protein each of us here can have according to our body weight (supposedly, one should eat 1,5grams of protein per kilogram of body weight). And based on the meat we get, we've estimated that there is more fat in ours than in what was measured for this chart.
Where did you guys find that figure? I'm curious, because Gedgaudas says 0.8 g/kg in PBPM.
 

Nicholas

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Re: Ketogenic Diet - Path To Transformation?

Approaching Infinity said:
Ailén said:
We have been doing rough calculations to see what amount of protein each of us here can have according to our body weight (supposedly, one should eat 1,5grams of protein per kilogram of body weight). And based on the meat we get, we've estimated that there is more fat in ours than in what was measured for this chart.
Where did you guys find that figure? I'm curious, because Gedgaudas says 0.8 g/kg in PBPM.
It is in Ailén's reading list.
This particular study: Ketogenic diets and physical performance.
 

Muxel

Dagobah Resident
Re: Ketogenic Diet - Path To Transformation?

To continue Ailén's thread of thought,

Oxidative Capacity, Lipotoxicity, and Mitochondrial Damage in Type 2 Diabetes

Neutral fatty acids that fail to be activated (converted to acyl-CoA) still manage to enter the mitochondrial matrix via a flip-flop mechanism. Once in, they lose their proton and become anionic. This lowers the proton gradient. ROS attacks the anions to produce lipid peroxides, which are highly reactive and can lead to oxidative damage of DNA, RNA, and enzymes in the matrix. Enter UCP3 to save the day. UCP3 exports fatty acid anions and peroxides to prevent damage. It lowers the proton gradient to reduce ROS generation.

During insulin resistance, UCP3 levels are decreased. So, levels of lipid peroxides are increased. The authors say this might lead to mitochondrial aberrations.

patients with type 2 diabetes are characterized by high plasma FFA [free fatty acid] levels and a reduced fat oxidative capacity. Under such conditions, fatty acids that cannot be oxidized will accumulate in the muscle cell, and the increased load of fatty acids on the mitochondrial membrane will lead to the entrance of neutral fatty acids into the mitochondrial matrix
UCP3 is upregulated under conditions of an abundance of fatty acid supply to the mitochondria, such as during fasting, high FFA levels, acute exercise, and high-fat feeding. On the other hand, downregulation of UCP3 occurs when fatty acid oxidation is increased or plasma FFA levels are lowered, such as with endurance training and weight reduction.
Here are my thoughts and conjectures. We are all diabetics, because sugar-burning is not a default pathway, but a subversion of one. Insulin prevents hydrolysis of stored triglycerides, and shuttles lipids from the blood into our tissues. When we became sugar-burners, there were two ways of surviving it: fatness and skinniness. Skinny people dealt with insulin spikes by increasing OXPHOS and UCP3. Fat people had a problem with their UCP3 mRNA expression. So, they had to decrease OXPHOS instead, or maybe increase UCP2 (white fat).

Maybe the strategy that fat people use is the same strategy that is used by old people. This could explain why the obese have shortened lifespans—they've skipped right to old-age compensation, and even that in overdrive.

in the elderly it was recently shown that muscular lipid accumulation is related to mitochondrial dysfunction and insulin resistance, and aging is associated with accumulation of ROS-induced mutations in control sites of mitochondrial DNA replication.
 

liffy

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Re: Ketogenic Diet - Path To Transformation?

Approaching Infinity said:
Ailén said:
We have been doing rough calculations to see what amount of protein each of us here can have according to our body weight (supposedly, one should eat 1,5grams of protein per kilogram of body weight). And based on the meat we get, we've estimated that there is more fat in ours than in what was measured for this chart.
Where did you guys find that figure? I'm curious, because Gedgaudas says 0.8 g/kg in PBPM.
It seems that Gedgaudas recommended protein intake is in the lower part of the spectrum of what different paleo-people recommend. If I remember correctly, though, she does say that this amount should be increased for persons that are doing resistance training.
 

mb

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Re: Ketogenic Diet - Path To Transformation?

liffy said:
Approaching Infinity said:
Ailén said:
We have been doing rough calculations to see what amount of protein each of us here can have according to our body weight (supposedly, one should eat 1,5grams of protein per kilogram of body weight). And based on the meat we get, we've estimated that there is more fat in ours than in what was measured for this chart.
Where did you guys find that figure? I'm curious, because Gedgaudas says 0.8 g/kg in PBPM.
It seems that Gedgaudas recommended protein intake is in the lower part of the spectrum of what different paleo-people recommend. If I remember correctly, though, she does say that this amount should be increased for persons that are doing resistance training.
Nora Gedgaudas, in Primal Body, Primal Mind, quotes the US RDA of 0.8 g/kg, with qualifications. One source I found credited this RDA value to Harvard School of Public Health. PBPM specifies this ratio as per kg of ideal body weight. She is not suggesting going below the RDA, but rather not going very much above it. (Emphasis in the quote below is in the original.)

Primal Body said:
So, how much is just enough? For most adults the RDA, roughly 0.8 g per kilogram (2.2 pounds) of ideal body weight (e.g., 150-pound ideal body weight (68 kg) × .8 g = 54 g), is probably sufficient for 97.5 percent of the adult population (one of the rare RDAs worth paying some attention to). The average would lie somewhere between 45 and 60 g of actual protein per day for the majority of adults. One study noted that the amount of protein needed to effectively retain lean tissue mass and quality physical performance in athletes was closer to 1.2 to 1.7 g/kg daily, translating to 60 to 80 g of protein per day, assuming adequate mineral intake (Phinney 2004). The same study also noted negative effects if this level of daily protein was exceeded by more than 25 percent of the daily energy expenditure, citing a drop in performance and suppression of ketogenesis.

Gedgaudas, Nora T. (2011-06-22). Primal Body, Primal Mind: Beyond the Paleo Diet for Total Health and a Longer Life (pp. 196-197). Healing Arts Press. Kindle Edition.
She is not talking about weight loss, however. The 1.5 g/kg figure appears in The Art and Science of Low Carbohydrate Living.

Now, for comparison, let’s contrast the response to this study with that to another similar study published 8 years later in 1984. Entitled ‘Metabolic effects of very low calorie weight reduction diets’, this study was done by Dr. Hoffer and colleagues at MIT and Harvard, and was also published in the Journal of Clinical Investigation[78]. So, similarly prestigious institutions and the same excellent journal. However Dr. Hoffer’s paper has only been cited 77 times – one third less often than the Van Itallie study. Why might this be?

Perhaps it is because Dr. Hoffer studied moderately overweight women given low and high carbohydrate diets of about 700 Calories per day for 6-8 weeks and found no difference in their rates of weight loss. But provocatively, what he also found was that his low carbohydrate diet (providing a more effective protein level for dieting subjects – 1.5 g/kg reference weight per day) resulted in significantly better preservation of lean tissue and physical performance compared to the same number of calories as a mixture of protein (0.8 g/kg – the current DRI) plus carbohydrate.

In essence, what Dr. Hoffer’s study demonstrated was that in the context of energy restriction, protein is more effective at preserving lean body mass than an equal number of calories as carbohydrate. But this was not what the mainstream nutrition consensus wanted to hear, so most of the ‘experts’ tried to ignore this well-controlled study done under conditions much more relevant to the real world of weight loss diets than Van Itallie’s short-term study of his low protein, high fat diet.

Phinney, Stephen; Volek, Jeff (2011-07-08). The Art and Science of Low Carbohydrate Living: An Expert Guide to Making the Life-Saving Benefits of Carbohydrate Restriction Sustainable and Enjoyable (pp. 148-149). Beyond Obesity LLC. Kindle Edition.
It can be difficult (or impossible) to lose weight while restricting protein intake, and trying to do so can result in consuming muscle and other vital tissue (bad!). I have had to increase my protein intake (while restricting carbs and not overdoing fat) to keep my appetite in check, but doing so has meant losing weight (or not -- it varies) without going hungry. So the 1.5 g/kg number sounds reasonable, depending upon the objective.
 

aragorn

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Re: Ketogenic Diet - Path To Transformation?

Megan said:
liffy said:
Approaching Infinity said:
Ailén said:
We have been doing rough calculations to see what amount of protein each of us here can have according to our body weight (supposedly, one should eat 1,5grams of protein per kilogram of body weight). And based on the meat we get, we've estimated that there is more fat in ours than in what was measured for this chart.
Where did you guys find that figure? I'm curious, because Gedgaudas says 0.8 g/kg in PBPM.
It seems that Gedgaudas recommended protein intake is in the lower part of the spectrum of what different paleo-people recommend. If I remember correctly, though, she does say that this amount should be increased for persons that are doing resistance training.
Nora Gedgaudas, in Primal Body, Primal Mind, quotes the US RDA of 0.8 g/kg, with qualifications. One source I found credited this RDA value to Harvard School of Public Health. PBPM specifies this ratio as per kg of ideal body weight. She is not suggesting going below the RDA, but rather not going very much above it. (Emphasis in the quote below is in the original.)
If I remember correctly, Nora G. recommends these figures, not only to stay in ketosis, but also to down-regulate the mTor pathway signaling (regulates longevity).

Apropos, it occured to me that even though we might not need that much supplementing following this diet, taking vitamin-C seems to be important in changing the mDNA. This is based on the following:

In all vertebrates, NAD can be synthesized by two pathways: de novo synthesis from tryptophan [3,4] and/or from vitamin precursors in the diet: NA, nicotinamide (NAM), and nicotinamide riboside (NAMR). [...] For the de novo pathway to be completed it is necessary to have adequate riboflavin (vitamin B2), pyridoxyl phosphate (vitamin B6), and ascorbate (vitamin C).
 

aragorn

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Re: Ketogenic Diet - Path To Transformation?

For those of you who don't have the book, here's a quote from Gedgaudas (her website) concerning protein intake:

_http://www.primalbody-primalmind.com/?p=295
So why would I recommend limiting protein intake at all…much less to the RDA of 44-56 grams…amounting to little more than about 6 ounces of natural protein per day??? This wouldn’t look much larger on a dinner plate than a deck of playing cards…only you’d be dividing that into 2 or 3 meals. Say WHAT??

*GASP*!!

Let’s just say I may have upset the applecart with a few die-hard carnivores…many of whom take on a “more is better” attitude toward their meat at mealtime. I can certainly sympathize. There was a time when I could have eaten a lot of them under the table and gone back for seconds when it came to a big juicy rare steak. I still love juicy rare steaks…I just limit the amount I consume at a meal nowadays.

Why on earth is that, you ask?

Am I trying to be more environmentally sensitive?

Am I trying to seem less insensitive to those suffering across the world from hunger?

Am I trying to lose weight?

Am I trying to avoid excess ammonia burden?

Am I trying to “go easy” on my digestive processes?

Am I trying to save money in these tough economic times?

Not necessarily. –Though a positive case could be made for any of this reasoning. The primary reason doesn’t have to do with any of the above…though I will say I don’t mind that a lot of these things are nice side-line benefits that come along with my primary incentive. What opened my eyes to the virtues of limited protein consumption wasn’t consideration from a Paleolithic, political, environmental or economic perspective but rather a more recent scientific one.

Turns out that 75 years of human longevity research and recent findings can help to uniquely wed our most primal nutritional requirements with a loophole that can help us all beat mother nature at her own game and stay healthier and younger much longer.

Research in just the last few years revealed a metabolic pathway that wasn’t known about before. This discovery revealed a new perspective on dietary protein that, together with insulin–can powerfully influence reproduction, aging, as well as susceptibility to degenerative illness and even cancer. Cynthia Kenyon’s important work back in the mid-1990′s revealed conclusively that the minimization of insulin is the single most important factor toward the enhancement of longevity and health. No small finding–even though it was hardly headline news (I could be persuaded by a conspiracy theory or two as to why it wasn’t at the time, but I digress). Her work pretty clearly showed the primary reason that caloric restriction–the single most effective of all anti-aging approaches–actually worked. –But it turns out there’s a secondary reason that caloric restriction seemed to confer a marked improvement in health and longevity, and resistance to degenerative processes and cancer. It has to do with something scientists found called mTOR–which stands for mammalian Target Of Rapamycin. I talk about this in my book at considerable length and won’t overly go into it here. Suffice it to say that this newly discovered metabolic pathway, “mTOR”, apparently serves as a sort of metabolic “protein sensor”. It belongs to something called the “P13K” pathway that is activated by insulin, nutrients and growth factors. It turns out that keeping mTOR down-regulated–by limiting protein intake to what is simply necessary for maintenance–is actually part of the key to maximizing our internal repair and regeneration, immune function–enhancing longevity, anti-aging and minimizing the risk of cancer. Coupled with maintaining low insulin levels, keeping the mTOR pathway largely down-regulated helps keep deterioration and disease at bay and helps keep us young. Ironically, dietary fat has no negative influence here.

Because mTOR is intimately involved with growth and reproduction, however, there may be instances–such as while seeking successful conception, pregnancy, extreme work loads, high level athletic training and critical growth periods from infancy through adolescence where the practice of limiting protein and mTOR might be less desirable. During time periods such as this the stimulation of cellular proliferation becomes more necessary. Apart from times like this, however, higher than needed amounts of protein can take away from your own maintenance and repair, lessen immunity, and make you far more susceptible to cancer.

Protein is not our enemy…but it is certainly true that too much protein is also arguably not necessarily our friend. I choose (with sound reason) to define “too much” as anything overly provoking of mTOR. Also, keep in mind that protein in excess of what is actually needed for repair and maintenance simply gets converted to glucose and is stored the same way.

I’ve also realized that 1) it’s not at all necessary to eat that big a portion of protein to truly have “enough” 2) it’s entirely possible to be fully satisfied with less, using sufficient accompanying dietary fat (this is KEY) 3) Past a certain amount in a meal protein ceases to be purely beneficial and really can place considerable demand on energy and digestive, etc. systems that can also lead to undesirable consequences (i.e., impaired digestion, excess ammonia burden, and potential weight gain). Former “carbovores” who try to switch to eating “high protein diets” may be just that much more efficient, too, at turning that excess protein into sugar and storing it the same way 4) it’s unnecessarily expensive to eat this much…and by restricting protein consumption in this way one can literally save thousands of dollars on grocery bills. –Not even counting the money you save avoiding processed junk, all the sugary and starchy carbs, juices, sodas and alcohol. Protein is often the most expensive thing we buy at the grocery store (not counting “specialty gourmet items”). Eating even THE best possible quality food becomes literally downright cheap. I kid you not. This amounts to literally the least expensive way to eat optimally well anywhere. Plus, you’re saving a fortune on medical bills in the long run, too—all the while you’re experiencing a rather astonishing enhancement of your energy, immune function and well-being. It’s a win-win–as long as you’ve also ditched the sugar and starch (and are eating enough natural fat).

Of course, you might not get to indulge in gorging yourself on that 10 oz side of beef–but truth be told, I doubt you’d much miss it.

Protein takes more energy than anything else to digest. By moderating your protein intake you lessen that burden and have more energy for a whole lot of other things. If you still want that 10 oz steak with dinner, go ahead. –But your appetite could be every bit as satisfied with less, you’d have better quality digestion, more energy and probably live longer and healthier than you otherwise would if you’d give the ideas in Primal Body-Primal Mind a try.

Besides, it may not be nice to fool mother nature, but it sure can be fun and a whole lot healthier beating her at her own game.

---
In the comments below the article, she adds:

"In short, yes–your weight and especially lean mass really do dictate your protein needs. Obviously, your activity level also makes a difference, which should be taken somewhat into account. In a conversation I just had with Ron Rosedale, MD (of “The Rosedale Diet”) who has exhaustively researched this very subject– although he liked my use of the protein RDA (44-56 grams/day) as a baseline average for most he also intimated this might very well even be too high for some! The idea is not to overly provoke the mTOR pathway or eat protein to excess of basic restructuring and maintenance need lest excesses go into energy production (i.e., conversion to sugar and potentially body fat and glycation).!"
 

aragorn

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Re: Ketogenic Diet - Path To Transformation?

While looking up the above, I found this study, which gives clues about how the mTOR pathway influences the mitocchondria:

_http://www.jbc.org/content/281/37/27643.long
p.27650:

DISCUSSION

In summary, we have provided evidence that mTOR activity and more precisely mTOR-raptor complex formation is tightly correlated with mitochondrial metabolism. In particular, cells sorted for spontaneous differences in resting mitochondrial respiration showed corresponding differences in their mTOR- raptor complexes and mTOR activity. Similarly disrupting mTOR-raptor complexes by either pharmacological means with rapamycin or genetically with RNAi resulted in a corresponding change in metabolism. There are at least two possible explanations for this relationship. The first is that increasing mTOR activity places a significant energetic load on the cell presumably through an increase in protein synthesis, ribosomal biogenesis, etc. that results in a corresponding reactive increase in mitochondrial activity. The second possibility is that mTOR can directly modulate mitochondrial metabolism in what might be described as a feed forward mechanism. Clearly these two possibilities need not be mutually exclusive. Although we cannot conclusively conclude which mechanism pre- dominates we believe that our observations do provide evidence for a feed forward pathway.

This primary regulation is supported by three observations. First, mTOR- raptor directly associated with the mitochondria, and disruption of mTOR-raptor resulted in a significant alteration in the mitochondrial phosphoproteome. Second, altering mTOR-raptor did not just affect the load-dependent property of basal oxygen consumption but also the total oxidative capacity of the cell, a measurement that is believed to reflect an intrinsic mitochondria property. Finally if the alteration in mitochondrial metabolism were merely secondary to changes in energetic demand we would not expect the relative balance of aerobic to glycolytic ATP generation to be altered. Rather we would expect that if cellular demand went up or down mitochondrial metabolism and cytosolic glycolysis would go correspondingly up or down but do so while maintaining their initial balance. Although our oxygen consumption measurements have limitations with regard to quantification, our data (Fig. 7A) do suggest that knockdown of raptor and TSC2 appears to alter the relative contribution of cytosolic glycolysis to mitochondrial metabolism. These observations, in our view, further support a primary regulatory role of mTOR on mitochondrial activity.

We performed our respiration experiments using intact cells, whereas the majority of previous studies have used isolated mitochondria. One somewhat surprising aspect of our data is that in our sorted cells the level of aerobic ATP production (i.e. oligomycin-sensitive oxygen consumption) and the mitochondrial membrane potential positively correlate (Fig. 1B). This is somewhat unusual because most events that increase the synthesis of ATP in isolated mitochondria that act solely through the F1F0-ATPase result in a lowering of membrane potential. A higher mitochondrial membrane potential in the face of higher respiration supports the notion that the overall capacity of the mitochondria to produce ATP has been enhanced. This supposition is also supported by our observation that oxidative capacity (maximal FCCP-stimulated respiration) increased as a function of mitochondrial membrane potential. We believe these observations highlight the potential utility of studying intact cells with intrinsic differences in endogenous mitochondrial activity and capacity rather then isolating and pooling mitochondria from metabolically heterogeneous tissues.

[...]
p.27651: Finally there is growing evidence that mitochondrial metabolism may play an important role in aging (2–4). Previous reports have indicated that in yeast, C. elegans, and Drosophila, inhibition of the TOR pathway results in life extension (13–16). An analysis of a large number of life-extending mutations in C. elegans has led to a hypothesis that these diverse genetic alterations may all function by inducing energetic shifts away from the mitochondria and toward alternative ATP-generating pathways (33). Our observation that mTOR activity tightly correlates with oxygen consumption and serves to regulate the balance between glycolysis and aerobic metabolism appears consistent with that theoretical framework.
 

Keit

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Re: Ketogenic Diet - Path To Transformation?

Laura said:
I can't say I'm all energized or anything, but then, I've probably got so much damaged mtDNA it'll take a week or longer to start experiencing any real changes.

It really does help to understand what is going on. So many times before when I would go into ketosis, since nothing really happened, I figured "it doesn't work for me" and said "heck with it". But now, understanding that the issue is probably a load of damaged mtDNA and how the system works to fix this and what the requirements are to help it along, well, it makes the experiment doable. All that is the theory, I want to see if it works on a hard case like me.
Don't know if it was already mention somewhere, but there is another, recently discovered, type of mitochondrial dysfunction- "selfish DNA". Here is an article on SOTT about it.

Researchers at Oregon State University have discovered, for the first time in any animal species, a type of "selfish" mitochondrial DNA that is actually hurting the organism and lessening its chance to survive - and bears a strong similarity to some damage done to human cells as they age. [...]

The mitochondria generally act for the benefit of the cell, even though it is somewhat separate. But the "selfish" DNA found in some plant mitochondria - and now in animals - has major differences. It tends to copy itself faster than other DNA, has no function useful to the cell, and in some cases actually harms the cell. In plants, for instance, it can affect flowering and sometimes cause sterility. [...]

What's also interesting, they say, is that the defects this selfish DNA cause in this roundworm are surprisingly similar to the decayed mitochondrial DNA that accumulates as one aspect of human aging. More of the selfish DNA is also found in the worms as they age.
 

seek10

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Re: Ketogenic Diet - Path To Transformation?

I was not really doing much fasting, as I still have low blood sugar issues. I think, I need to wait until the blood sugar normalizes and I need to increase my sugar levels. Though I don't feel tired or any thing for 15 hrs of food break , I still see symptoms of low blood sugar and glucometer shows low values. Even after eating stomach full of high fat meat, my blood sugar is still lingers at 80 mg/dL. I still need to read some papers though.
 

seek10

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Re: Ketogenic Diet - Path To Transformation?

seek10 said:
I was not really doing much fasting, as I still have low blood sugar issues. I think, I need to wait until the blood sugar normalizes and I need to increase my sugar levels. Though I don't feel tired or any thing for 15 hrs of food break , I still see symptoms of low blood sugar and glucometer shows low values. Even after eating stomach full of high fat meat, my blood sugar is still lingers at 80 mg/dL. I still need to read some papers though.

Is this still true?
_http://paleodietlifestyle.com/intermittent-fasting-paleo-diet/

Who shouldn’t IF?

While most healthy adults following a Paleo diet should have no trouble with intermittent fasting, it’s not for everyone. Before adding IF to your routine, make sure your body has fully adjusted to eating Paleo. Fasting is a stressor to your body, so it can do more harm than good if you’re already under any kind of chronic stress. If you’re sleep-deprived, suffering the effects of overtraining or chronic lifestyle stress, leptin resistant, or if you have blood sugar problems, IF is not for you. You should not feel sick, dizzy, or inexplicably exhausted during a fast: if you do, eat something. Think of IF as the cherry on top of your Paleo chocolate pudding: first work on the fundamentals (adjusting to the dietary changes, getting enough sleep, and reducing chronic stressors), and then consider adding it to your routine.
 

Hesper

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Re: Ketogenic Diet - Path To Transformation?

I'm still trying to expand my understanding of the ketone bodies and the specifics of how this diet works, and I happened to stumble upon this book: "Cancer as a Metabolic Disease" by Thomas Seyfried. It's pretty expensive on Amazon but it looks like a really good read. This is an editorial review:


A groundbreaking new approach to understanding, preventing, and treating cancer

Supported by evidence from more than 1,000 scientific and clinical studies, this groundbreaking book demonstrates that cancer is a metabolic disease and, more importantly, that it can be more effectively managed and prevented when it is recognized as such. Moreover, the book provides detailed evidence that the traditional view of cancer as a genetic disease has been largely responsible for the failure to develop effective therapies and preventive strategies.

Cancer as a Metabolic Disease reevaluates the origins of cancer based on the latest research findings as well as several decades of studies exploring the defects in tumor cell energy metabolism. Author Thomas Seyfried is a biochemical geneticist who has been investigating the lipid biochemistry of cancer for thirty years. In this book, he carefully establishes why approaching cancer as a metabolic disease leads to better understanding and management of all aspects of the disease, including inflammation, vascularization, cell death, drug resistance, and genomic instability. In addition, the book explores:

Origin of metastasis
New treatment strategies that target tumor cell energy metabolism, including the ketogenic diet
More effective prevention strategies in light of the metabolic origin of cancer
Case studies and perspectives from the point of view of physicians, patients, and caregivers

Throughout the book, tables, figures, and graphs summarize key information and clarify complex concepts. In addition, the renowned cancer biochemist Peter Pedersen from Johns Hopkins Medical School also provides a historical perspective on the importance of the information presented in his foreward to the book.

Cancer as a Metabolic Disease is essential reading for all cancer researchers and clinicians as well as public health professionals. By treating cancer as a metabolic disease, the book sets readers on a new, more promising path to understanding the origins of cancer and developing new, more effective strategies to treat and prevent it.
About the Author

THOMAS N. SEYFRIED, PhD, has taught and conducted research in the fields of neurogenetics, neurochemistry, and cancer for more than twenty-five years at Yale University and Boston College. He has published more than 150 scientific articles and book chapters and is on the editorial boards of Nutrition & Metabolism, Journal of Lipid Research, Neurochemical Research, and ASN Neuro.
Has anyone read this one? It's on Google Books so I have had a chance to look through a bit of it, and it does seem like a good read. It not only covers the science but also the history of the metabolic theory and how it's been attacked by big shot cancer researchers. Seems great to me so I'll see if the library could get a copy, though school is starting again soon so I'm not sure how much time I could devote to digging into it.

Here's the link to it on Google Books: _http://books.google.com/books?id=j7ODau5zCzUC&pg=PA108&lpg=PA108&dq=sidney+weinhouse&source=bl&ots=hKvQ6v2X0a&sig=sNEG7-V-lK8y-ggsqmWlK55FDn0&sa=X&ei=PsknUIaYK4382gXRyoCYDg&ved=0CBsQ6AEwBjgU#v=onepage&q=sidney%20weinhouse&f=false
 

Approaching Infinity

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Re: Ketogenic Diet - Path To Transformation?

Nicolas said:
Approaching Infinity said:
Ailén said:
We have been doing rough calculations to see what amount of protein each of us here can have according to our body weight (supposedly, one should eat 1,5grams of protein per kilogram of body weight). And based on the meat we get, we've estimated that there is more fat in ours than in what was measured for this chart.
Where did you guys find that figure? I'm curious, because Gedgaudas says 0.8 g/kg in PBPM.
It is in Ailén's reading list.
This particular study: Ketogenic diets and physical performance.
Thank you, Nicolas! Hadn't gotten to that one yet.
 

mb

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Re: Ketogenic Diet - Path To Transformation?

Hesper said:
I'm still trying to expand my understanding of the ketone bodies and the specifics of how this diet works, and I happened to stumble upon this book: "Cancer as a Metabolic Disease" by Thomas Seyfried. It's pretty expensive on Amazon but it looks like a really good read...
The research article by the same name and from the same author is available at
_http://www.nutritionandmetabolism.com/content/7/1/7

Reading that would be a good starting point. I only had time to skim it, but it is similar to other metabolism-related papers I have been examining.

Conclusions
Evidence is reviewed supporting a general hypothesis that cancer is primarily a disease of energy metabolism. All of the major hallmarks of the disease can be linked to impaired mitochondrial function. In order to main- tain viability, tumor cells gradually transition to sub- strate level phosphorylation using glucose and glutamine as energy substrates. While cancer causing germline mutations are rare, the abundance of somatic genomic abnormalities found in the majority of cancers can arise as a secondary consequence of mitochondrial dysfunc- tion. Once established, somatic genomic instability can contribute to further mitochondrial defects and to the metabolic inflexibility of the tumor cells. Systemic metastasis is the predicted outcome following protracted mitochondrial damage to cells of myeloid origin. Tumor cells of myeloid origin would naturally embody the capacity to exit and enter tissues. Two major conclu- sions emerge from the hypothesis; first that many can- cers can regress if energy intake is restricted and, second, that many cancers can be prevented if energy intake is restricted. Consequently, energy restricted diets combined with drugs targeting glucose and glutamine can provide a rational strategy for the longer-term man- agement and prevention of most cancers.
 

mb

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Re: Ketogenic Diet - Path To Transformation?

Nicolas said:
Approaching Infinity said:
Ailén said:
We have been doing rough calculations to see what amount of protein each of us here can have according to our body weight (supposedly, one should eat 1,5grams of protein per kilogram of body weight). And based on the meat we get, we've estimated that there is more fat in ours than in what was measured for this chart.
Where did you guys find that figure? I'm curious, because Gedgaudas says 0.8 g/kg in PBPM.
It is in Ailén's reading list.
This particular study: Ketogenic diets and physical performance.
This appears to be the 2004 paper by Phinney, cited in Primal Body, Primal Mind within the text I quoted above. I haven't gone over it yet (too many things to do!), and I couldn't assess the context for the 1.5 g/kg/d figure (used three times in the paper) by simply skimming. As in PBPM, the reference is to 1.5 g/kg of "reference" (i.e. ideal) body weight. It doesn't mean to simply weigh yourself and then do the calculation, if you are overweight.

My approach has been to adjust protein intake so that it is just enough to stabilize my appetite (or a little more), which does indeed bring it somewhere near this value, rather than setting a target based upon "average" requirements. But then pre-diet I only burned around 1800 kcal/day, which is not "average" for someone 6 feet tall, and I think it may be even less now (I don't count it any more). Unless you are "average," be careful about using average targets.
 
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