Not all of us are built for high fat/low carb diets. I, for one, tolerated the diet well for the first few months, and then my body began to crumble.  Judging from your general symptoms, it would seem that your body is kindly screaming at you to stop the experiment. However, as a type 2 diabetic, ketosis may benefit your metabolism in some ways--so long as you use the diet intermittently and very carefully. But let me ask a few questions before saying much more:

How long have you been on the diet for? The adaptation curve for a ketogenic diet can be rather steep, and typically people experience negative side effects for the first few days, up to a couple of weeks.

What fat/protein ratios are you working with?

Are you eating fresh organs along with muscle meats?

Are you getting at least 30-40g carbs per day for your brain's glucose needs?

How is your gut health?

Regarding the weight loss, what you are experiencing does not seem to be completely out of the ordinary, as ketogenic diets have a tendency to initially cause a significant decrease in the body's ability to store water, I.E., reducing water weight. As a diabetic, though, you should be extra cautious with sudden drops in weight.

As a final thought, I think balance is key when it comes to a functional, optimal diet. Going down the strictly fruitarian path is as problematic as reducing carbs to a negligible amount. You can still reap the metabolic benefits of a moderately low carb diet even if you include some more fruits, greens, and certain vegetables. For some of us, being in either ketosis or ultra-high carb mode constantly can really take its toll on our health. Again, think balance.

This has to be one of the most biased, unscientific post I’ve read in a while.

I had been waiting for someone else to pull the “unscientific” card. I'll address your concerns in their order of appearance. A bibliography is attached at the end of this response.

“By and large, carnivorous mammals across the world exhibit lower average lifespans than omnivorous creatures.” Really? Please show any evidence of this.

[http://www.demogr.mpg.de/longevityrecords/0203.htm]

This comes straight from the Max Planck institute for Demographic Research. The average life span data for each species is supported by peer-reviewed studies.

If you look through the document, you'll notice that strictly and/or predominantly carnivorous mammals exhibit lower average life spans than their omnivorous counterparts. While I don't have the time to construct a chart which explicitly compares the two groups (or which deals with the statistical significance of the data), I will pick out some quick examples that address the underlying concerns in a succinct manner:

1) Hippopotamus (omnivorous) in relation to the lion (classic, cliche example of carnivorous animal).
2) Suborder mysteceti whales (fin whales, blue whales, etc.) in relation to carnivorous whales.
3) Eurasian brown bear (predominantly omnivorous since the middle ages) in relation to the polar bear (predominantly carnivorous).

On a tangential note, it would seem that whales possess metabolic adaptations to predominantly carnivorous diets that allow them to live longer than most land carnivores. However, this all comes with a rather large caveat: within the whale groups themselves, the filter-feeders, or baleen whales, exhibit larger average life spans than the predominantly carnivorous species. For the baleens, consuming zooplankton means that phytoplankton is difficult to avoid, and indeed, perhaps even constitutes an important dietary element for the aquatic mammals. Zooplankton depends primarily on phytoplankton for survival, and the two are seldom found separated in the oceans. “The physical factor that influences zooplankton distribution the most is mixing of the water column…along the coast and in the open ocean….that affects nutrient availability and, in turn, phytoplankton production” (Lalli et al. 1993). At least for certain species such as the bowhead whale, research has demonstrated that phytoplankton is an important, if consequential, aspect of their diets. “Each adult [bowhead] whale consumes on the order of 100 metric tons of zooplankton prey, which in tum represents a much larger ( -10 times) biomass of phytoplankton” (Schell 2000). Finally, here is a quote from an accessible article which ties the levels of phytoplankton in the world's oceans to the diets of blue whales: [http://www.theguardian.com/environment/2010/jul/28/phytoplankton-decline-nature].

Another user on this forum (Edmon) posited that the differences in carnivore/omnivore life spans are due to the expression of the simple mechanisms of survival involved in predatory activities. To take his claims further, the logic supporting such a statement is as follows: If a hunter feasts solely on meat, then the hunter's capacity to survive is tied directly to their hunting skills, and hunting skills are tougher to maintain than grazing faculties. Edmon argued that carnivorous animals typically die while attempting to secure their prey, in fights with other predators, and of infections/other illnesses. While we can accept such an Occam's razor-like approach to the life span problem in carnivores, and immediately cease considering a myriad variables, a series of critical, thought-provoking questions will yet remain: All things considered, why does the wild carnivore's survival functions—namely, the capacity to engage in a successful hunt, acquire nourishment, and deflect other predators, pathogens, etc.—decline at a faster rate than the omnivore's, thereby leading to observable differences in life spans? In other words, why does the carnivorous mammalian, which is supposedly well-adapted to hunting and the consumption of an all-meat diet, fail to adequately maintain its physical faculties for longer than the omnivore's? Is it simply that hunting full-time is harder work than foraging and scavenging? What does such harder work constitute, in a metabolic sense? Harder work in what specific terms? What of the omnivores, who hunt, scavenge, and forage, depending on the seasons, their needs, desires? Capturing live prey obviously involves a great deal of exertion and stressors, but are the lion's overall stressors necessarily greater than the hippo's per se?

The emergence of these questions led me to the eventual exploration of the mechanisms of action involved in the mammalian body's metabolic pathways. Before I get into the theoretical and scientific underpinnings of my section dealing with the human’s metabolic pathways, let me tackle your point regarding "the validity of a diet to optimal health:"

And even if this was true, it means nothing about the validity of a diet to optimal health. Optimal health means heath level during life, not how long that life lasts.

Since I refuse to play a game of semantics, I'm going to assign a very specific definition to my usage of the concept of optimization, so that there may be no confusion regarding what I'm referring to.

Optimization involves the process of making something as effective, sustainable, and fully-functional as possible. The optimization of a system refers to the maximization of productivity and the minimization of refuse. In the context of my discussion, optimization is directly tied to temporal sustainability, and therefore, by extension, to life span.

Simply put, the form of optimization that I seek does not only account for the short-term benefits of efficiency; I am far more compelled by the notion of efficiency as it relates to sustainability and longitudinal performance. Thus, I initially frame optimization within the context of life span because I am asking how we can optimize both the quality and duration of human life. You seem to be arguing that the quality of a life is all that matters for an organism's existence. In this sense, it does not matter whether a person lives past their forties, so long as they have experienced an acceptable level of health throughout their active moments. I disagree with this rather simplistic and limited conceptualization of health and optimization. My argument attempts to push beyond the strictly qualitative domain and into the temporal and quantitative.

Mice are herbivores, but they live less long than a cat that feeds on them, if they both die of old age.

I’m not exactly certain as to why you are bringing up herbivorous mice. At no point did I address the life spans of herbivorous species. However, if we want to go down that road, then I will note that large mammalian herbivores, such as ruminants, do tend to live longer than large carnivores (where ‘large’ refers to animals bearing an average body weight of over 150 lbs.), if subjects are allowed to die strictly of old age. But—and this is a huge but—the encephalization quotients, as do the brain sizes, of herbivores (Deaner et al. 2007; Nelson et al. 2001) tend to be much lower than omnivores and carnivores, thereby revealing an apparent deficit in the cognitive abilities of the herbivorous group—which would make sense from an evolutionary perspective that considers brain growth as tied to the consumption of animal proteins and fats.) Of course, we can get into extended and unfruitful discussions of what constitutes intelligence within a particular species. For the sake of simplicity, I am using the rubrics of the encephalization quotient and total brain size to describe mental processes as they become appreciable to our human understandings of intellect.

The evolutionary ideas, while “somewhat” valid as empirical evidence (is there any evidence that animals in the wild tend to eat what is best for them?

It does not matter whether you believe that “animals in the wild tend to eat what [is or isn’t] best for them.” (Although there are numerous people on this forum—“instinctos”—that will strongly dispute this point in relation to human evolution.) The point of my discourse is to emphasize the fact that countless years of human evolutionary adaptations have laid the biological foundations for the execution of a potential diet which utilizes rational, historically-valid reasoning to provide the body with its optimal requirements. You are attacking my usage of evolutionary ideas by mobilizing a completely unrelated assertion. Evolutionary theories do not ipso facto rely on optimization apparatuses to describe animal bodies; evolutionary theories present us with frameworks for approaching the adaptations and survival dynamics that allow for the reproduction, transformation, and destruction of a species. I am drawing on evolutionary theories insofar as they reveal the present conditions of human metabolic pathways, and allow for us to make informed judgments regarding the optimal means by which to expand the living performance of bodies. I am not, as you crudely assume, drawing on evolutionary theories to supply evidence for the supposed “natural” existence of optimization mechanics in the “wild.” Do not misconstrue my words.

However, no one knows what earlier humans ate. It’s all guesses and suppositions. They had element “X” in their environment, it’s edible, they probably ate it. Again, why would people assume that they would eat what is good for them rather then what they might stumble upon is beyond me.

Absolutely irrelevant to my argument. I highly doubt that ancient humans were thinking of how to grow larger brains when they decided to hunt other animals. I would not be so naïve and foolish to claim this. Rather, the evolutionary result of the ancient human’s dietary decisions contributed, directly and indirectly, to the development of specific bodily facets—namely, the larger brain. Evolution is not akin to optimization, but dietary optimization theories must draw on evolutionary knowledge to pass grounded judgments. Your failure to grasp my assertions makes me wonder whether you even read my opening post before engaging in this unfounded collection of attacks.

Worse, using arguments of authority is dishonest. “reading up on a great deal of scientific studies and informal experiences” What’s that supposed to mean? Every doctor I’ve ever heard talk about nutrition…

I don’t even feel the need to quote that statement in its entirety. Your ad hominem tactics are infuriating, at the very least, and, at most, rather disheartening. Considering the overt assaults on my character, if your response to my post were to appear in a scholarly journal, I would feel no need whatsoever to offer you a rebuttal. Thankfully, this is a public forum, and I’ll gladly humor your offensive reply for the sake of fostering public knowledge.

I am not marshaling “arguments of authority” in any way whatsoever. If your definition of arguments of authority means that I declared my knowledge of the subject that I am describing, then yours is truly an atypical approach to the expression. The reason why I stated that I read up on a significant number of scientific studies and informal experiences is because I did. As for informal experiences, my own encounter with a sustained ZC diet has led to heart issues that I am still recovering from. At several moments throughout my ZC experiment, I was dealing with ridiculous and unexplainable palpitations; my extremities were becoming cold, my emotions were receding, and I was consistently irritable. If you would like to talk about the problems that others have experienced while on a sustained ZC diet, just ask PaleoPhil about the symptoms that he dealt with. On Carbsane and other forums, informal evidence for symptoms of what has been termed “VLC/ZC torpor” have emerged as well. PaleoPhil, I’m sure, would be glad to provide you with actual links to the pages where people talk about their problems while on ZC diets.

Regarding the formal underpinnings of my theories, I have drawn on specific scientific studies which demonstrate the inefficient properties of gluconeogenesis (Hendrick et al. 1990; Veldhorst 2009; Veldhorst 2012; Baba et al. 1994) while in a deep ketogenic state (Tagliabue A 2012), and relative to glucose metabolism (Mcdonald 1998; Prince et al. 2013); as well as revealing the difficulties associated with the production of glucose from fatty acids (Kaleta et al. 2011); and the limitations on the potentially therapeutic overall uptake of ketones by the brain (Devivo et al. 1978; Seyfried et al. 2003; Lahanna et al. 2009; Cahill 2006). All of these studies address periods of deep ketosis as exceptional for the mammalian body, with Lahanna (2009) and Seyfried (2003) particularly making use of such exceptional circumstances to augment the validity of their experimental procedures. Taken in tandem, these studies point to the short-term therapeutic benefits of a ZC or VLC diet (for the metabolically deranged, epileptic, etc.), but direct us toward challenging the long-term metabolic stressors that arise from the sustained inefficiencies of the aforementioned key metabolic pathways. I will return to this last point soon.

The body does not tend towards an optimal state. It maintains a “minimal” state. Enough to not die, nothing more. Lie down in a bed for a few months, eating the best diet you can. Your bones will still end up brittle, your muscles will be almost inexistent. Even if you eat a lot of protein and fat. Why? Because your body does the least in can if it has the option.

The body tends toward homeostasis, which is absolutely different from the “minimal” caloric state that you are describing. Your definition of minimal begs interrogation. If you are defining the human’s basal caloric requirements as being constitutive of a minimal state or set-point, then even at this level, homeostasis involves a conglomerate of intensely erratic, fluctuating processes. Homeostasis is about balancing and stabilizing the entropic reactions of a semi-structured body. Confronted with an obviously necessary minimal caloric intake (which is about the only minimal element of a human existence), the entropic body incessantly attempts to adapt and respond to the chaos generated both by and within metabolic processes.
Homeostasis, for one, cannot be separated from hormesis, which details the body’s responses to disordered metabolic chains. Even the subject lying on a bed will be exposed to organic stressors (atrophy, etc.) that cause their body to reflexively manipulate key metabolic pathways in response to sedentary functions. Oftentimes, these metabolic pathways involves seriously disruptive physical processes that make maximum use of inefficient metabolic structures, such as gluconeogenesis and ketosis, and which may not contribute to the optimal health of the subject, but which certainly allow for the subject to survive and adapt.
This is all to say that what you perceive as the body doing “enough to not die,” is actually the body doing enough to survive and reproduce; and there is a massive, indisputable difference between these two expressions. Your fatalistic approach to human existence is wholly unsupported by science. Humans have been shown to possess psychological and physical regulatory mechanisms that further the pursuit of reproduction, survival, and survival beyond reproduction. The body does the most it can to survive and reproduce, not the least it can to ward off death. The body, in fact, is not concerned with life and death--this Christian dichotomy that so many scientists submit to. The human body, the mammalian, animal body, is invested in the protection of reproductive faculties that are inextricably bound to the adaptive survival of an entropic organism. Survival is about adaptation and reproduction, not death and a minimalistic quality of degeneration.

 

So the fact that gluconeogenesis and ketosis are very inefficient (on a calorific) and taxing (on the organs) is irrelevant. That’s like saying that a jet is not optimal because it consumes too much energy and stresses its components, so a bicycle is better.

The underlying logic here is absolutely flawed. You moved from A to B without adequately connecting the two thoughts.

A) "The body does not tend towards an optimal state. It maintains a “minimal” state."
B) "So the fact that gluconeogenesis and ketosis are very inefficient (on a calorific) and taxing (on the organs) is irrelevant.

So, “if the body does not tend towards an optimal state,” then “the fact that gluconeogenesis and ketosis are very inefficient…and taxing on the organs….is irrelevant.”

What? How have you established the irrelevance of point B in relation to point A? In legal-speak, this is what we call a non-sequitur.

The notion of a minimal state serves no purpose in addressing the particular metabolic inefficiencies of gluconeogenesis and ketosis. As I stated above, the only minimal state in the human body is the basal need for calories that defines survival. To reiterate: optimization, as per my discussion, entails rationally reflecting (an anti-‘natural’ process) on the specific qualities of metabolic pathways so as to determine their maximum performance levels in relation to life spans and health.

That’s like saying that a jet is not optimal because it consumes too much energy and stresses its components, so a bicycle is better.

Do you really want to get into the thermodynamics of using petroleum to power jets? I'm just going to marginalize this. By all means, keep believing that jet planes are efficient machines.

If you are going to take your own arguments as a basis for optimal behavior, then you should be against exercise. After all, exercise is inefficient, it taxes many organs, including the heart, wastes energy, and produces many “dangerous” chemical reactions.

Now we are getting deeper into ad-hominem territory. That's fine, though. I'll play along.
To begin with, I am not against exercise, and at no point did I imply or state this. Most exercise does not involve a sleuth of chronic stressors, and exercise satisfies many of the hormetic requirements of a homeostatic system. Hormesis, though, is not the same as systematic degeneration. Provided that a body is properly nourished, exposure to exercise allows for the optimization of life span and health viz. the enhancement of metabolic flexibility. Many forms of exercise satisfy the conditions of adaptive and sustainable optimization that I embrace within my writings. I am, without a doubt, against endurance training, for I believe (as do other scholars) that it places undue stress on the organ systems of the human body (Benito et al. 2011; Wilson et al. 2011). Do you see the difference here? There is a huge gap between short-term hormetic stressors and chronic degenerative stressors.

The very fact that gluconeogenesis is associated to cortisol levels should send up some red flags” So again, are you against exercise? Exercise is strongly associated to cortisol levels. Cortisol is associated with stress. Stress is good for the body. Absence of stress is bad. Why don’t you tell astronauts how the absence of stress on their joints is good for them?

You are foolishly misconstruing my arguments. I am not claiming that short-term stressors are unnecessary for human health; I am writing against the long-term stressors emerging from a chronic ZC diet and its inefficient metabolic pathways. The reason why cortisol sends up a red flag in relation to gluconeogenesis is because while in a deep ketogenic diet, a subject is constantly engaged in gluconeogenesis, and therefore exhibits elevated cortisol levels (Swain et al. 2012). Dichotomizing stress as good/bad is a ridiculous proposition. Stress is neither good nor bad; stress is a physical signifier that directs our attention toward bodily processes that may indicate the absence or presence of particular adaptive mechanisms. I have opted to question which adaptive mechanisms are optimal for both longevity and maximum health.

However, if you want to argue along the dichotomy of “stress is good” and the “absence of stress” is bad, you’d do best to research how the body deals with the elevated cortisol levels of exercise. A little hint: as the body becomes used to stressors, cortisol levels begin to decrease. Chronically elevated cortisol levels are a serious problem, leading to heart disease, etc., but cortisol released in response to short-term stressors allows for the body to adapt to the demands of exercise.

Retrieved from: [http://www.livestrong.com/article/86687-exercise-cortisol-levels].

Negative Effects [of cortisol]
Unfortunately, the negative effects of cortisol outweigh the positive. Cortisol has an immunosuppressive effect, meaning that if your body constantly has high levels of cortisol, you are more susceptible to illness or infection. Also, because cortisol is a response to stress and the goal is to increase fuels in the blood, it will increase blood calcium by inhibiting bone formation and decreasing intestinal calcium absorption. This may result in a decrease in bone density over time. Cortisol also inhibits the pathway that releases sex hormones (gonadotropins), so if you are constantly stressed, you may experience a decreased libido and, in some cases, infertility or difficulty conceiving. Women who have high levels of cortisol in combination with low body weight may have amenorrhea (loss of menstrual cycle).
Training Effects
Because cortisol is released in response to stress, exercise training will increase the threshold of cortisol release. For example, if you begin an exercise program walking at a 20-minutes per mile pace, cortisol will be released at that intensity. However, as your training progresses and you begin walking at a 15-minutes per mile rate, the body will not perceive the 20-minutes per mile pace to be as stressful and will not release as much cortisol.

Finally, telling people that they should seriously switch their diets if they start feeling sick is irresponsible. People get sick irrespective of their diets. You trying to be an authority on what people should or should not do is laughable.

Using the internet’s anonymity to make hostile, assumptive statements against my intents involves a great deal of cowardice, to say the least.

When did I say that anybody should stop eating a ZC diet? I was trying to help others on this forum by presenting my theories and understandings of the problematic attributes of a chronic ZC diet. I am not trying to brainwash or control anyone. Do whatever you want. If you feel fantastic and want to continue on the ZC diet, then by all means, go right on ahead. I am presenting people with my understanding of what an optimal human diet does and does not contain, and my conclusions are, despite what you may believe, supported by science.

I know I said finally, but I lied. Here is some pure wisdom: The true optimal form is to be dead. Then you consume nothing, you experience no stress, and you have no chance of having any disease.

The so-called purity of your wisdom leaves much to be desired.

But that is not what I want. I want to be as strong and vigorous as I can. I don’t seek to be free from pain and stress, I want for everything that doesn’t kill me to make me stronger. I don’t want an easy life, I want the strength to endure a hard one.

I applaud you on the rhetorical flourish; truly, I was nearly brought to tears.

Works cited
Baba, H., Zhang, X. J., & Wolfe, R. R. (1994). Glycerol gluconeogenesis in fasting humans. Nutrition (Burbank, Los Angeles County, Calif.), 11(2), 149-153.

Benito, B., Gay-Jordi, G., Serrano-Mollar, A., Guasch, E., Shi, Y., Tardif, J. C., ... & Mont, L. (2011). Cardiac Arrhythmogenic Remodeling in a Rat Model of Long-Term Intensive Exercise TrainingClinical Perspective. Circulation, 123(1), 13-22.

Cahill Jr, G. F. (2006). Fuel metabolism in starvation. Annu. Rev. Nutr., 26, 1-22.

Deaner, R. O., Isler, K., Burkart, J., & van Schaik, C. (2007). Overall brain size, and not encephalization quotient, best predicts cognitive ability across non-human primates. Brain, Behavior and Evolution, 70(2), 115-124.

Devivo, D. C., Leckie, M. P., Ferrendelli, J. S., & McDougal, D. B. (1978). Chronic ketosis and cerebral metabolism. Annals of neurology, 3(4), 331-337.

Hendrick, G. K., Frizzell, R. T., Williams, P. E., & Cherrington, A. D. (1990). Effect of hyperglucagonemia on hepatic glycogenolysis and gluconeogenesis after a prolonged fast. American Journal of Physiology-Endocrinology And Metabolism, 258(5), E841-E849.

Iwaniuk, A. N., Nelson, J. E., & Pellis, S. M. (2001). Do big-brained animals play more? Comparative analyses of play and relative brain size in mammals. Journal of Comparative Psychology, 115(1), 29.

Kaleta, C., de Figueiredo, L. F., Werner, S., Guthke, R., Ristow, M., & Schuster, S. (2011). In Silico Evidence for Gluconeogenesis from Fatty Acids in Humans PLoS Computational Biology, 7 (7) DOI: 10.1371/journal.pcbi.1002116

Lalli, C.M. and Parsons, T.R. (1993). Biological Oceanography, an Introduction. 30 Corporate Drive, Burlington, MA 01803: Elsevier. p. 314. ISBN 0-7506-3384-0.

LaManna, J. C., Salem, N., Puchowicz, M., Erokwu, B., Koppaka, S., Flask, C., & Lee, Z. (2009). Ketones suppress brain glucose consumption. In Oxygen Transport to Tissue XXX (pp. 301-306). Springer US.

McDonald, L. (1998). The ketogenic diet. A complete guide for the dieter and practitioner. Austin TX: Morris Publishing.

Prince, A., Zhang, Y., Croniger, C., & Puchowicz, M. (2013). Oxidative Metabolism: Glucose Versus Ketones. In Oxygen Transport to Tissue XXXV(pp. 323-328). Springer New York.

Schell, D. M. (2000). Declining carrying capacity in the Bering Sea: isotopic evidence from whale baleen. Limnology and Oceanography, 45(2), 459-462.

Seyfried, T. N., Sanderson, T. M., El-Abbadi, M. M., McGowan, R., & Mukherjee, P. (2003). Role of glucose and ketone bodies in the metabolic control of experimental brain cancer. British journal of cancer, 89(7), 1375-1382.

Ebbeling CB, Swain JF, Feldman HA, Wong WW, Hachey DL, Garcia-Lago E, Ludwig DS. (2012). Effects of dietary composition on energy expenditure during weight-loss maintenance. 27; 307(24):2627-34.

Tagliabue A, Bertoli S, Trentani C, Borrelli P, Veggiotti P (2012). Effects of the ketogenic diet on nutritional status, resting energy expenditure, and substrate oxidation in patients with medically refractory epilepsy: a 6-month prospective observational study. Clin Nutr 31(2):246–249

Veldhorst, M. A., Westerterp-Plantenga, M. S., & Westerterp, K. R. (2009). Gluconeogenesis and energy expenditure after a high-protein, carbohydrate-free diet. The American journal of clinical nutrition, 90(3), 519-526.

Veldhorst, M. A., Westerterp, K. R., & Westerterp-Plantenga, M. S. (2012). Gluconeogenesis and protein-induced satiety. British Journal of Nutrition,107(4), 595.

Wilson, M., O'Hanlon, R., Prasad, S., Deighan, A., MacMillan, P., Oxborough, D., ... & Whyte, G. (2011). Diverse patterns of myocardial fibrosis in lifelong, veteran endurance athletes. Journal of Applied Physiology, 110(6), 1622-1626.

aem42290, I do appreciate your specifying that it is that complete Raw Zero Carb or pure Carnivory that you are harping against and making it clear in this thread.

And I do appreciate other people chiming in with their experiences.

Let's all be welcoming to each other's sharing... we are a very small number of global practitioners and every experience counts.

So please don't "lose patience".

This is all good conversation.

I agree, GS. Thank you for that reminder. It's important to retain a sense of community while discussing our points. Honestly, I appreciate all of the perspectives that have been shared on this post--whether I agree with them or not. We are a very small group of people, relatively speaking, and at the heart of all of these topics resides the fact that most of us have adopted a rare and condemned diet for the sake of improving our health.

On the contrary, you were insisting that  hysterical, science-free, dubious  "warning" threads should be put in the RZC forum, but did not insist on other forums being so afflicted.  That is almost as bad as banning a  particular dietary path.

I echo PaleoPhil in saying that, as a moderator, your callous and irreverent language sets a very poor example for the broader quality of exchanges on this site. And since you have been so neglectful of the scientific data in my opening post, I am going to assume that you are treating my thread as one of the "hysterical" texts. If so, then this would be the first time in my life that I have been called hysterical, and while I do take some offense to your erratic and implicitly ad-hominem condemnation, I will gladly provide you with a substantial bibliographical document to support all of my conclusions. Perhaps then your thirst for "truths" will be satisfied.

Yes, intermittent fasting and intermittent ZCing do appear to be beneficial and none of my warnings were regarding it. They were regarding chronic long-term ZC.

I'm with Edmon and PaleoPhil: I am not disputing the short-term use-value of a ZC ketogenic diet (so long as there exists an adequate understanding of the numerous variables involved in the diet's execution), and I am especially not challenging the benefits of intermittent fasting, which I engage in on a frequent basis. Rather, I am questioning the long-term health effects of a ZC diet for the majority of humans. In this sense, I am using 'optimization' to express an index of and for sustainable metabolic efficiency, which, by extension, contributes to the conditions and intricacies of establishing longevity.

I do IFing and intermittent ZC myself. My posts had nothing to do with that.

Indeed.

In the end what is optimal is unique to the individual.

I strongly disagree with this. Although it is tempting to assume that individuals should always be at the center of discussions regarding optimization and dietary health, the fact remains that core metabolic processes function in comparable manners for most humans on the planet. To offer some counterpoints: I would argue that most humans would benefit from incorporating an intermittent fasting plan in their diets; most humans would benefit from eliminating grains entirely; and most humans would benefit from ceasing the consumption of antibiotics. There is a fine line between structure and particular that I believe dietary advice must tread. In regards to optimization, this line must be drawn along the terrain of temporality. A short-term dietary success is likely to correct individual problems, but a long-term dietary failure is likely to reveal structural (i.e., human) vulnerabilities.

I'd like to continue this debate if you would indulge me, though in a more gentlemanly manner. I must say its been a while since I have researched any of this and its possible that there is new knowledge out there. This is one of those things where you can't just take any study and run with it because there are vested interests that like to fudge numbers and mislead people when health is at stake.

Of course, Edmon. We'll continue the debate. I must say that I have been rather busy as of late, and have thus been unable to post here as frequently as I'd like.

I'm going to take some time later on today to address a few of the key points brought up by others. Namely, I'd like to tackle:
1) The role of glial cells in relation to ketosis. (Edmon171)
2) Ketogenic diets as possessing healing qualities, short-term. (Sabertooth)
3) Why "differing/critical posts, which would serve as warnings about potential risks for people to make their own judgments " should be allowed in their respective forums. (PaleoPhil)
4) Epigenetic adaptations to ZC/ketogenic and high carb diets. (Sabertooth)

I'm sorry, but I don't buy any of this thesis. Writing a post that is 10 miles long does not add to its validity.

At what moment did I state that the validity of my post is augmented by its length? A rather weak and unnecessarily confrontational point.

There is no account for the glycerol that is released on fat breakdown being easily converted to glucose.

You must have missed the section about the acetyl CoA cycle. Or perhaps you are not familiar with the fact that glycerol is converted into pyruvate, which later becomes acetyl CoA, and finally turns into glucose (viz. a highly complex and inefficient series of metabolic interactions)? Whatever the case, you failed to properly engage with what I have written.

By the way, I will stress that the generation of glucose from fatty acids is not easy work for the human body (as you make it seem.) A recent (2011) study explored the metabolic pathways involved in the generation of glucose from acetyl CoA. Their conclusion? "Analyzing the detected pathways in detail we found that their energetic requirements potentially limit their capacity." Activating the systems that concert fatty acids and glycerol involves inefficient metabolic structures that require fair amounts of labor on behalf of the liver.

There is no account for glycogen consumed in muscle and organ meats converting easily to glucose. There is no account for glucose being consumed directly in fresh blood.

Are you aware that the glycogen in most meats turns into lactic acid shortly after slaughter?

For a very simple and clear expression of this: http://sciencewa.net.au/topics/agriculture/item/1391-muscle-glycogen-related-to-meat-quality-post-slaughter.html/1391-muscle-glycogen-related-to-meat-quality-post-slaughter.html

If you are still not convinced:
"During the post slaughter period the muscle cells are still capable of converting glycogen to lactic acid -
the process takes about 48 hours for completion (at refrigeration temperatures) - electrical stimulation of
carcasses speeds this process so as the reactions are complete by 24 hours" (Kastner et al. 1993).

Consider the fact that very few people (myself included) in industrial societies have access to a steady supply of freshly gathered meat. Therefore, unless one is consuming an animal immediately upon securing the kill, glycogen in muscle tissue rapidly degenerates into lactic acid, and your point about deriving glucose from muscle tissue is rendered wholly moot.

There is no account for glucose being consumed directly in fresh blood.

Ah, I've heard this one before. To frame the question in a familiar context: Do you know how much sugar is in the blood of a  a typical human's body? About 82 mg/dl to 110 mg/dl (4.4 to 6.1 mmol/l) following the successful digestion of a meal. Other mammals aren't too far off from these numbers. This means that an adult human male with about 5 liters of blood at 100mg/dl will have a measly 5g of glucose in their blood at most moments throughout the day. 5 grams of glucose is very little, even on a ZC diet. So, If you were to drink a whole 5 liters of mammalian blood, you'd get 5g or so of glucose. Quite a trivial source of glucose, considering how difficult raw blood is to obtain for most ZCers.

At best, gluconeogenesis is a temporary condition that is used to provide up to 100g of glucose per day until one is fully adapted to ketosis.

Do you have any evidence to substantiate this claim? Unless you are asserting that the human brain can run on ketones exclusively, your statement is completely inaccurate. Gluconeogenesis is not a "temporary" phase for ZC dieters; it is a constant process that must be accounted for within a metabolic environment that is forced to meet the needs of a glucose-dependent organ (the brain.) So far, studies demonstrate that the brain, even when fully keto-adapted, requires 30-50g of glucose to function properly.

Albeit misconstrued, your argument regarding glycerol does not get away from the fact that the conversion of fatty acids to glucose is an energy intensive process in relation to the absorption of sugars from carbohydrates.  In the context of my piece, optimization is related directly to metabolic efficiency at numerous levels. I am not arguing against a LC diet (so long as LC provides at least 30g glucose per day.) I am decrying the naive and historically unnatural pursuit of a long-term, completely ZC diet (carried out in industrial settings) that ignores all plant foods for the sake of trendiness, ignorance, or unreflexivity. 

The short life span in carnivores is explained by the fact that their food and their competition is trying to kill them almost every time they eat. Eventually they get old and get gouged in a hunt or a fight and succumb to an infection or bleed-out. There is no need to complicate it any further than that.

I'll write a response to this later.

As an afterthought, before you approach this thread with such a dismissive disposition, I would urge you to seriously research the processes that you are narrowly describing. To be frank, I am glad that ZC is working for you. As Francois (Iguana) once said on these forums: we (the imagined human species) are honored to have you as an experimenter in the name of superior health. Thank you for subjecting yourself to the conditions of a dietary plan that very few humans in the history of our planet have exposed themselves to. If things continue to go well for you, then so be it. If matters take a turn for the worse, then consider taking into account some of the points that I have made.

Yes, there is room for criticism, this thread was not deleted not censored, this is why this raw paleo diet forum exists and Tyler and the other mods try to keep a balance.

There are those who really follow the zero carb thing and it works for them and just to respect what is working for them, criticisms are placed in the hot topics section.

I am not a zero carber, but I respect this zero carb section.

I whole heartedly agree with many points of the very very nicely written piece.  Thank you. 

And I would have to agree with Tyler it still belongs to the hot topics section.

Thank you for your kind response, GS. For the many years that I've been lurking these forums, I have consistently found your nutritional suggestions to be highly useful and well-balanced.

My point of contention remains that I believe ZCers (and ex-ZCers, such as myself) should be exposed to critical arguments directly--out of respect, even. What is respect if not the desire to take someone's actions seriously enough to critique them?

aem42290,
I am wondering if you gained  benefits initially from VLC that were worthwhile, and if you had started to very slowly increase carbs early on that might have worked well?

I have been interested in reading the research of Paul and Shou-Ching Jaminet (The Perfect Health Diet book). In regards to carbs their findings are that the ideal is 30% of energy from carbs (Typically ~600 calories), from 'safe starches' like potatoes, rice and bananas, to provide for the bodies glucose needs, and the rest from fat.

Here is Paul's investigation of ideal glucose levels for longevity and dialog with Ron Rosedale:
http://perfecthealthdiet.com/2011/11/safe-starches-symposium-dr-ron-rosedale/

Thank you for this information. I will be looking into the research shortly. At a quick glance, it seems that this website offers some very intelligent pieces of advice, and that, generally, arguments are grounded in rigorous scientific studies.

As for the viability of a ZC diet, I do believe that the temporary elimination of plant-foods offers a therapeutic value for many people, specifically those who are metabolically deranged (GS has stated this before as well.) The body in deep ketosis will choose to keep only the strongest of cells. This culling  process has obvious benefits. However, for the long-term subsistence of a human, the ZC diet comes attached to some critical and alarming factors.

This post is wholly inappropriate for the ZC forum. I will put it in the hot topics forum instead.

Tyler,
With all due respect, I believe that putting this post in the "hot topics" section is unjust. Inappropriate in what sense? What I have written is a reflexively critical piece that deals with ZC diets directly. Is there no place for intellectual criticism on these forums? I do believe that those on a ZC diet have the right to be exposed to what is on the other side of the fence. Moving this post to "hot topics" seems almost punitive.

I appreciate the thought put into this 'thesis'.   May I suggest that you post this to Ron Rosedale, he has a blog, and see if he'd care to respond to your conclusions.   I for one would love to see his response.  I think it would add value as I'm sure, if he did respond, he would include some science to ponder over. 
    One of the difficulties of using say the Inuit as a barometer is that they didn't eat for longevity, except you might call it longevity of the moment, or simply to survive the day.     Another way to say this is, I wouldn't use a wine drinking alcoholic to study the health benefits of wine.
    There may never have been any group of peoples who knew how to use diet to maximize longevity.    For sure we know of no strictly raw eating peoples..    That is why I say one has to dig deeper, or be willing to experiment with one's self.    But please, blog Ron, see if he'll respond.   thanks

Hey, Van. Thanks for your response and for your (earlier) reply to my PM. Really appreciate it.

I agree, we do need to continue experimenting. I wrote this thesis to dispel the notion that ZC diets are optimal/healthy long term. I feel strongly about this, considering that the diet eventually took a silent and fairly insidious toll on my body. Hence why I thought it'd be meaningful to share my knowledge with this excellent community.

How would I go about posting this to his blog? Should I leave it as a comment to any specific threads?

Welcome, aem42290.That sounds much like a nocturnal panic attack, which happened to me in the past.
43-45 resting heart rate is very low for any adult who isn't an elite long-distance runner. I also had low RHR in the past. Low RHR is common among people who have been on diets too low in carbs, prebiotics and/or calories for too long. See Ray Peat's info on this (ex: http://raypeat.com/articles/articles/hypothyroidism.shtml).
Have you had any other symptoms of LC torpor, like low basal temperature, cold extremities, lightheadedness after exertion, reduced sleep quality, dry skin, skin rash, high and rising FBG, high and rising LDL, low T3, ...? http://perfecthealthdiet.com/category/zero-carb-dangers/
How did you run an EKG on yourself?

Hey, Paleophil.
First off, thanks for your prompt response. I'll try to systematically answer/comment on your thoughts.
1. I question the notion that what I experienced was a panic attack. My disbelief here is justified by the elevated resting heart rate following the incident (an unnecessarily elevated resting heart rate that I am still dealing with.) I have dealt with panic attacks before while on the SAD, and I am rather aware of the symptoms that come attached to them (feelings of limited breathing, imminent death, heightened anxiety levels, etc.) I'm relatively convinced that this heart episode was something else entirely.
2. I agree that my RHR is low, but I don't consider this to be an indicator of any underlying problems. Rather, there are genetic factors involved in the RHR factor (my father has a low RHR, and my grandfather before him), and, further, I was, in fact, a sprinter for much of my undergrad college career. My heart has always been one of my healthiest features. Which makes all of this much more distressful. I ran the EKG on myself using a fully-functional personal EKG device that was gifted to me by an old med school mentor. His technology firm created the apparatus in late 2000s.
3. I have experienced only one other symptom of what you refer to as low carb torpor: cold extremities. My basal metabolic rate seems to be within acceptable limits, and my thyroid blood profile is very solid. I am, at least in the eyes of most knowledgeable people, in top-notch shape at this moment—and yet, my heart is still behaving erratically.
4. Berries seem to irritate my throat. As per your advice, I will look for other forms of carbs.

I don't quite know what to say because I understand that this is something that happened only once in six months of RPD. You sound like you've read enough information to know how to eat low carb - the "secret" of getting a variety of organs and enough fat - at any rate, if there were a problem like protein poisoning, you'd have a set of definitive symptoms.
As far as colds go, I've never been prone to catching cold. Again, if I got one cold, I wouldn't think too much about it.
Are you in a health-care profession? That might make you prone to running mental diagnostics. Personally, I try to "dumb myself down" about a lot of modern medical knowledge. Waiting for things to happen more than once has made it easier for me to notice valid trends, such as which foods make me have certain symptoms. That being said, I'm not a science-y person, so I might be missing something.

Thank you for responding, Eve.
1. You are wholly correct: I have researched the LC carnivorous diet extensively. I've been consuming moderately high fat amounts; watching my protein intake; eating a fair amount of fresh raw organs; and I have been selecting only the finest wild and grass-fed organic meats. To the best of my knowledge, I've done this experiment as well as is humanly possible.
2. Interesting that you have never caught a cold. I felt invincible while on this diet for most of my days, but following recent events, I stress that it is sometimes important to confront humbling experiences with a reflexive eye.
3. You called it. I was a med school student for three years. Although I am not currently in the healthcare world, I do have a substantial amount of medical knowledge (and the lofty burden of critical inquisitiveness that comes along.) I should probably put aside minor issues and wait for a repeat, but I am too cautious and observational to marginalize any physical ailments. ?

I will soon be creating another post where I address numerous conclusions that I've arrived at following my heart incident. I will address elements of the ZC/V-VLC carnivorous diet in detail.