Author Topic: Ketogenic Diet - Path To Transformation?  (Read 291084 times)

Offline Laura

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Ketogenic Diet - Path To Transformation?
« on: August 03, 2012, 10:42:20 PM »
This thread was split off from Life Without Bread which is one of the most active threads on the forum.   After reading a few pages of this thread, the reader will begin to understand why we included "Path to Transformation" in the subject field.


I just want to report that we made a nice taboule with quinoa, bits of tomato, cucumber, onion, and mint leaves.  It was dressed with olive oil and lemon juice.   I didn't eat much, but I've been sick all day after with something like acid reflux.  I guess I just can't handle any grains at all anymore.

Which makes me wonder: if, when we start getting back to fat burning, paleo eating, we find that eating grains is so darn taxing to the body, we have to think that nobody would ever have started eating them at all unless they had nothing else to eat.  Imagine how things might have been after a cataclysm and all the animals were either killed or driven away, and some people survived in an area where some grains sprouted up rather quickly.  Maybe there were dead creatures about that they dried or smoked and were able to survive on for a bit, but after awhile, no more critters to eat, only the grains on that grass out there... so they began to eat it.  It was very unsatisfactory, but it kept them alive, barely.  And soon, the gluten had them addicted, so even when animals returned, they continued to eat grains.  I can't imagine it happening otherwise because nobody in their right mind would think that farming is less labor intensive than hunting, and it's pretty clear to me that eating grains etc could NOT have been agreeable to the digestive systems of our ancestors.

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Offline Kniall

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Re: Ketogenic Diet - Path To Transformation?
« Reply #1 on: August 03, 2012, 11:04:38 PM »
That makes a whole lot of sense, that they were forced by temporarily severe environmental conditions to eat their food's food (grains that would otherwise be eaten by animals).
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Offline SeekinTruth

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Re: Ketogenic Diet - Path To Transformation?
« Reply #2 on: August 04, 2012, 06:07:37 AM »
That makes a whole lot of sense, that they were forced by temporarily severe environmental conditions to eat their food's food (grains that would otherwise be eaten by animals).

Yeah, that does make a lot of sense. Then, agriculture was probably spread by force by pathological "leaders"/dominators and the whole "neolithic civilization values" spread and became entrenched? I think this could be plausible once people became addicted to opiods?
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Offline Chu

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Re: Ketogenic Diet - Path To Transformation?
« Reply #3 on: August 04, 2012, 02:04:38 PM »
That makes a whole lot of sense, that they were forced by temporarily severe environmental conditions to eat their food's food (grains that would otherwise be eaten by animals).

Indeed! I tell ya', that bit of quinoa on our bellies was NOT what the body is meant to eat.

I was reading a paper on the ketogenic diet yesterday, and at one point it says:

Quote
In a previous study, a 48-h fast, which results in similar short-term ketosis as that achieved by the ketogenic diet, was found to protect rats against neuronal loss in the striatum, neocortex, and hippocampus produced by 30-min four-vessel occlusion (Marie et al., 1990). There was also a reduction in mortality and the incidence of postischemic seizures in fasted animals. Thus, there is evidence that the ketogenic diet has neuroprotective activity in both traumatic and ischemic brain injury. An additional study found that rats receiving a ketogenic diet are also resistant to cortical neuron loss occurring in the setting of insulin-induced hypoglycemia (Yamada et al., 2005).

It is so blatantly obvious that the body needs to be in ketosis! You stop eating for 48hours, and it immediately uses ketogenic bodies. Duh...

The rest of the paper is here: Neuroprotective and disease-modifying effects of the ketogenic diet

It has some interesting studies. But it's funny how they can't really say that it's better overall. They mention that high fat consumption is "unpalatable and unhealthy", and that a ketogenic "pill" would be preferable. Either they do it in order to avoid getting censured, or they are working for pharmaceutical companies, or their brains are fried from not being in ketosis themselves.

Here is the entire paper, if anyone is interested:

Quote
Neuroprotective and disease-modifying effects of the ketogenic diet
Maciej Gasior,a Michael A. Rogawski,a and Adam L. Hartmana,b
Author information ► Copyright and License information ►
The publisher's final edited version of this article is available at Behav Pharmacol

The ketogenic diet has been in clinical use for over 80 years, primarily for the symptomatic treatment of epilepsy. A recent clinical study has raised the possibility that exposure to the ketogenic diet may confer long-lasting therapeutic benefits for patients with epilepsy. Moreover, there is evidence from uncontrolled clinical trials and studies in animal models that the ketogenic diet can provide symptomatic and disease-modifying activity in a broad range of neurodegenerative disorders including Alzheimer’s disease and Parkinson’s disease, and may also be protective in traumatic brain injury and stroke. These observations are supported by studies in animal models and isolated cells that show that ketone bodies, especially β-hydroxybutyrate, confer neuroprotection against diverse types of cellular injury. This review summarizes the experimental, epidemiological and clinical evidence indicating that the ketogenic diet could have beneficial effects in a broad range of brain disorders characterized by the death of neurons. Although the mechanisms are not yet well defined, it is plausible that neuroprotection results from enhanced neuronal energy reserves, which improve the ability of neurons to resist metabolic challenges, and possibly through other actions including antioxidant and anti-inflammatory effects. As the underlying mechanisms become better understood, it will be possible to develop alternative strategies that produce similar or even improved therapeutic effects without the need for exposure to an unpalatable and unhealthy, high-fat diet.
Keywords: Alzheimer’s disease, cellular energetics, epilepsy, ketone bodies, ketogenic diet, mitochondria, neuroprotection, Parkinson’s disease, stroke, traumatic brain injury

Introduction

The ketogenic diet is a high-fat content diet in which carbohydrates are nearly eliminated so that the body has minimal dietary sources of glucose. Fatty acids are thus an obligatory source of cellular energy production by peripheral tissues and also the brain. Consumption of the ketogenic diet is characterized by elevated circulating levels of the ketone bodies acetoacetate, β-hydroxybutyrate and acetone, produced largely by the liver. During high rates of fatty acid oxidation, large amounts of acetyl-CoA are generated. These exceed the capacity of the tricarboxylic acid cycle and lead to the synthesis of the three ketone bodies within liver mitochondria. Plasma levels of ketone bodies rise, with acetoacetate and β-hydroxybutyrate increasing three-fold to four-fold from basal levels of 100 and 200 µmol/l, respectively (Musa-Veloso et al., 2002). In the absence of glucose, the preferred source of energy (particularly of the brain), the ketone bodies are used as fuel in extrahepatic tissues. The ketone bodies are oxidized, releasing acetyl-CoA, which enters the tricarboxylic acid cycle.

The ketogenic diet is an established and effective nonpharmacological treatment for epilepsy (Vining et al., 1998; Stafstrom, 2004; Sinha and Kossoff, 2005). Although the diet is useful in people of all ages, clinical experience suggests that it may be more valuable in children, if only because adults have greater difficulty adhering to it. Importantly, the diet is often effective in pharmacoresistant forms of common epilepsies as well as in the difficult to treat catastrophic epilepsy syndromes of infancy and early childhood such as West Syndrome, Lennox–Gastaut Syndrome, and Dravet Syndrome (Crumrine, 2002; Trevathan, 2002; Caraballo et al., 2005).

Recently, there has been interest in the potential of the ketogenic diet in the treatment of neurological disorders other than epilepsy, including Alzheimer’s disease and Parkinson’s disease. Studies in these neurodegenerative disorders have led to the hypothesis that the ketogenic diet may not only provide symptomatic benefit, but could have beneficial disease-modifying activity applicable to a broad range of brain disorders characterized by the death of neurons. Here, we review evidence from clinical studies and animal models that supports this concept.

Ketogenic diet

The classic ketogenic diet is a high-fat diet developed in the 1920s to mimic the biochemical changes associated with periods of limited food availability (Kossoff, 2004). The diet is composed of 80–90% fat, with carbohydrate and protein constituting the remainder of the intake. The diet provides sufficient protein for growth, but insufficient amounts of carbohydrates for the body’s metabolic needs. Energy is largely derived from the utilization of body fat and by fat delivered in the diet. These fats are converted to the ketone bodies β-hydroxybutyrate, acetoacetate, and acetone, which represent an alternative energy source to glucose. In comparison with glucose, ketone bodies have a higher inherent energy (Pan et al., 2002; Cahill and Veech, 2003). In adults, glucose is the preferred substrate for energy production, particularly by the brain. Ketone bodies are, however, a principal source of energy during early postnatal development (Nehlig, 2004). In addition, ketone bodies, especially acetoacetate, are preferred substrates for the synthesis of neural lipids. Ketone bodies readily cross the blood–brain barrier either by simple diffusion (acetone) or with the aid of monocarboxylic transporters (β-hydroxybutyrate, acetoacetate), whose expression is related to the level of ketosis (Pan et al., 2002; Pierre and Pellerin, 2005).

Today, several types of ketogenic diets are employed for treatment purposes. The most frequently used is the traditional ketogenic diet originally developed by Wilder in 1921, which is based on long-chain fatty acids (Wilder, 1921). In the 1950s, a medium-chain triglyceride diet was introduced, which produces greater ketosis (Huttenlocher et al., 1971). This modification has not been widely accepted because it is associated with bloating and abdominal discomfort and is no more efficacious than the traditional ketogenic diet. A third variation on the diet, known as the Radcliffe Infirmary diet, represents a combination of the traditional and medium-chain triglyceride diets (Schwartz et al., 1989). Its efficacy is also similar to the traditional ketogenic diet.

Although the ketogenic diet was a popular treatment approach for epilepsy in the 1920s and 1930s, its medical use waned after the introduction of phenytoin in 1938. The recognition that the diet may be an effective therapeutic approach in some drug-resistant epilepsies, particularly in children, has led to a resurgence of interest in the last 15 years. The popularization of various low carbohydrate diets for weight loss, such as the Atkins diet (Acheson, 2004), probably also has increased interest in the dietary therapy of epilepsy. In fact, a modified form of the Atkins diet, which is easier to implement than the various forms of the traditional ketogenic diet, may be an effective epilepsy treatment approach (Kossoff et al., 2006).


Clinical studies
Epilepsy


At present, strong evidence exists that the ketogenic diet protects against seizures in children with difficult-to-treat epilepsy (Freeman et al., 1998). Recent reports have raised the possibility that the diet may also improve the long-term outcome in such children (Hemingway et al., 2001; Marsh et al., 2006). In these studies, children with intractable epilepsy who remained on the ketogenic diet for more than 1 year and who experienced a good response to the diet, often had positive outcomes at long-term follow-up 3–6 years after the initiation of diet. Forty-nine percent of the children in this cohort experienced a nearly complete (≥ 90%) resolution in seizures. Surprisingly, even those children who remained on the diet for 6 months or less (most of these children terminated the diet because of an inadequate response) may have obtained a long-term benefit from exposure to the diet. Thirty-two percent of these children had a ≥ 90% decrease in their seizures and 22% became seizure free even without surgery. The diet also allowed a decrease or discontinuation of medications without a relapse in seizures. Of course, in the absence of a control group, it is not possible to be certain that the apparent good response in these children is simply the natural history of the epilepsy in the cohort studied, although these children had, by definition, intractable epilepsy before starting the diet. In any case, the results raise the possibility that the ketogenic diet, in addition to its ability to protect against seizures, may have disease-modifying activity leading to an improved long-term outcome. It is noteworthy that none of the currently marketed antiepileptic drugs has been demonstrated clinically to possess such a disease-modifying effect (Schachter, 2002; Benardo, 2003). Determining whether the ketogenic diet truly alters long-term outcome will require prospective controlled trials.

Alzheimer’s disease

Recent studies have raised the possibility that the ketogenic diet could provide symptomatic benefit and might even be disease modifying in Alzheimer’s disease. Thus, Reger et al. (2004) found that acute administration of medium-chain triglycerides improves memory performance in Alzheimer’s disease patients. Further, the degree of memory improvement was positively correlated with plasma levels of β-hydroxybutyrate produced by oxidation of the medium-chain triglycerides. If β-hydroxybutyrate is responsible for the memory improvement, then the ketogenic diet, which results in elevated β-hydroxybutyrate levels, would also be expected to improve memory function. When a patient is treated for epilepsy with the ketogenic diet, a high carbohydrate meal can rapidly reverse the antiseizure effect of the diet (Huttenlocher, 1976). It is therefore of interest that high carbohydrate intake worsens cognitive performance and behavior in patients with Alzheimer’s disease (Henderson, 2004; Young et al., 2005).

It is also possible that the ketogenic diet could ameliorate Alzheimer’s disease by providing greater amounts of essential fatty acids than normal or high carbohydrate diets (Cunnane et al., 2002; Henderson, 2004). This is because consumption of foods or artificial supplements rich in essential fatty acids may decrease the risk of developing Alzheimer’s disease (Ruitenberg et al., 2001; Barberger-Gateau et al., 2002; Morris et al., 2003a, b).

Parkinson’s disease

One recently published clinical study tested the effects of the ketogenic diet on symptoms of Parkinson’s disease (VanItallie et al., 2005). In this uncontrolled study, Parkinson’s disease patients experienced a mean of 43% reduction in Unified Parkinson’s Disease Rating Scale scores after a 28-day exposure to the ketogenic diet. All participating patients reported moderate to very good improvement in symptoms. Further, as in Alzheimer’s disease, consumption of foods containing increased amounts of essential fatty acids has been associated with a lower risk of developing Parkinson’s disease (de Lau et al., 2005).

Studies in animal models
Epilepsy


Anticonvulsant properties of the ketogenic diet have been documented in acute seizure models in rodents (Appleton and De Vivo, 1973; Huttenlocher, 1976; Hori et al., 1997; Stafstrom, 1999; Likhodii et al., 2000; Thavendiranathan et al., 2000, 2003; Bough et al., 2002). Moreover, there is accumulating evidence from studies in models of chronic epilepsy that the ketogenic diet has antiepileptogenic properties that extend beyond its anticonvulsant efficacy. Thus, in the rat kainic acid model of temporal lobe epilepsy, the development of spontaneous seizures was attenuated by the ketogenic diet and there was a reduction in the severity of the seizures that did occur (Muller-Schwarze et al., 1999; Stafstrom et al., 1999; Su et al., 2000). In addition, animals fed the diet have reduced hippocampal excitability and decreased supragranular mossy fiber sprouting in comparison with rats fed a normal diet. Further evidence supporting the antiepileptogenic activity of the ketogenic diet is the demonstration that the development of spontaneous seizures in inbred EL/Suz mice, a genetic model of idiopathic epilepsy, is retarded by the diet (Todorova et al., 2000). In other studies, caloric restriction, which often occurs with the ketogenic diet, has also been demonstrated to have antiepileptogenic effects in EL/Suz mice (Greene et al., 2001; Mantis et al., 2004). (Although the ketogenic diet is designed to provide calories adequate for growth, patients and animals may eat less because the diet may be unpalatable to some. Thus, the ketogenic diet may be accompanied by an unintentional caloric restriction.)

Alzheimer’s disease

Epidemiological studies have implicated diets rich in saturated fat with the development of Alzheimer’s disease (Kalmijn et al., 1997; Grant, 1999; Morris et al., 2003a, b, 2004; but see Engelhart et al., 2002). Moreover, in transgenic mouse models, high-fat diets increase the deposition of amyloid β (Aβ) peptides (Levin-Allerhand et al., 2002; Shie et al., 2002; George et al., 2004; Ho et al., 2004). These studies, however, did not examine the effects of ketogenic diets rich in fats, when the high lipid content is administered along with severe carbohydrate restriction. Indeed, in a recent series of experiments using a transgenic mouse model of Alzheimer’s disease, a ketogenic diet was found to improve Alzheimer’s pathology. The mice used in this study, which express a human amyloid precursor protein gene containing the London mutation (APP/V717I), exhibit significant levels of soluble Aβ in the brain as early as 3 months of age and show extensive plaque deposition by 12–14 months (Van der Auwera et al., 2005). They also demonstrate early behavioral deficits in an object recognition task. Exposure to a ketogenic diet for 43 days resulted in a 25% reduction in soluble Aβ(1–40) and Aβ(1–42) in brain homogenates, but did not affect performance on the object recognition task. Caloric restriction has also been demonstrated to attenuate β-amyloid depositions in mouse models of Alzheimer disease (Patel et al., 2005; Wang et al., 2005). How the ketogenic diet and caloric restriction affect β-amyloid levels and whether this effect could be disease modifying in Alzheimer’s disease requires further study.

The ketogenic diet could have beneficial effects in Alzheimer’s disease apart from effects on β-amyloid disposition. For example, essential fatty acids in the diet may have beneficial effects on learning, as demonstrated with studies of spatial recognition learning in rodent models of Alzheimer’s disease (Hashimoto et al., 2002, 2005; Lim et al., 2005). Alternatively, the diet might protect against β-amyloid toxicity. Thus, direct application of β-hydroxybutyrate in concentrations produced by the ketogenic diet has been found to protect hippocampal neurons from toxicity induced by Aβ(1–42) (Kashiwaya et al., 2000).

Parkinson’s disease

The most widely used animal model of Parkinson’s disease is based on the neurotoxin MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine). Exposure to MPTP causes degeneration of mesencephalic dopamine neurons, as in the human clinical condition, and is associated with parkinsonian clinical features. The ketogenic diet has not yet been studied in the MPTP or other animal models of Parkinson’s disease. As in epilepsy and Alzheimer’s disease models, however, caloric restriction has been found to have beneficial effects in MPTP models of Parkinson’s disease. This was first demonstrated in rats fed on an alternate-day schedule so that they consume 30–40% less calories than animals with free access to food. The calorie-restricted animals were found to exhibit resistance to MPTP-induced loss of dopamine neurons and less severe motor deficits than animals on the normal diet (Duan and Mattson, 1999). More recently, it has been reported that adult male rhesus monkeys maintained chronically on a calorie-restricted diet are also resistant to MPTP neurotoxicity (Maswood et al., 2004; Holmer et al., 2005). These animals had less depletion of striatal dopamine and dopamine metabolites and substantially improved motor function than did animals receiving a normal diet. In other studies in mice, caloric restriction has been reported to have beneficial effects even when begun after exposure to MPTP (Holmer et al., 2005).

In addition to caloric restriction, several recent reports have indicated that β-hydroxybutyrate may be neuroprotective in the MPTP model. MPTP is converted in vivo to 1-methyl-4-phenylpyridinium (MPP +), which is believed to be the principal neurotoxin through its action on complex 1 of the mitochondrial respiratory chain. In tissue culture, 4 mmol/l β-hydroxybutyrate protected mesencephalic neurons from MPP + toxicity (Kashiwaya et al., 2000). Moreover, subcutaneous infusion by osmotic minipump of β-hydroxybutyrate for 7 days in mice conferred partial protection against MPTP-induced degeneration of dopamine neurons and parkinsonian motor deficits (Tieu et al., 2003). It was proposed that the protective action is mediated by improved oxidative phosphorylation leading to enhanced ATP production. This concept was supported by experiments with the mitochondrial toxin 3-nitropropionic acid (3-NP). 3-NP inhibits oxidative phosphorylation by blocking succinate dehydrogenase, an enzyme of the tricarboxylic acid cycle that transfers electrons to the electron transport chain via its complex II function. The protective effect of β-hydroxybutyrate on MPTP-induced neurodegeneration in mice was eliminated by 3-NP. Moreover, in experiments with purified mitochondria, β-hydroxybutyrate markedly stimulated ATP production and this stimulatory effect was eliminated by 3-NP. Thus, it seems likely that β-hydroxybutyrate is protective in the MPTP model of Parkinson’s disease by virtue of its ability to improve mitochondrial ATP production (Tieu et al., 2003). Whether the ketogenic diet would also be protective in Parkinson’s disease models as a result of increased β-hydroxybutyrate production remains to be determined. It is noteworthy that β-hydroxybutyrate is not anticonvulsant and is unlikely to directly account for the antiseizure activity of the ketogenic diet (Rho et al., 2002). Whether β-hydroxybutyrate contributes in some other way to the beneficial activity of the ketogenic diet in epilepsy therapy remains to be studied.

Ischemia and traumatic brain injury

Much of the neurological dysfunction that occurs in stroke, cerebral ischemia, and acute traumatic brain injury is due to a secondary injury process involving glutamate-mediated excitotoxicity, intracellular calcium overload, mitochondrial dysfunction, and the generation of reactive oxygen species (ROS) (McIntosh et al., 1998). Consequently, the underlying pathophysiological mechanisms may have features in common with those in classical neurodegenerative disorders. Recently, Prins et al. (2005) have reported that the ketogenic diet can confer up to a 58% reduction in cortical contusion volume at 7 days after controlled cortical injury in rats. The beneficial effects of the diet, administered after the injury, only occurred at some postnatal ages despite similar availability of ketone bodies at all ages studied. This led the authors to conclude that differences in the ability of the brain to utilize ketones at different developmental stages may influence the protection conferred (Rafiki et al., 2003; Vannucci and Simpson, 2003; Pierre and Pellerin, 2005). In a previous study, a 48-h fast, which results in similar short-term ketosis as that achieved by the ketogenic diet, was found to protect rats against neuronal loss in the striatum, neocortex, and hippocampus produced by 30-min four-vessel occlusion (Marie et al., 1990). There was also a reduction in mortality and the incidence of postischemic seizures in fasted animals. Thus, there is evidence that the ketogenic diet has neuroprotective activity in both traumatic and ischemic brain injury. An additional study found that rats receiving a ketogenic diet are also resistant to cortical neuron loss occurring in the setting of insulin-induced hypoglycemia (Yamada et al., 2005).

Although the mechanism whereby the ketogenic diet confers protection in these diverse injury models is not well understood, β-hydroxybutyrate could play a role. The ketone body would presumably serve as an alternative energy source to mitigate injury-induced ATP depletion. In fact, exogenous administration of β-hydroxybutyrate can reduce brain damage and improve neuronal function in models of brain hypoxia, anoxia, and ischemia (Cherian et al., 1994; Dardzinski et al., 2000; Suzuki et al., 2001, 2002; Smith et al., 2005). In addition, the other ketone bodies, acetoacetate and acetone, which are β-hydroxybutyrate metabolites and can also serve as alternative energy sources, have similar neuroprotective effects (Garcia and Massieu, 2001; Massieu et al., 2001, 2003; Noh et al., 2006). Interestingly, in rats receiving a ketogenic diet, neuronal uptake of β-hydroxybutyrate is increased after cortical impact injury in comparison with animals receiving a standard diet (Prins et al., 2004). Thus, the ketogenic diet may promote delivery of β-hydroxybutyrate to the brain.

Cellular mechanisms underlying the neuroprotective activity of the ketogenic diet
Effects on energy metabolism


As noted above, ketone bodies, including β-hydroxybutyrate, that are produced during consumption of the ketogenic diet may serve as an alternative source of energy in states of metabolic stress, thus contributing to the neuroprotective activity of the diet. In fact, β-hydroxybutyrate may provide a more efficient source of energy for brain per unit oxygen than glucose (Veech et al., 2001). Recently, using microarrays to define patterns of gene expression, Bough et al. (2006) made the remarkable discovery that the ketogenic diet causes a coordinated upregulation of hippocampal genes encoding energy metabolism and mitochondrial enzymes. Electron micrographs from the dentate/hilar region of the hippocampus showed a 46% increase in mitochondrial profiles in rats fed the ketogenic diet. Thus, the ketogenic diet appears to stimulate mitochondrial biogenesis. Moreover, there was a greater phosphocreatine : creatine ratio in the hippocampal tissue, indicating an increase in cellular energy reserves, as expected from the greater abundance of mitochondria. In sum, during consumption of the ketogenic diet, two factors may contribute to the ability of neurons to resist metabolic stress: a larger mitochondrial load and a more energy-efficient fuel. In combination, these factors may account for the enhanced ability of neurons to withstand metabolic challenges of a degree that would ordinarily exhaust the resilience of the neurons and result in cellular demise.

Effects on glutamate-mediated toxicity

Interference with glutamate-mediated toxicity, a major mechanism underlying neuronal injury, is an alternative way in which the ketogenic diet could confer neuroprotection, although the available evidence supporting this concept is scant. Thus, acetoacetate has been shown to protect against glutamate-mediated toxicity in both primary hippocampal neuron cell cultures; however, a similar effect occurred in an immortalized hippocampal cell line (HT22) lacking ionotropic glutamate receptors (Noh et al., 2006). Acetoacetate also decreased the formation of early cellular markers of glutamate-induced apoptosis and necrosis, probably through the attenuation of glutamate-induced formation of ROS, as discussed below.

Effects on γ-aminobutyric acid systems

Another possible way in which the ketogenic diet may confer neuroprotection is through enhancement of γ-aminobutyric acid (GABA) levels, with a consequent increase in GABA-mediated inhibition (Yudkoff et al., 2001). Thus, ketone bodies have been demonstrated to increase the GABA content in rat brain synaptosomes (Erecinska et al., 1996), and, using in-vivo proton two-dimensional double-quantum spin-echo spectroscopy, the ketogenic diet was associated with elevated levels of GABA in some but not all human subjects studied (Wang et al., 2003). Rats fed a ketogenic diet did not, however, show increases in cerebral GABA (al-Mudallal et al., 1996).

Antioxidant mechanisms

Enhancement of antioxidant mechanisms represents an additional potential mechanism of neuroprotection. For example, ketone bodies have been shown to reduce the amount of coenzyme Q semiquinone, thereby decreasing free radical production (Veech, 2004).

A key enzyme in the control of ROS formation is glutathione peroxidase, a peroxidase found in erythrocytes that prevents lipid peroxidation by reducing lipid hydroperoxides to their corresponding alcohols and reducing free hydrogen peroxide to water. The ketogenic diet induces glutathione peroxidase activity in the rat hippocampus (Ziegler et al., 2003).

The ketogenic diet also increases production of specific mitochondrial uncoupling proteins (UCPs) (Sullivan et al., 2004). For example, in mice fed a ketogenic diet, UCP2, UCP4, and UCP5 were increased, particularly in the dentate gyrus. UCPs serve to dissipate the mitochondrial membrane potential, which, in turn, decreases the formation of ROS. Thus, juvenile mice fed a ketogenic diet had higher maximum mitochondrial respiration rates than those fed a control diet. Oligomycin-induced ROS production was also lower in the ketogenic diet-fed group. The ketogenic diet likely induces UCP production via fatty acids (Freeman et al., 2006). Levels of many polyunsaturated fatty acids are elevated in human patients on the ketogenic diet (Fraser et al., 2003). In fact, in patients with epilepsy, levels of one polyunsaturated fatty acid, arachidonate, were found to correlate with seizure control, although it has not yet been shown that arachidonate induces UCP production.

Effects on programmed cell death

The ketogenic diet may also protect against various forms of cell death. For example, the diet was protective against apoptotic cell death in mice induced by the glutamate receptor agonist and excitotoxin kainate, as evidenced by reductions of markers of apoptosis, including terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick-end labeling and caspase-3 staining, in neurons in the CA1 and CA3 regions of the hippocampus (Noh et al., 2003). Activation of caspase-3, a member of a larger family of cysteine proteases, has been implicated in neuronal cell death produced by different brain insults including seizures and ischemia (Gillardon et al., 1997; Chen et al., 1998). Apoptosis in seizure models can proceed via a number of molecular pathways (McIntosh et al., 1998; Fujikawa, 2005). One molecule that may play a role is calbindin, which is increased in mice on the ketogenic diet (McIntosh et al., 1998; Noh et al., 2005a). Calbindin is believed to have neuroprotective activity through its capacity to buffer intracellular calcium, which is a mediator of cell death (Mattson et al., 1995; Bellido et al., 2000). Further, protection by the ketogenic diet may be mediated by the prevention of kainic acid-induced accumulation of the protein clusterin (Noh et al., 2005b), which can act as a prodeath signal (Jones and Jomary, 2002).

Anti-inflammatory effects

It is well recognized that inflammatory mechanisms play a role in the pathophysiology of acute and chronic neurodegenerative disorders (Neuroinflammation Working Group, 2000; Pratico and Trojanowski, 2000; Chamorro and Hallenbeck, 2006). Inflammation has also been hypothesized to contribute to the development of chronic epilepsy (Vezzani and Granata, 2005). It is therefore of interest that fasting (a state associated with ketonemia, as in the ketogenic diet) or a high-fat diet has been associated with effects on inflammatory mechanisms (Palmblad et al., 1991; Stamp et al., 2005). A link between the ketogenic diet, anti-inflammatory mechanisms, and disease modification of neurological disease is still highly tentative. It is, however, noteworthy that intermittently fasted rats have increased expression of the cytokine interferon-γ in the hippocampus, and it was further shown that the cytokine conferred protection against excitotoxic cell death (Lee et al., 2006). The high fatty acid load of the ketogenic diet may also activate anti-inflammatory mechanisms. For example, it has been shown that fatty acids activate peroxisome proliferator-activated receptor α, which may, in turn, have inhibitory effects on the proinflammatory transcription factors nuclear factor-κB and activation protein-1 (Cullingford, 2004).

Carbohydrate restriction as a protective mechanism

A key aspect of the ketogenic diet is carbohydrate restriction. The role of decreased carbohydrates in neuroprotection has been investigated through the use of 2-deoxy-d-glucose (2-DG), a glucose analog that is not metabolized by glycolysis. Lee et al. (1999) found that administration of 2-DG to adult rats at a nontoxic dose (200 mg/kg) for 7 consecutive days produced dramatic protection against hippocampal damage and functional neurological deficits induced by the seizure-inducing excitotoxin kainate. In addition, 2-DG was protective against glutamate-induced and oxidative stress-induced neuronal death in cell culture. The authors also found that reduced glucose availability induces stress proteins, including GRP78 and HSP70, which they proposed act to suppress ROS production, stabilize intracellular calcium, and maintain mitochondrial function.

Conclusions

A wide variety of evidence suggests that the ketogenic diet could have beneficial disease-modifying effects in epilepsy and also in a broad range of neurological disorders characterized by death of neurons. Although the mechanism by which the diet confers neuroprotection is not fully understood, effects on cellular energetics are likely to play a key role. It has long been recognized that the ketogenic diet is associated with increased circulating levels of ketone bodies, which represent a more efficient fuel in the brain, and there may also be increased numbers of brain mitochondria. It is plausible that the enhanced energy production capacity resulting from these effects would confer neurons with greater ability to resist metabolic challenges. Additionally, biochemical changes induced by the diet – including the ketosis, high serum fat levels, and low serum glucose levels – could contribute to protection against neuronal death by apoptosis and necrosis through a multitude of additional mechanisms, including antioxidant and antiinflammatory actions. Theoretically, the ketogenic diet might have greater efficacy in children than in adults, inasmuch as younger brains have greater capacity to transport and utilize ketone bodies as an energy source (Rafiki et al., 2003; Vannucci and Simpson, 2003; Pierre and Pellerin, 2005).

Controlled clinical trials are required to confirm the utility of the diet as a disease-modifying approach in any of the conditions in which it has been proposed to be effective. A greater understanding of the underlying mechanisms, however, should allow the diet to be more appropriately studied. Indeed, there are many as yet unanswered questions about the use of the diet. For example, in epilepsy, how long an exposure to the diet is necessary? Do short periods of exposure to the diet confer long-term benefit? Why can the protective effects of the diet be readily reversed by exposure to carbohydrates in some but not all patients? In situations of acute neuronal injury, can the diet be administered after the neuronal injury, and if so, what time window is available? Does monitoring the diet through measurements of biochemical parameters improve efficacy and, if so, what is the best marker to monitor? Finally, the most fundamental research questions are what role ketosis plays, if any, in the therapeutic effects of the diet, and whether low glucose levels contribute to or are necessary for its symptomatic or proposed disease-modifying activity.

Moreover, a better understanding of the mechanisms may provide insights into ketogenic diet-inspired therapeutic approaches that eliminate the need for strict adherence to the diet, which is unpalatable, difficult to maintain, and is associated with side effects such as hyperuricemia and nephrolithiasis, and adverse effects on bone health and the liver (Freeman et al., 2006). A variety of approaches have been devised that allow ketosis to be obtained without the need to consume a high fat, low carbohydrate diet. The simplest is the direct administration of ketone bodies, such as through the use of the sodium salt form of β-hydroxybutyrate. Toxicological studies in animals have demonstrated that β-hydroxybutyrate sodium is well tolerated, and that theoretical risks such as acidosis and sodium and osmotic overload can be avoided by careful monitoring of blood parameters (Smith et al., 2005). Intravenous β-hydroxybutyrate has the potential to provide neuroprotection against ischemia during some surgical procedures, such as cardiopulmonary bypass. Owing to its short half-life, β-hydroxybutyrate sodium is, however, not suitable for long-term therapy in the treatment of chronic neurodegenerative disorders. In these circumstances, orally bioavailable polymers of β-hydroxybutyrate and its derivatives with improved pharmacokinetic properties may be of utility (Veech, 2004; Smith et al., 2005). Another interesting alternative to the ketogenic diet is the administration of metabolic precursors of ketone bodies. Among potential precursor molecules, 1,3-butanediol and 1,3-butanediol acetoacetate esters have been most extensively studied. These compounds are metabolized in a chain of enzymatic reactions in the plasma and liver to the same ketone bodies that are produced during the ketogenic diet (Desrochers et al., 1992, 1995; Ciraolo et al., 1995). Although each of the aforementioned alternatives is still early in development, the idea of developing the ketogenic diet in a ‘pill’ is very attractive and may be approachable.

Acknowledgements

We thank Amy French and Jessica Yankura for their helpful comments.

Sponsorship: This work was supported by the Intramural Research Program of the NINDS, NIH.

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Offline seek10

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Re: Ketogenic Diet - Path To Transformation?
« Reply #4 on: August 04, 2012, 03:05:14 PM »
That makes a whole lot of sense, that they were forced by temporarily severe environmental conditions to eat their food's food (grains that would otherwise be eaten by animals).

  It does make sense. How many times simple explanations make  more sense instead of dramatic explanations ( like ET's , GOD's  etc.)
“In the life of warriors it was extremely natural to be sad for no overt reason. Whenever the boundaries of the known are broken, a mere glimpse of the eternity outside is enough to disrupt the coziness of our controlled awareness. The best way to get rid of melancholy is to make fun of it.”(carlos)

Offline QuantumLogic

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Re: Ketogenic Diet - Path To Transformation?
« Reply #5 on: August 04, 2012, 05:57:20 PM »


I was reading a paper on the ketogenic diet yesterday, and at one point it says:

Quote
In a previous study, a 48-h fast, which results in similar short-term ketosis as that achieved by the ketogenic diet, was found to protect rats against neuronal loss in the striatum, neocortex, and hippocampus produced by 30-min four-vessel occlusion (Marie et al., 1990). There was also a reduction in mortality and the incidence of postischemic seizures in fasted animals. Thus, there is evidence that the ketogenic diet has neuroprotective activity in both traumatic and ischemic brain injury. An additional study found that rats receiving a ketogenic diet are also resistant to cortical neuron loss occurring in the setting of insulin-induced hypoglycemia (Yamada et al., 2005).

It is so blatantly obvious that the body needs to be in ketosis! You stop eating for 48hours, and it immediately uses ketogenic bodies. Duh...



I obviously don't know for sure, but as I stated in a previous post, from time to time before starting the ketogenic diet I would fast for a week. I wonder if that is why I have not had a hard time changing to this diet, since for brief periods I could have been in a state of ketosis (obviously not the same effects as a full blown diet change, though). I am on my 4th week now, and one of the things I find interesting is that I can read faster and comprehend easier. This effect may not be from ketosis, as I have eliminated everything else but meat, lots of fat, and a few non-inflammatory vegetables. All I can say for sure is that after the first two weeks, my energy level and sustainability grew exponentially higher than before.

I found this interesting as well-

Quote
Fermented vegetables like sauerkraut, kim chi, sauerruben and cortido are excellent alternatives for people with gut issues. First, the fermentation process “pre-digests” the vegetables and makes them easier to absorb. Second, fermented veggies contain probiotic microorganisms that help heal the gut.

I have eaten home canned vegetables that were grown organically for 35 years, since I was a small child. I have a photocopy of the old canning book my father used, complete with all of the modifications and experimental recipes he tried over the years. Sauerkraut is one of my favorite things to eat, and has been my entire life. It is easy and cheap to make, and keeps almost indefinitely in proper conditions. I eat it everyday, so that may explain why I have not had any gut or digestion issues throughout my life. I even drink the juice once the jar is empty. I would never have thought that it had any health benefits. Great info!

My body definitely seems to like eating this way. I do not get hungry as often, and the meat and fat are very filling. The LWB book is absolutely amazing, and I learned a great deal from it. I still have to read PMPB, but now that I can concentrate much easier (before it seemed I had to really work at it) it should be equally enlightening. Thanks to everyone here for the work and research you do finding these gems of wisdom. I feel like I am on a good, sustainable path now, and I am deeply grateful.


Offline Aragorn

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Re: Ketogenic Diet - Path To Transformation?
« Reply #6 on: August 04, 2012, 05:58:44 PM »
Moreover, a better understanding of the mechanisms may provide insights into ketogenic diet-inspired therapeutic approaches that eliminate the need for strict adherence to the diet, which is unpalatable, difficult to maintain, and is associated with side effects such as hyperuricemia and nephrolithiasis, and adverse effects on bone health and the liver (Freeman et al., 2006). A variety of approaches have been devised that allow ketosis to be obtained without the need to consume a high fat, low carbohydrate diet. The simplest is the direct administration of ketone bodies, such as through the use of the sodium salt form of β-hydroxybutyrate. Toxicological studies in animals have demonstrated that β-hydroxybutyrate sodium is well tolerated, and that theoretical risks such as acidosis and sodium and osmotic overload can be avoided by careful monitoring of blood parameters (Smith et al., 2005).

[...] Although each of the aforementioned alternatives is still early in development, the idea of developing the ketogenic diet in a ‘pill’ is very attractive and may be approachable.

This whole passage is just unbelievably biased, and simply bad science. Then again, not that surprising. The comment about the diet being 'unpalatable' made me laugh :)

Basically, yet another study that brings out the truth, but with clever formulation and a few inserted "plants" - that makes the reader doubt the whole thing - the results are watered down. Or not, if you can see through the manipulation.

Looking up the study by Freeman et al., 2006, shows that the associated side effects of the ketogenic diet (in that study) are labeled as 'early onset adverse effects'. And then, look at this, they state:

_http://www.matthewsfriends.org/jh/KDPaviaEpilepsyResearch.pdf
Quote
Most of the early onset adverse effects of the diet (Table 4) {the early onset effects} are transient and can be carefully managed with conservative strategies (Freeman et al. 2006, 165).

So, there we go again! Cherry picking the data...  :cool2:

ADDED: Funny they don't bring up the role of caloric restriction (CR), which benefits for longevity and health are shown in multiple other studies. Guess they didn't want to go there, since the diet would be too unpalatable. :)
« Last Edit: August 04, 2012, 06:00:41 PM by Aragorn »
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Offline QuantumLogic

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Re: Ketogenic Diet - Path To Transformation?
« Reply #7 on: August 04, 2012, 06:21:09 PM »
Well, just the mention of "unpalatable" would be enough to make most interested readers cringe- their minds immediately thinking "Oh, it doesn't taste good". It goes to show the easiest way to manipulate the masses is through their mouths. I found it interesting that even with the data provided, they immediately look to some alternative to changing one's diet permanently. As you have pointed out, Aragorn, they seem to be attempting to frighten people with short-lived side effects in an effort to dissuade anyone from doing what is proven (more every week, it seems)- change your diet, and you will, over time, be healthier.

The commentary offered by the researchers is seemingly in direct conflict with the data itself. They are so transparent it is truly laughable.

Offline Laura

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Re: Ketogenic Diet - Path To Transformation?
« Reply #8 on: August 05, 2012, 12:46:11 PM »
Something else that comes up in the ketogenic diet papers is intermittent fasting.   One study was done on mice that were fed on alternate days.  Results were dramatic and included turning on the SIRT2 genes.  Here is an article that talks about this sort of thing in a general way.  What it doesn't mention explicitly is the advantage of doing this on a ketogenic diet.  The way this article describes it might be more doable for some of the folks who have issues with mitochondrial dysfunction.  I think I'll be doing it this way, not total fasting, but restriction on alternate days.

Quote
http://www.bbc.co.uk/news/health-19112549

Scientists are uncovering evidence that short periods of fasting, if properly controlled, could achieve a number of health benefits, as well as potentially helping the overweight, as Michael Mosley discovered.

I'd always thought of fasting as something unpleasant, with no obvious long term benefits. So when I was asked to make a documentary that would involve me going without food, I was not keen as I was sure I would not enjoy it.

But the Horizon editor assured me there was great new science and that I might see some dramatic improvements to my body. So, of course, I said, "yes".

I am not strong-willed enough to diet over the long term, but I am extremely interested in the reasons why eating less might lead to increased life span, particularly as scientists think it may be possible to get the benefits without the pain.

How you age is powerfully shaped by your genes. But there's not much you can do about that.

Calorie restriction, eating well but not much, is one of the few things that has been shown to extend life expectancy, at least in animals. We've known since the 1930s that mice put on a low-calorie, nutrient-rich diet live far longer. There is mounting evidence that the same is true in monkeys.
Growth hormone

The world record for extending life expectancy in a mammal is held by a new type of mouse which can expect to live an extra 40%, equivalent to a human living to 120 or even longer.

It has been genetically engineered so its body produces very low levels of a growth hormone called IGF-1, high levels of which seem to lead to accelerated ageing and age-related diseases, while low levels are protective.

A similar, but natural, genetic mutation has been found in humans with Laron syndrome, a rare condition that affects fewer than 350 people worldwide. The very low levels of IGF-1 their bodies produce means they are short, but this also seems to protect them against cancer and diabetes, two common age-related diseases.

The IGF-1 hormone (insulin-like growth factor) is one of the drivers which keep our bodies in go-go mode, with cells driven to reproduce. This is fine when you are growing, but not so good later in life.

But it turns out IGF-1 levels can be lowered by fasting. The reason seems to be that when our bodies no longer have access to food they switch from "growth mode" to "repair mode".

As levels of the IGF-1 hormone drop, a number of repair genes appear to get switched on according to ongoing research by Professor Valter Longo of the University of Southern California.
Intermittent fasting

One area of current research into diet is Alternate Day fasting (ADF), involving eating what you want one day, then a very restricted diet (fewer than 600 calories) the next, and most surprisingly, it does not seem to matter that much what you eat on non-fast days.

Dr Krista Varady of the University of Illinois at Chicago carried out an eight-week trial comparing two groups of overweight patients on ADF.

"If you were sticking to your fast days, then in terms of cardiovascular disease risk, it didn't seem to matter if you were eating a high-fat or low-fat diet on your feed (non-fast) days," she said.

I decided I couldn't manage ADF, it was just too impractical. Instead I did an easier version, the so-called 5:2 diet. As the name implies you eat normally 5 days a week, then two days a week you eat 500 calories if you are a woman, or 600 calories, if you are a man.

There are no firm rules because so far there have been few proper human trials. I found that I could get through my fast days best if I had a light breakfast (scrambled eggs, thin slice of ham, lots of black tea, adding up to about 300 calories), lots of water and herbal tea during the day, then a light dinner (grilled fish with lots of vegetables) at night.

On my feed days I ate what I normally do and felt no need to gorge.

I stuck to this diet for 5 weeks, during which time I lost nearly a stone and my blood markers, like IGF-1, glucose and cholesterol, improved. If I can sustain that, it will greatly reduce my risk of contracting age-related diseases like cancer and diabetes.

Current medical opinion is that the benefits of fasting are unproven and until there are more human studies it's better to eat at least 2000 calories a day. If you really want to fast then you should do it in a proper clinic or under medical supervision, because there are many people, such as pregnant women or diabetics on medication, for whom it could be dangerous.

I was closely monitored throughout and found the 5:2 surprisingly easy. I will almost certainly continue doing it, albeit less often. Fasting, like eating, is best done in moderation.
He who learns must suffer
And even in our sleep pain that cannot forget
Falls drop by drop upon the heart,
And in our own despair, against our will,
Comes wisdom to us by the awful grace of God.
Agamemnon, Aeschylus

Offline Hildegarda

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Re: Ketogenic Diet - Path To Transformation?
« Reply #9 on: August 05, 2012, 07:29:54 PM »
Something else that comes up in the ketogenic diet papers is intermittent fasting.   One study was done on mice that were fed on alternate days.  Results were dramatic and included turning on the SIRT2 genes.  Here is an article that talks about this sort of thing in a general way.  What it doesn't mention explicitly is the advantage of doing this on a ketogenic diet. 

I have recently come to the same idea!  One of the stated benefits of fasting is that it puts you into ketogenic state.  This is why after fasting for 2 days or so you get a second wind and feel energetic, for a while anyway.  Breaking the fast with vegetable juices, honeyed tea or rice however, as is often recommended, appears completely wrong, because it whacks you out of ketogenic state fast and messes you up in all various ways.  I used to fast more or less regularly, but stopped about three years ago, when I got shakes and symptoms of sugar crash after breaking fast and thought, this can't be good for me.  Now, doing it while on ketogenic diet will not produce this effect and in fact should be easy and natural.  After all, our ancestors on primal diets had to deal with food shortages constantly, and the evolution has got to already have established a way for our physiology to manage it. 
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Offline Oxajil

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Re: Ketogenic Diet - Path To Transformation?
« Reply #10 on: August 05, 2012, 08:20:56 PM »
I've noticed that I feel pretty light and energetic on days when I'm more or less fasting.

Here's another article on this:

_http://paleodietlifestyle.com/intermittent-fasting-paleo-diet/
Quote
Intermittent Fasting And The Paleo Diet

Most people in the developed world spread their food intake out over the whole day – breakfast, lunch, dinner, and maybe a snack or two in between. But humans evolved and thrived on an irregular meal schedule well before grocery stores and modern food preservation made “three squares a day” possible. And far from being unhealthy, skipping an occasional meal or two has several benefits for health and weight loss. Essentially, fasting is a beneficial stressor, and when your body responds to the stress, it becomes stronger and healthier.

What is Intermittent Fasting?

Intermittent fasting, or IF, means incorporating regular periods of fasting into your meal schedule. Some people fast for 24 hours once or twice a week, while others incorporate shorter but more frequent fasts by restricting their daily caloric intake to a window of 4-8 hours. Fasting is most commonly understood to involve no food consumption at all, but Paul Jaminet at the Perfect Health Diet also argues for the consumption of coconut oil or bone broth during a fast.

Intermittent fasting is a logical extension of the Paleo diet, for people who want to eat not only what they evolved to digest, but when they evolved to digest it. Eating Paleo also makes fasting relatively easy: if you avoid refined carbohydrates, your energy levels don’t spike and crash with every meal, so you shouldn’t experience wooziness or “brain fog” during a fast.

Fasting and weight loss


Conventional diet wisdom discourages skipping meals, which is often associated with eating disorders and unsustainable crash diets. Deliberately practiced intermittent fasting, however, can be a powerful tool for weight loss.

Most obviously, fasting involves caloric restriction – and many people find it easier to fast than to count calories. When you fast, you quickly stop feeling hungry and can turn your attention to other things, and then conclude the fast with a satisfying meal. Counting calories, on the other hand, makes it easy to fixate on restricting food intake, leading to persistent feelings of hunger and deprivation as you eat several unsatisfying meals throughout the day.

Hormonal changes involved in fasting also promote weight loss, even if you don’t restrict calories. Fasting lowers the body’s levels of insulin, a hormone that prevents the release of stored body fat. With lower insulin levels, your body turns to stored fat for energy. Additionally, fasting increases other hormones called catecholamines, which trigger your body to use energy at a faster rate. This makes fasting a particularly useful tool for dieters, since it promotes the loss of fat rather than muscle mass.

Fasting and athletic performance


At first glance, athletic training in a fasted state seems contradictory: how can your body perform without fuel? But intermittent fasting can actually improve athletic performance, as long as you don’t fast for too long.

For endurance athletes, the benefits of fasting come from a two-pronged approach: training in the fasted state, and competing in the fed state. Fasted training can improve performance by forcing your body to adapt to lower glycogen stores and use glycogen more efficiently. Essentially, training in the fasted state adds another stressor, forcing your body to compensate and become stronger. This sets you up to get a huge boost from competing in the fed state – your body will make maximum use of your pre-workout fuel.

Short-term fasting is also useful for power athletes. While fasting for several days at a time will hurt your progress, intermittent fasts less than 24 hours will not cause muscle loss or send your body into “starvation mode,” as long as you consume adequate calories and protein when you do eat. On the contrary, when you lift in a fasted state, your body uses protein more efficiently afterwards, boosting muscle growth. Weightlifters seeking to gain lean mass without also gaining fat should look into Martin Berkhan’s Leangains program, which specifies an eight-hour “feeding window” and a sixteen-hour fast every day.

Other benefits of fasting

As well as weight loss and increased athletic performance, your body’s response to the beneficial stress of fasting can help promote health and longevity in a variety of other ways.

First, fasting can help cancer patients. Although the relevant research was conducted on animals, one study showed that rats who fasted every other day showed greater ability to fight off chronic diseases like diabetes and cancer, and improved heart health. Fasting helps fight these diseases because when you stress your cells by fasting, they enter “survival mode,” giving them increased resistance to stress, while cancer cells remain in “normal mode:” this gives your cells the advantage. In study on humans, scientists found that fasting can also reduce the risk of heart disease.

Fasting also promotes health by reducing oxidative stress. Oxidative stress, or damage to your cells from a harmful build-up of oxidized proteins, is linked to the harmful effects of aging. Fasting helps your cells get rid of these oxidized proteins. A study done on humans with asthma showed a reduction in oxidative stress and improved heart health on an alternate-day fasting regimen even when the “fasting days” actually involved very low food intake.

As well as benefitting your body, fasting is also good for your brain. In the same way that it helps your other cells, it increases brain cells’ ability to repair themselves and eliminate potentially harmful waste material. It also triggers the body to release more of a protein called brain-derived neurotrophic factor (BDNF), which supports healthy brain function and prevents degenerative disorders like Alzheimer’s disease.

On top of its other health benefits, intermittent fasting also helps some people who suffer from troublesome circadian rhythms, since circadian rhythms are even more strongly tied to eating patterns than to light exposure. Even if your circadian rhythms are normally fine, fasting can help beat jet lag by “resetting” your internal clock to the new time zone.

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.

Conclusion

If your body is able to handle the additional stress, intermittent fasting can lead to faster weight loss, improved athletic performance, and a long list of other health improvements. Easy to practice and safe for most people, IF can be a great addition to a Paleo diet.
"It is important for us all to remember that our goal in this life is not to be become 'super' men or women, but to relearn how to become normally functioning human beings."
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Offline liffy

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Re: Ketogenic Diet - Path To Transformation?
« Reply #11 on: August 05, 2012, 10:25:46 PM »
I used to do the whole intermittent fasting thing for a while (before turning paleo, but low-carb whole foods), and it's quite neat, considering that there are longer periods where preparing and eating food isn't an issue.

One thing that has been mentioned countless times in the diet forums here has to do with the necessity of eating the biggest meal in the morning, and then gradually decreasing meal size throughout the day, which certainly isn't something one does on an everyday basis when fasting (either through delaying meals until early afternoon, or doing days without food/with low amounts of food).

I'm not saying that the optimal solution is to eat a huge, late dinner, but could there be a possibility that meal-timing isn't as important, as long as the necessary nutrients are present over time?
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Offline Laura

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Re: Ketogenic Diet - Path To Transformation?
« Reply #12 on: August 05, 2012, 10:31:13 PM »
Something else that comes up in the ketogenic diet papers is intermittent fasting.   One study was done on mice that were fed on alternate days.  Results were dramatic and included turning on the SIRT2 genes.  Here is an article that talks about this sort of thing in a general way.  What it doesn't mention explicitly is the advantage of doing this on a ketogenic diet. 

I have recently come to the same idea!  One of the stated benefits of fasting is that it puts you into ketogenic state.  This is why after fasting for 2 days or so you get a second wind and feel energetic, for a while anyway.  Breaking the fast with vegetable juices, honeyed tea or rice however, as is often recommended, appears completely wrong, because it whacks you out of ketogenic state fast and messes you up in all various ways.  I used to fast more or less regularly, but stopped about three years ago, when I got shakes and symptoms of sugar crash after breaking fast and thought, this can't be good for me.  Now, doing it while on ketogenic diet will not produce this effect and in fact should be easy and natural.  After all, our ancestors on primal diets had to deal with food shortages constantly, and the evolution has got to already have established a way for our physiology to manage it.

We've really been digging into a whole stack of papers on the whole ketogenic diet and after reading and collecting the best info it seems that the intermittant fasting as described in the article I posted - though doing it from a paleo diet - would work extremely well on healing mitochondria, correcting mtDNA errors, possibly reversing mutation issues, etc.  And make no mistake about it, nearly every problem - if not ALL - that has been brought up on this forum relating to health, is a mitochondrial issue. 

We'll get a list of links to the papers up.  Some of them are very technical and some have to be read with a grain or more of salt because it seems that scientists nowadays don't have a lot of common sense when they design studies. 

We think that instead of calling it "restriction" or "fasting" we'll just call it the Rhythm Method of eating... and we began our experimenting today and will report results.  We've got several different states/conditions involved, so it's a good sample just in the house here.   Some of you peeps with energy issues might want to try this because it apparently can begin to show very good results in something like 8 to 10 days. 
He who learns must suffer
And even in our sleep pain that cannot forget
Falls drop by drop upon the heart,
And in our own despair, against our will,
Comes wisdom to us by the awful grace of God.
Agamemnon, Aeschylus

Offline Laura

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Re: Ketogenic Diet - Path To Transformation?
« Reply #13 on: August 05, 2012, 11:06:32 PM »
I've noticed that I feel pretty light and energetic on days when I'm more or less fasting.

Here's another article on this:

_http://paleodietlifestyle.com/intermittent-fasting-paleo-diet/
Quote
<snip>
Conclusion

If your body is able to handle the additional stress, intermittent fasting can lead to faster weight loss, improved athletic performance, and a long list of other health improvements. Easy to practice and safe for most people, IF can be a great addition to a Paleo diet.

The fact that many people who need to invoke the healing of their mtDNA and other systems most cannot tolerate this stress is why I'm suggesting the Rhythm Diet which is not a total fast but very, VERY light eating on alternating days.   And if, on the days they eat normally, they are still eating a ketogenic diet, that is, very, very low carbs, somewhat low protein, and high fat, then they can have the same benefits without the stress. 

We'll be getting some hard-core info up over the next couple of days and even if they are technical, it will help for everyone to read the papers.  Just try to follow what's being said without getting bogged down in the jargon or the exact processes when they wander off into detailed descriptions of cellular processes.   The fact is, there is NO ONE SIZE FITS ALL solution except for the fact that the ketogenic diet itself, in some form or another, seems to be the one common beneficial/healing factor.   Over the last few days, as we have read through this material, we have arrived at some understanding of why various people participating in this thread have had certain problems, and why supplementation should be handled very carefully.  Getting into the state of mild ketosis and then doing the things that can change your DNA, and in many cases, even reverse the progression of disease has to be approached from different directions for different people.  Some people's mitochondria are so compromised that even ketosis itself must be approached carefully.  And you can't overload one system that then brings detriment to another.  Without access to a major lab and tons of tests, you have to pay close attention to how you feel/react in order to make adjustments, and you have to understand what is going on in your body to be able to report or assess. 

What struck me as I was reading all this material is this: what if the "ascension process" much touted in esoterica is exactly this: figuring out how to heal and activate DNA?  What if, by these studies and experiments, we manage to activate/accelerate "soul seating" capacity and "receivership capability"???  What if this is part of "it's not where you are, but who you are and what you see"?  Perhaps, by aligning with our paleolithic ancestors who painted caves and decorated the earth with megaliths, and restoring our DNA to that more similar to theirs, we might acquire, along the way, some of their abilities?
He who learns must suffer
And even in our sleep pain that cannot forget
Falls drop by drop upon the heart,
And in our own despair, against our will,
Comes wisdom to us by the awful grace of God.
Agamemnon, Aeschylus

Offline Laura

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Re: Ketogenic Diet - Path To Transformation?
« Reply #14 on: August 05, 2012, 11:10:25 PM »
I used to do the whole intermittent fasting thing for a while (before turning paleo, but low-carb whole foods), and it's quite neat, considering that there are longer periods where preparing and eating food isn't an issue.

One thing that has been mentioned countless times in the diet forums here has to do with the necessity of eating the biggest meal in the morning, and then gradually decreasing meal size throughout the day, which certainly isn't something one does on an everyday basis when fasting (either through delaying meals until early afternoon, or doing days without food/with low amounts of food).

I'm not saying that the optimal solution is to eat a huge, late dinner, but could there be a possibility that meal-timing isn't as important, as long as the necessary nutrients are present over time?

For the sake of the HPA axis issues that many people in modern society have, I think it is still a good idea to eat breakfast on the partial fasting days.  And that it should be the main, or only meal on that day.

He who learns must suffer
And even in our sleep pain that cannot forget
Falls drop by drop upon the heart,
And in our own despair, against our will,
Comes wisdom to us by the awful grace of God.
Agamemnon, Aeschylus