Low fat ketogenic diet menu list,exercises to do at home to lose weight quickly,can you lose weight by eating green beans - Step 2

16.01.2015
Scientist say a low-carb, high-fat ketogenic-style diet is better for weight loss, diabetes, and metabolic syndrome than diets focused obsessively on calorie restriction. Obesity experts say the longstanding emphasis on calorie counting has failed, and we need to move beyond the "calories in, calories out" dogma if we're serious about defeating the global tsunami of obesity and diabetes. According to Ludwig, the true cause of weight gain isn't eating too many calories, but eating a high-carb diet that's rich in refined carbs. Ludwig join a growing list of medical experts who are dispelling the myth that eating fat makes you fat, and that calorie restriction is best for weight loss. Eating refined carbs like a 100-calorie pack of jelly beans (which are fat-free) produces a huge insulin spike that signals your fat cells to store calories. You'll also feel fuller, longer, after eating the nuts, while the jelly beans will make your blood sugar surge and promptly crash, causing you to quickly feel hungry again. Surges in blood sugar and insulin also leads to diabetes, inflammation and metabolic syndrome, so by curbing these with a low-carb, high-fat diet such as the Atkins and ketogenic diets, we simultaneously stem several diseases in one fell swoop. Ludwig's JAMA commentary comes on the heels of new scientific research suggesting that unprocessed saturated fat is not the cause of weight gain, diabetes or heart disease. What fuels weight gain and disease is inflammation — which is caused by a high-carb diet — especially one high in sugar, said Dr.
The irony is that the foods we were taught are good for us — breads, cereals, pasta, rice, potatoes — are the very ones that are killing us, said Westman. Westman has been aware of the health benefits of dietary fat for years and is glad there's a growing vindication of this important macronutrient.
Studies show the ketogenic diet is better than drugs for managing epilepsy-induced seizures, can reverse type 2 diabetes, and manage cancer. Volek, author of The Art and Science of Low Carbohydrate Living, is encouraged by the increasing popularity of high-fat diets like the ketogenic diet, as more people are beginning to accept that eating fat does not make you fat. Kate Middleton Royal Tour of India : The Duchess of Cambridge style guide Kate Middleton wore several stylish outfits during her recent Royal visit to India. The Ketogenic Diet in some form or another has been labeled by many different names in recent times, and started gaining traction again with Dr.
This diet is not new, however, as it was seen as a therapeutic diet that produced better results than drugs in treating epilepsy way back in the 1920s.
When the Atkins diet gained media popularity several years ago, many critics complained that there were no long-term studies done on the diet. The research that is starting to be published on the effectiveness of the Ketogenic Diet in curing disease is nothing less than amazing. Dietary and metabolic therapies have been attempted in a wide variety of neurological diseases, including epilepsy, headache, neurotrauma, Alzheimer disease, Parkinson disease, sleep disorders, brain cancer, autism, pain, and multiple sclerosis.
This review article explores the rationale for using the KD and related dietary treatments in neurological disorders outside of epilepsy, and summarizes the clinical experience to date. Over the past decade, investigators have identified numerous mechanisms through which the KD may provide neuroprotective activity. Two hallmark features of KD treatment are the rise in ketone body production by the liver and a reduction in blood glucose levels. In the end, there are likely many other mechanisms that could contribute to the neuroprotective properties of the KD.
Aging involves the gradual decrease in function, and at times outright degeneration, of neurons and neural circuits.
Thus, there is growing evidence that the KD may be an effective treatment for AD through a variety of metabolism-induced mechanisms that reduce oxidative stress and neuroinflammation, and enhance bioenergetic profiles - largely through enhanced mitochondrial functioning. The primary pathophysiology in Parkinson disease (PD) is excitotoxic degeneration of dopaminergic neurons in the substantia nigra, leading to abnormalities of movement, and to an increasing extent, in cognition and other cortical functions.
Amyotrophic lateral sclerosis (ALS) is a rapidly progressive disease due to degeneration of motor neurons of the cortex and anterior horn of the spinal cord. One potentially important consideration in this regard - applicable to all neurodegenerative diseases - is determining whether timing of intervention is crucial for a protective effect by KD treatment.
While clinical validation of this phenomenon is not yet forthcoming, there are several case reports suggesting that the KD may be efficacious in humans with brain tumors. To date, no clinical trials of the KD have been performed in patients with stroke, but several animal studies of hypoxia-ischemia support the potential beneficial effect of the diet. Unfortunately, the incidence of brain injury is increasing in both civilian and military contexts. Several recent animal studies support this idea, and investigators have principally focused on ketone bodies (Prins, 2008a). With respect to anti-epileptogenesis following head injury, the data regarding KD effects are mixed.
Mood stabilizing properties of the KD have been hypothesized (El-Mallakh and Paskitti, 2001), but no clinical studies have been conducted as of this writing.
Autism is a neurodevelopmental disorder that affects language development and social function. Migraine is a paroxysmal neurological disorder having considerable clinical phenotypic overlap with epilepsy (Rogawski, 2008). Interestingly, the first report of using the KD for migraine came in 1928, only a few years after the diet's first use for epilepsy (Schnabel, 1928). Despite the relative lack of clinical data, there is an emerging literature supporting the broad use of the KD (and its variants) against a variety of neurological conditions.
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Slideshare uses cookies to improve functionality and performance, and to provide you with relevant advertising. Clipping is a handy way to collect and organize the most important slides from a presentation. From the Center for Health Services Research in Primary Care, Department of Veterans Affairs Medical Center, and Duke University Medical Center, Durham, North Carolina. Over 24 weeks, a low-carbohydrate diet program led to greater weight loss, reduction in serum triglyceride level, and increase in HDL cholesterol level compared with a low-fat diet. PlayNancy says after her husband died undergoing gastric bypass surgery, her son, Rob, began using food to cope with his grief.
The ketogenic diet is showing amazing results in curbing obesity and improving cognition, Alzheimer's disease and schizophrenia.
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Canada sees Fentanyl OD surge: Picking their battles in OD state of emergencyCanada is seeing a surge in Fentanyl OD deaths, so much so, that they have called a state of emergency as the death toll rises due to the OD cases involving this drug. What constitutes an optimal physique?  This is different based on each individual’s unique genetic potential but researchers would agree that we should have a moderate to thin structure and good muscular development.
While many have sought after a thin physique, the mantra of the 21st century is that strong is the new thin!  We want to have a good body fat percentage (6-15% for men and 15-30% for women) and have developed well-toned musculature.
There is a popular idea that the body needs carbohydrates and protein immediately after exercising in order to properly recover.  However, with the application of a properly formulated ketogenic diet to achieve a keto-adapted state this is not necessary. Now, I eat 2 meals a day between a 4-8 hour eating window and consume around 3500-4000 calories with approximately 60-70% fat, 20-25% protein and 10-15% carbohydrates on average. The results – I am stronger in my upper and lower body and feel significantly better than I did in my teens and 20’s. Some individuals do well with the inclusion of a higher carbohydrate meal two or 3 times a week while others will do better staying in ketosis for a month at a time.  You will have to experiment to find what you feel best with. Each night I have a treat (a few pieces of homemade fudge and some dried fruit) and 1-2 glasses of a good quality wine.
Initially on this programme my blood glucose was spiking super high (7-8 in the morning, 8-9 post exercise, 7-10 postprandial).
According to my ketostix (not the best method of testing, I think) – I am hovering in and out of a mild nutritional ketosis. I’ve never been so level in terms of appetite and energy, so I am hoping my programme is good enough. With well over 1,000 members and dozens of contributing authors, Primal Docs is an impressive collection of ideas from thought leaders in the Ancestral Health and Functional Medicine space. David Ludwig, director of the Obesity Prevention Center at Boston Children’s Hospital, wrote in JAMA. This is because our body stores fat when we experience insulin spikes, which are caused by eating too much sugar and processed grains like white bread. The way to lose weight is to prevent insulin spikes, which the LCHF Atkins and ketogenic diets do. The true cause of obesity, cardiovascular disease, high cholesterol and diabetes is a high-carb diet, especially one high in sugar. Eric Westman champions a low-carb, high-fat ketogenic-style diet for weight loss and reversing type 2 diabetes. Westman said eating a diet high in healthy fats such as olive oil, whole eggs, grass-fed beef, and pastured butter not only accelerates weight loss, but reduces inflammation.


For people who want to lose weight without deprivation and enjoy optimal health, Westman wholeheartedly champions a low carb, high-fat (LCHF) diet.
Volek has followed a ketogenic diet for the past 20 years, and credits it for his excellent health. Volek explained that by drastically reducing carbs in our diet and replacing them with healthy, unprocessed fats, we boost fat-burning, eliminate nagging carb cravings, experience more stable blood sugar levels, and enjoy better mood. A graduate of the University of Pennsylvania, Samantha enjoys running, cycling and taking photos.
Today, the diet is being studied in the medical community with applications to all kinds of diseases. However, there are plenty of studies on the Ketogenic Diet and there has never been any negative effects recorded from long-term use.
The impetus for using various diets to treat - or at least ameliorate symptoms of - these disorders stems from both a lack of effectiveness of pharmacological therapies, and also the intrinsic appeal of implementing a more "natural" treatment.
Even in patients with medically refractory epilepsy who have remained seizure-free on the KD for 2 years or more, it is not uncommon for clinicians to observe that both anticonvulsant medications and the diet can be successfully discontinued without recrudescence of seizures (Freeman et al., 2007). An underlying theme of such diet-based therapies is that nutrients and metabolic substrates can exert profound effects on neuronal plasticity, modifying neural circuits and cellular properties to enhance and normalize function. Many of these mechanisms are thought to relate principally to the KD's anticonvulsant effects, but some if not all of them could contribute to cellular homeostasis and preventing neuronal injury or dysfunction.
After its introduction in 1920, the KD was used as a first or second-line treatment for severe childhood epilepsy. It is possible that by altering energy metabolism with the KD, rates of degeneration of certain neural structures and functions might be slowed (Balietti et al., 2010a). While the essential pathological processes of AD involves neuronal degeneration with accumulation of abnormal cellular products such as fibrillary plaques and tangles, recent evidence points to alterations in the function of extant neural circuits and mitochondrial homeostasis (Kapogiannis and Mattson, 2011). A randomized double-blind, placebo-controlled trial of a MCT KD resulted in significantly improved cognitive functioning in APO?4-negative patients with AD but not in patients with a APO?4 mutation (Henderson et al., 2009).
AGE accumulation is a process of normal aging that is accelerated in AD; proteins are non-enzymatically glycosylated and this cross-linking of proteins accentuates their dysfunction.
However, caution should be exercised in extrapolating findings in animals to humans, as discrepancies in terms of both clinical efficacy and untoward side-effects have been noted.
As a consequence, voluntary motor activity gradually deteriorates, leaving the affected individual profoundly weak despite largely retained cognitive functioning. Neurological disorders in late stages of progression may have such extreme neuronal dysfunction and death to allow a "re-fueling" with metabolic substrates to help recover integrity and function.
Most of these models entail pre-treatment with the KD (or with BHB), resulting in decreased structural and functional damage from the stroke. At the same time, it must be considered that inherent mitochondrial dysfunction might predispose individuals to adverse toxicities from high fatty acid loads that could overwhelm ?-oxidation within the mitochondrial matrix. KD treatment - either before or after fluid percussion injury in rats - did not alter later seizure sensitivity to fluorothyl, even though the degree of hippocampal cell loss was reduced by pre- but not post-treatment (Schwartzkroin et al., 2010). The heterogeneous etiologies leading to autism spectrum disorders, plus the uncertainty about what causes autism in the majority of "idiopathic" cases, has hampered the development of a universally beneficial treatment, aside from symptomatic treatment of autism-related behaviors such as aggression or anxiety.
Although the intrinsic mechanisms underlying seizures and migraine attacks differ in many fundamental respects, there are theoretical reasons to consider the KD for chronic migraine.
Nine of 28 patients reported "some improvement," although the validity of this clinical study is uncertain and some patients admitted poor compliance. A Low-Carbohydrate, Ketogenic Diet versus a Low-Fat Diet To Treat Obesity and Hyperlipidemia: A Randomized, Controlled Trial.
These effects on weight loss and serum triglyceride level are similar to those in 4 randomized, controlled trials of the low-carbohydrate diet (7–10). Would love to hear about your experiences with a cyclic ketogenic diet in the comments box below. A diabetes nurse told me it is because the pancreas needs regular stimulation to produce insulin, which sounded like bollocks to me, and I couldn’t find any references to support this. While their opinions may vary, every one of them have much more in common than they are different and all share the common philosophy that lifestyle, nutrition, and movement are the key components in not only treating chronic health problems, but more importantly, preventing them in the first place. Sugar raises insulin, which causes inflammation, which is the fundamental cause of heart disease.
Restricting carbs allows the body to use stored fat for fuel rather than the limited fuel obtained from carb intake, he told me. Volek doesn't have a weight problem, but follows the ketogenic diet for its many health benefits, which include reduced inflammation, improved mood, and protection from diabetes and heart disease.
Dominic D'Agostino told me the ketogenic diet can prevent and treat metastatic cancer because cancer is a metabolic disease, and cancer cells thrive on sugar. Today's latest fad diet, the "paelo diet" is another example of a diet based on the ketogenic principles. Of course, most of the medical interest in the diet is to try and develop a line of "ketone" drugs to mimic the diet.
The enormous spectrum of pathophysiological mechanisms underlying the aforementioned diseases would suggest a degree of complexity that cannot be impacted universally by any single dietary treatment. This intriguing clinical observation forms the basis of the hypothesis that the KD may possess anti-epileptogenic properties. At a fundamental level, any disease in which the pathogenesis is influenced by abnormalities in cellular energy utilization - and this implies almost every known condition - would theoretically be amenable to the KD. An important caveat, however, is that yet unidentified mechanisms may operate in diseases outside of epilepsy, and this possibility presents further opportunities for examining the pleiotropic effects of this metabolism-based therapy at a mechanistic level.
With the introduction of anticonvulsant medications in convenient pill form, the use of the KD waned, only to resurge later in the early 1990s, due largely to the efforts of concerned parents who brought the diet back to greater public awareness (Wheless, 2008). However, KDs may induce differential morphological effects in structures such as the hippocampus, perhaps as a consequence of region-specific neuronal vulnerability during the late aging process (Balietti et al., 2008). This view is bolstered by the higher incidence of seizures in patients with AD as compared to the unaffected population (Palop and Mucke, 2009).
In this study, the primary cognitive end-points measured were the mean change from baseline in the AD Assessment Scale-Cognitive subscale, and global scores in the AD Cooperative Study - Clinical Global Impression of Change (Henderson et al., 2009).
Transgenic AD mice fed 2DG demonstrated better mitochondrial function, less oxidative stress, and reduced expression of amyloid precursor protein and ?-amyloid compared to control animals (Yao et al., 2011). One proposed mechanism is increased ROS and free radical formation, which, as discussed above, hampers mitochondrial function. The essential pathophysiological mechanisms that underlie this relentless disorder are yet to be fully elucidated, but similar to other neurodegenerative disorders, the involvement of energy-producing systems likely play a role and mitochondrial dysfunction probably contributes to disease pathogenesis. Certainly, this appears to be the case in a small pilot study of KD treatment in patients with Lafora body disease (Cardinali et al., 2006). Despite this well documented cellular observation, the KD has only recently been considered as a clinical treatment in the oncology field. Experimental data described above attest to significant improvements in mitochondrial function, and many lines of evidence point to the rationale of therapeutically targeting mitochondrial bioenergetics for other disease states (Wallace et al., 2010), but is there any clinical evidence in patients with intrinsic mitochondrial disorders? Further, the occurrence of epilepsy months to years following brain trauma adds to the morbidity of affected individuals, and speaks to the emergence of hyperexcitable neuronal circuits over time. Similarly, in the lithium - pilocarpine model of temporal lobe epilepsy, KD treatment prior to induction led to morphological neuroprotection in the hippocampus but did not affect latency to onset of spontaneous recurrent seizures (Linard et al., 2010). Now, limited clinical evidence raises the intriguing possibility that the KD might be helpful to alleviate some of the abnormal behaviors seen in children with autism spectrum disorders.
Both disorders involve paroxysmal excitability changes in the brain, and there is considerable overlap in the array of pharmacological agents used to treat these conditions.
Compliance might be better with the less restrictive modified Atkins diet, which has also shown promise for migraine treatment (Kossoff et al., 2010). How can a simple dietary change lead to improvement in disorders with such a huge span of pathophysiological mechanisms? Ketogenic diets: an historical antiepieptic therapy with promising potentialities for the aging brain.
A ketogenic diet increases succinic dehydrogenase (SDH) activity and recovers age-related decrease in numeric density of SDH-positive mitochondria in cerebellar Purkinje cells of late-adult rats. Ketogenic diets cause opposing changes in synaptic morphology in CA1 hippocampus and dentate gyrus of late-adult rats. Benefits of caloric restriction on brain aging and related pathological states: understanding mechanisms to devise novel therapies. Peroxisome proliferator-activated receptor alpha and the ketogenic diet.Epilepsia 49(Suppl. Peroxisome proliferator activated receptor ? ligands as anti-cancer drugs targeting mitochondrial metabolism. Ketogenic foods need to be low-carb, rich in good fat (and low in bad, transfat and saturated fat), plus high protein and full of good dietary fiber. Superfood acai and blueberries are loaded with fiber and fatty acid-rich seeds that blast fat. Fish (especially salmon and tuna) are off-the-charts with protein and omega 3 and other omega oils.
Ketones, which our body can produce during fasting or "starvation," is an alternative energy source for those who are insulin resistant.


Yet, it is conceivable that alterations in certain dietary constituents could affect the course and impact the outcome of these brain disorders. It is important to acknowledge that much of the data discussed here are preliminary and anecdotal, and hence need to be validated by well-controlled prospective studies. Specifically, it has been shown that the medium-chain triglyceride (MCT) form of the KD may induce detrimental synaptic changes in CA1 stratum moleculare, but beneficial effects in the outer molecular layer of the dentate gyrus (Balietti et al., 2008). Therefore, there is a rationale for hypothesizing that the KD might have a beneficial role in patients with AD (Balietti et al., 2010a), in addition to the potential benefits to the aging process as noted above. This significant clinical improvement was considered to be secondary to improved mitochondrial function, since ketone bodies (specifically, beta-hydroxybutyrate or BHB) have been shown to protect against the toxic effects of ?-amyloid on neurons in culture (Kashiwaya et al., 2000). In animal models of PD produced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), BHB administration ameliorated the mitochondrial respiratory chain damage that ordinarily results from that toxin (Kashiwaya et al., 2000).
One group found that the KD reduces ROS production in malignant glioma cells, and gene microarray expression profiling demonstrated that the KD induces an overall reversion to patterns seen in non-tumor specimens and a reduction in the expression of genes encoding signal transduction pathways and growth factors known to be involved in glioma growth (Stafford et al., 2010). Hence, in light of the clinical problem of post-traumatic epileptogenesis and the fact that the KD can reduce seizure activity, the notion has emerged that dietary therapy might ameliorate brain injury and possibly, long-term consequences such as epilepsy.
Later, they showed that cognitive and motor functioning was also improved with KD treatment (Appelberg et al., 2009).
Using a KD variant consisting of MCT, 10 of 18 autistic children demonstrated moderate or significant behavioral improvement (by a blinded rater) after a 6-month trial of providing the diet for 4weeks of KD diet treatment alternating with 2weeks of normal diet, in 6-week cycles (Evangeliou et al., 2003).
Although it might seem unlikely that an individual with migraine would undertake such a complicated dietary regimen as the KD, in light of suboptimal alternatives, this choice is worthy of consideration, particularly in the medically refractory population (Maggioni et al., 2011).
The magnitude of weight loss that we observed compares favorably with that achieved with use of weight loss medications approved by the U.S. Flaxseed, millet, oatmeal and quinoa are complex carbohydrates with loads of fiber fatty acids. It is still official government dietary policy today, due to the influence of the vegetable oil industry which produces their products from the highly subsidized corn and soy bean crops.
So with no side effects from a natural diet, it is highly unlikely that any pharmaceutical products will see the same success the Ketogenic Diet is seeing today.
Further, it is possible that a final common neurometabolic pathway might be influenced by a variety of dietary interventions. Along similar lines of improved bioenergetics, the KD has been shown to stimulate mitochondrial biogenesis, resulting in stabilized synaptic function (Bough et al., 2006). The KD has now become an integral part of the armamentarium of most major epilepsy centers throughout the world (Kossoff and McGrogan, 2005). In MCT-fed aged rats compared to aged rats receiving a normal diet, mitochondrial density and function in cerebellar Purkinje cells were significantly increased, suggesting that the KD can rescue age-related mitochondrial dysfunction (Balietti et al., 2010b). Alternatively, the KD may actually decrease amounts of ?-amyloid deposition (VanderAuwera et al., 2005). Additional evidence supporting the potential benefits of ketone bodies in PD is provided by in vitro experiments demonstrating the protective effects of these substrates against mitochondrial respiratory chain dysfunction induced exogenously by complex I and II inhibitors rotenone and 3-nitropropionic acid, respectively (Kim do et al., 2010), and even anti-inflammatory actions of the KD on MPTP-induced neurotoxicity (Yang and Cheng, 2010). Administration of a KD to these mutant mice led to both histological (higher motor neuron counts) and functional improvements (preserved motor function on the rotorod test) compared to non-KD fed animals (Zhao et al., 2006).
It is also interesting to note that PPAR?-activated by nutrients such as fatty acids - is now a target for developing anti-cancer drugs that target mitochondrial metabolism (Grabacka et al., 2010).
This study was carried out on the island of Crete, where the frequency of autism is high but the possibility of genetic inbreeding is also significant. Notwithstanding this limitation, laboratory investigations have found that both short-term and long-term treatment with either MCT or long-chain triglyceride forms of the KD resulted in a significant reduction in the velocity of cortical spreading depression (CSD) velocity in immature rats (de Almeida Rabello Oliveira et al., 2008). Food and Drug Administration, such as orlistat (decrease of about 9% at 6 months) (18–19) and sibutramine (decrease of about 8% at 6 months) (20). The most notable example of a dietary treatment with proven efficacy against a neurological condition is the high-fat, low-carbohydrate ketogenic diet (KD) used in patients with medically intractable epilepsy.
Thus, the potential for interesting and novel applications of the KD and related dietary therapies is almost limitless (Stafstrom, 2004). These observations imply certain risks, but also potential benefits of the KD for the aging brain. Interestingly, other diets such as the Mediterranean diet are showing some promise in AD (Gu et al., 2010), possibly through a reduction in systemic inflammation and improved metabolic profiles. Further, in a pilot trial of the KD in 16 patients with advanced metastatic tumors, six individuals reported improved emotional functioning and less insomnia, indicating that in some instances, the KD may lead to improved quality of life (Schmidt et al., 2011). Other researchers have hypothesized that the neuroprotective properties of ketone bodies might be related to up-regulation of hypoxia inducible factor (HIF1-?) which is important in angiogenesis and anti-apoptotic activity (Puchowicz et al., 2008).
These authors observed that half of these patients became seizure-free on the KD, and only four patients failed to respond.
Thus, at this juncture, there is no consensus regarding whether the KD is anti-epileptogenic following a variety of traumatic insults and manipulations. Therefore, these findings need to be interpreted cautiously and larger longitudinal studies are needed. Another intriguing aspect of this study was the observation that triheptanoin - an anaplerotic substrate that enhances tricarboxylic acid cycle function - had a notable effect in retarding CSD, consistent with a later report that triheptanoin supplementation raised pentylenetetrazol tonic seizure threshold and delayed the development of corneal kindled seizures (Willis et al., 2010). Ultimately, the details of how that altered metabolism reduces neuronal excitability, abrogates ongoing neurodegeneration, or mitigates functional disability remain unknown. The effects of a ketogenic diet on behavioral outcome after controlled cortical impact injury in the juvenile and adult rat. Ketogenic diet prevents alterations in brain metabolism in young but not adult rats after traumatic brain injury. 2-Deoxy-D-glucose reduces epilepsy progression by NRSF-CtBP-dependent metabolic regulation of chromatin structure. Caloric restriction inhibits seizure susceptibility in epileptic EL mice by reducing blood glucose. Here are ketogenic diet foods with the three-pronged low-carb, good fat, high protein combination. Coconut oil--another superfood--is high in CLA, ALA and GLA (conjugated, alpha and gamma linolenic acids) that melt bad stored body fat away! While the mechanisms through which the KD works remain unclear, there is now compelling evidence that its efficacy is likely related to the normalization of aberrant energy metabolism.
However, the fact that the KD reduces oxidative stress and its downstream consequences provides a reasonable rationale for considering this type of treatment to retard the adverse consequences during aging (Freemantle et al., 2009). Mitochondria from these mutant mice demonstrated increased ATP synthesis, countering the inhibition of complex I of the electron transport chain. In contrast, a retrospective examination of five patients with tuberous sclerosis complex treated with the KD indicated either a lack of tumor suppression or further tumor growth (Chu-Shore et al., 2010).
In that study, pre-treatment with BHB (via intraventricular infusion, followed by middle cerebral artery occlusion) led to significant increases in brain succinate content, as well as elevations in HIF1-? and Bcl-2, an anti-apoptotic protein.
Hence, these preliminary data suggest that the KD is not necessarily contraindicated in patients with mitochondrial respiratory chain abnormalities. Consistent with these observations, it was found that fasting - which shares the key feature of ketosis with the KD - led to significant tissue sparing in brain following CCI injury, and that again ketosis (with improved mitochondrial functioning) rather than the relative hypoglycemia seen with fasting was the important determinant of neuroprotection (Davis et al., 2008). The potential involvement of adenosine, an endogenous neuromodulator and anticonvulsant, in ameliorating autistic behaviors raises the possibility of overlap with KD mechanisms (Masino et al., 2011). Herein lay rich opportunities for further investigation, in both the laboratory and the clinic, in the broad realm of translational neurosciences.
The concept that many neurological conditions are linked pathophysiologically to energy dysregulation could well provide a common research and experimental therapeutics platform, from which the course of several neurological diseases could be favorably influenced by dietary means. As an example, T-maze and object recognition performance were improved in aged rats by KD administration, suggesting a potential functional benefit in cognition (Xu et al., 2010). It is important to note that approximately 20% of the familial cases of ALS have SOD1 mutations, and hence the possibility arises that the KD may be of benefit to patients with ALS. Thus, it may be that distinct tumor types within different organ systems may respond differently to the KD or other dietary treatments and that such differences may reflect variations in the metabolic vulnerability of specific tumor types, perhaps through intrinsic differences in the expression of metabolism-related genes (Stafford et al., 2010). To be clinically meaningful, of course, a positive effect must be demonstrable after, and not before, an ischemic event.
As a caveat, many children with autism poorly tolerate changes in dietary and other routines, which could impact implementation of dietary therapies, which require strict adherence. Here we provide an overview of studies using the KD in a wide panoply of neurologic disorders in which neuroprotection is an essential component.
Finally, it should be noted that because of its similarities to calorie restriction (as noted above), the KD is likely to involve other neuroprotective mechanisms that could ameliorate pathological aging - especially when occurring in the context of neurodegeneration (Contestabile, 2009). Nevertheless, such studies imply that biochemical alterations that favor energy metabolism would be protective against acute forms of severe brain injury. Thus, it is critical to determine the specific mitochondrial defect when considering treatment with the KD, to avert clinical deterioration. Burn fat with a high protein, superfood, ketogenic diet shake of coconut milk, almonds, blueberries, chia seeds, flaxseed, Greek yogurt and avocado.



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