High fat diet ibs,low fat high energy meal plan,how do bulimics lose weight so fast,diet to lose weight fast youtube - And More

20.07.2014
The low-fat diet has been on life support since 2006, when the failure of the WHI trial was published. About 7,500 people were randomized to either get advice on a low-fat diet or a Mediterranean diet with more fat, specifically olive oil or nuts. All the ratios and micronutrient percentages are like this: almost identical across the three studies. It's almost as if they were trying to keep the macronutrient rations identical, so they could claim that the benefits were the result of the olive oil and the nuts, who coincidentally sponsored the study. What this study does do, is compare a standard diet to a diet that raises either nuts or olive oil. Results -- There was no significant reduction in heart attacks, death from cardiovascular causes, or death from any cause.
One wonders if it is even possible for people with a specific point of view to read such reports without self administered distortion. 4Mike HFebruary 25 2013It is funny to me that the "Mediterrannan Diet" seems to be the politically correct term for low carb. The statistically significant difference was in the primary endpoint: major cardiovascular events. If they are uses as the typical "low fat" model, then you need to look at 10% of calories as fat. This study is good and useful, but only when looking closely at the actual facts, groups, and diets involved. I could easily tell a person on a standard diet to follow this version of the Mediterranean diet assuming they were unlikely to do anything more intensive. Wouldn't it be wonderful if we were all devoted to finding the healthiest diet, and not our preconceived notions. What I find amusing is that the critics of this latest study argue that anybody who considers the study valid is filled with preconceived notions.
I've visited other blogs that caught my interest, only to discover that I do not agree with the points of view being expounded there.
I'm a mother of 16 month old twins and ever since they were born my body has been deteriorating from lack of sleep and stress from working, going to school, chasing babies, and still having to get dinner on the table. Oh and side note: Not even a slight increase in exercise and I still got all these amazing results! One thing the study didn't have in Table 1, however, was besides the recommendation to avoid baked goods it didn't mention anything about avoiding or recommending pasta in the mediterranean part. I have looked at the table re dietary advice given in this study, and it does indeed look like standard low fat diet advice. 29vkoolNovember 7 2013Low-fat diet did not succeed in preventing heart disease but it is still a good diet to follow. Synthetic oils of the last 200 years high in omega 6 and low or zero omega 3's like corn oil, soy oil, canola oil etcetera that are mnufactured at high temperatures are cheap and everywhere. You don’t even have to eat more calories, eating the same amount of calories, but simply eating more fat, changed muscle function. Processed food manufacturers are in the business of making and therefore selling their food. Foods that contain higher levels of salt, sugar, fat are the most likely to alter brain chemistry and cause people to overeat. Swedish researchers tracked the increase of processed (116%) and ultra processed foods (142% increase) from 1960-2000.
And the last study I read recently that I found fascinating and related is that high fat diets change your behaviour, and you probably already guessed it, not in a good way. High fat diets cause a number of problems, heart attacks and strokes are the most common, but now science has found that high fat diets can cause depression and other psychiatric problems. 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.
Anybody can claim one diet is better than another, but it's not worth listening if they don't present sound evidence.
Both of my shoulders were going out almost everyday for the past year and a half, my knees have been constantly hurting since February 2012, i'd gained 65 lbs since I had the twins and about 3 months ago I started to feel an arthritic-like pain in my hands.
And I say that as someone who is firmly convinced that the overall evidence is indeed in its favour. I think that this study say that if one get free olive oil or nuts, one eat those and cut out other foods! They may initially comply; but over time people drift back to the average 15 to 20 percent of calories from protein. There are plenty of times you might eat high fat foods, not only on holidays and vacations, and it only takes 5 days to change your metabolism. Since 1980, when 857 million were classified as obese or overweight to 2013 when that number rose to 2 billion, 3-4 million people die yearly from related complications. Another study that just came out proves that the more highly processed foods are linked to addictive eating. Instead of being satisfied, eating these salt, fat, sugar combos are more likely to cause you to want more. Processed foods have high calorie density but low nutritional density and the increased intake mirrors the obesity rates in Sweden.


Processed food did with all the variations on how we can eat it, then we couldn’t stop.
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. We are committed to maintaining a lively but civil forum for discussion, so we ask you to avoid personal attacks, and please keep your comments relevant and respectful.
Instead people with pre-existing heart disease had a 30 percent increase in risk of heart disease!
There was a reduction in cardiovascular causes only when these were pooled with deaths from stroke . His studies included multiple variables and to state that the variable that mattered was fat is simply unproven.
If you have time, I'd be interested to hear you thoughts on this specific point, rather than linking back to "what the diet looked like"? Was on low fat diet for diabetes ldl 325, weight 340, high blood pressure, high cholesterol, every health marker bad. Your muscles make up about 30% of your weight and are responsible for breaking down or storing glucose for energy. Muscle is critical for normal glucose metabolism and can have dramatic consequences to your health if normal metabolism is changed. The doctor and lawyer David Kessler, author of The End of Overeating, says the food industry manipulates our brain’s neurological response and designs foods to make us eat more then we should. 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. If you encounter a comment that is abusive, click the "X" in the upper right corner of the comment box to report spam or abuse. It would help Dean Ornish's argument if he actually performed a valid experiment instead of just speculating. It doens't even say where this supposed research came from or what kind of study it is which is very important.. I'm a walker and i've probably taken a 30-35 minute walk almost everday since I was about 11. 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). 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). A new study tracking more than 157,000 US households for one year shows that highly processed foods make up more than 60% of the calories in the food we are buying.
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. I've tried weight watchers, jenny craig, doing it on my own, and other various "lifestyle changes" none of which lasted very long and most of which left me hungry most of the time. 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.



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