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A new study published this month (April 2014) compared two diets with overweight diabetic people.
The other group, almost in direct contrast to the ADA diet, was encouraged to eat a a very low carbohydrate, high fat, non calorie-restricted ketogenic diet. The ADA diet group, despite eating far fewer calories per day than the ketogenic diet group, did not lose as much weight as the ketogenic diet group. This study is simply another of many studies looking at the ketogenic diet and its effects on health, as compared to the standard USDA approved diet, which is now linked to promoting disease rather than health. The health benefits of carbohydrate restriction (NOT calorie restriction) and healthy fats were once common knowledge, as this clip from the popular 1960s Andy Griffith show portrays. A Randomized Pilot Trial of a Moderate Carbohydrate Diet Compared to a Very Low Carbohydrate Diet in Overweight or Obese Individuals with Type 2 Diabetes Mellitus or Prediabetes.
Does an Italian village filled with cigarette smoking centenarians hide the secret to long life? For to be free is not merely to cast off one's chains, but to live in a way that respects and enhances the freedom of others.
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. September 2009 – I eliminated most sources of sugar in my diet (for a definition of “sugar” click here) six days per week.
January 2011 – I reduced starch intake to one serving per day, but continued to eat fruits and vegetables in an unrestricted manner. May 2011 – Reduced carbohydrate intake to less than 50 grams per day and reduced protein intake to approximately 120 grams per day, entering a state of nutritional ketosis.
Another way to see the implications of these changes on my actual intake is shown in the figure below.
The most externally obvious change that occurred as I ratcheted down my carbohydrate intake was a decrease in body fat.
The other (profoundly simple) “test” I used to track my weight loss was my waist measurement. Between February 2010 and July 2010 I had a bad bout of swine flu, which left me in pretty rough shape for a while. Pay more attention to fat mass, separately, than overall body weight, and do the same with lean mass. Most people, especially physically active people, probably experience some seasonal variation in body fat, especially at low levels.
Establishing the metabolic state of ketosis even for a short period of time has many outstanding benefits. Establishing this metabolic state of ketosis even for a short period of time has many outstanding benefits. The main benefit of ketosis is that it increases the body's ability to utilize fats for fuel, which gets very lazy on a high-carbohydrate diet. Another benefit has to do with the low levels of insulin in the body, which causes greater lipolysis and free-glycerol release compared to a normal diet when insulin is around 80-120.
Another small but very important benefit of the ketogenic diet is that when in the state of ketosis, ketones, along with a high protein intake, seem to suppress appetite.3 A high-carbohydrate diet, on the other hand, increases hunger levels.
Fatty acid production in fat tissue is stimulated by epinephrine and glucagon, and inhibited by insulin. When the body's glycogen stores begin to get depleted, rates of beta-oxidation increase, resulting in the mobilization of free fatty acids from fat tissue. I feel the benefits of the ketogenic diet outweigh the pitfalls, but as with any diet, speak with your doctor first. During the first few weeks of the ketogenic diet, the body has to go through the "metabolic shift," as Dr.
Once the body gets used to manufacturing ketones as the main energy substrate, the body actually has more energy than it previously had, and you won't have to be fighting through all those low-blood-sugar crashes your high-carb meals previously gave you.
Blood-lipid profile is also a concern on the ketogenic diet due to the staggering amounts of saturated fats in the diet, although the diet can be centered around healthier unsaturated fats—which isn't as fun as eating an egg and cheese omelet, fried in butter, with bacon on the side! Blood-lipid-profile issues are experiencing much debate; some people following the ketogenic diet will experience a drop in cholesterol levels, but for some people, cholesterol levels will increase.
Because carbohydrates are restricted to less than 50 grams a day, the issue of micronutrient deficiencies can occur. Ketoacidosis occurs when the level of ketones in the blood gets out of control, which poses a severe health risk for diabetics.
Ketosis is different, because, when in the state of ketosis, the brain will prefer ketones over glucose. Through experimentation, I have found that the best way to get into the metabolic state of ketosis is by starting off using a fairly high-fat intake with smaller amounts of protein. Ultimately, you want your macronutrient range to look something like this— Fats should comprise the majority of your calories, anywhere from 60 to 70 percent of your daily caloric intake. DIETLow-Carb Ketogenic Diet Beats Low-Fat, Low-Calorie Diet For Weight Loss Says Harvard DoctorBy Samantha Chang, January 4th, 2016Physician and Harvard professor Dr. A low-carb, high-fat ketogenic-style diet promotes weight loss and prevents diabetes and metabolic syndrome better than a low-fat, low-calorie diet, says Harvard professor and physician Dr. The true cause of weight gain isn’t eating too many calories, but a diet that’s high in refined carbs and sugars. Ludwig join a growing number of medical experts who are dispelling the myth that eating fat makes you fat and calorie restriction is best for weight loss. The most effective way to lose weight is to prevent blood-sugar and insulin spikes, which the LCHF Atkins and ketogenic diets do, say obesity scientists. Eating refined carbs such as a 100-calorie pack of jelly beans (which are fat-free) causes a massive 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 fuel inflammation, which in turn contribute to diabetes, heart disease, Alzheimer’s and cancer. An avalanche of new scientific research suggests unprocessed saturated fat is not the cause of weight gain, diabetes or heart disease as we have long been told. What fuels weight gain and disease is inflammation — which is caused by a high-carb diet — especially one high in sugar, explained 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 slowly killing us, said Westman, who has helped hundreds of people lose thousands of pounds on a LCHF diet. Westman has been aware of the health benefits of unprocessed dietary fat for years and is glad there’s a growing vindication of this important macronutrient.
Restricting carbs and eating more healthy fats allows the body to use stored fat for fuel rather than the limited fuel obtained from carb intake, said Volek, who has followed a ketogenic diet for the past 20 years, and credits it for his excellent health.
Volek doesn’t have a weight problem, and follows the ketogenic diet for its many health benefits, which include reduced inflammation, improved mood, and protection from diabetes and heart disease. Volek, author of The Art and Science of Low Carbohydrate Living, is encouraged by the increasing popularity of high-fat diets such as the ketogenic diet, as more people are beginning to accept that eating fat does not make you fat. 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. Scientific studies show the ketogenic diet is better than drugs for managing epilepsy-induced seizures, can reverse type 2 diabetes, and manage cancer, said Boston College professor Thomas Seyfried.
Seyfried’s decades of research suggests the low-carb ketogenic diet can fight cancer because cancer is a metabolic — not a genetic — disease.
For tips on how to lose weight without hunger and prevent heart disease, dementia and cancer, check out Dr. Their goal was to reach a state of "ketosis," defined as a blood beta-hydroxybutyrate level between 0.5 and 3 mM, as measured twice a week at home using blood ketone test strips.


7 out of 11 ketogenic dieters (64%) were able to reduce their anti-diabetic medications, whereas only 2 out of 13 ADA dieters did (15%). The ketogenic diet was originally developed by John Hopkins Hospital in the 1920s as an effective method of curing epilepsy and seizures in children, when drugs did not work. Aunt Bee's apple pie is seen as something to limit or even skip because of the dangerous "carbohydrates and glucose", while meatloaf was seen as healthier. 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.
As a result, I probably lost more lean mass than I would have liked, or expected to, even transiently.
My body fat probably fluctuations between 7 and 10% over the course of year now, often a function of activity type (more than activity level).
The metabolic state of ketosis simply means that the quantity of ketone bodies in the blood have reached higher-than-normal levels. When on high-carbohydrate diets, the body can usually expect an energy source to keep entering the body. Since the body has copious quantities of fat, this means there is no need to oxidize protein to generate glucose through gluconeogenesis. Insulin has a lipolysis-blocking effect, which can inhibit the use of fatty acids as energy.
Because you have to consume a lot of fat on a ketogenic diet, which hold 9 calories per gram, you are not getting much food volume. Additionally, hydration should be an area of high priority, especially before, during, and after exercise. Thiamin, folate, calcium, iron, potassium, and magnesium are typically inadequate in low-carb diets. When massive quantities of ketones are produced, the pH level of the blood drops, creating a high-acidic environment. After your body gets into ketosis, the fat intake can be reduced and the protein intake can be increased. Protein intake should be around 20 to 30 percent of your daily calorie intake, and carbs should not exceed 50 grams per day. We are your personal trainer, your nutritionist,your supplement expert, your lifting partner, your support group. David Ludwig says you can enjoy weight loss without hunger with a low-carb ketogenic-style diet.
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.
In contrast, eating 100 calories of nuts (which are high-fat and low-carb) will produce a negligible insulin spike.
By curbing these pro-inflammatory blood-sugar spikes with a low-carb, high-fat diet, you can stem several diseases in one fell swoop and slow down cellular aging. The true cause of obesity, cardiovascular disease, high cholesterol and diabetes is a high-carb diet, especially one high in sugar.
Eric Westman also champions a low-carb, high-fat ketogenic-style diet for weight loss and reversing type 2 diabetes. Sugar raises insulin, which causes inflammation, which is the fundamental cause of heart disease. 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. Thomas Seyfried says his decades of research show cancer is a metabolic disease that can be managed with a low-carb ketogenic diet. 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.
My goal was to reduce my waist to 32 inches and I calculated I would need to lose 20 pounds of fat, without losing any muscle mass, to do this. Lean mass took a big hit initially (although I believe in my case, the prolonged illness didn’t help), but then recovered. But in the state of ketosis, the body has to become efficient at mobilizing fats as energy. Also, when insulin is brought to low levels, beneficial hormones are released in the body, such as growth hormone and other powerful growth factors. Insulin's purpose is to keep blood glucose levels in check by acting like a driver, pushing the glucose into cells. This usually happens when a person skips meals, or does not consume adequate amounts of carbohydrates for an extended period of time.


Others can be partially oxidized to form the substrate acetoacetate, which is then converted to beta-hydroxybutyric acid; collectively, these are termed ketone bodies. While going through this, the body will experience a small degree of fatigue, brain fog, and even dehydration due to the increased water loss associated with ketoic-induced diuresis and water loss from depletion of glycogen stores. The best thing to do to avoid this is to make sure you take a high-quality multivitamin to ensure you get 100 percent of the daily value.
Nondiabetics need not fear, as the regulated and controlled production of ketone bodies allows the blood pH to remain within normal limits.
Added to that, some dieters do copious amounts of aerobic exercise when dieting, which can cause further breakdown of muscle. We provide the technology, tools, andproducts you need to burn fat, build muscle, and become your best self. 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’s a pretty remarkable test that is now the gold standard for measuring body composition. As silly as this sounds, I recall, back in the spring of 2009 while stuck in an airport, using calculus to integrate the volume of fat I needed to lose from my waist (both visceral – around my organs – and under my skin) to get down to a 32-inch waist. Total body weight is shown on top of each bar, while the blue bar represents lean tissue and the red bar represents fat.
The body will start breaking down your own body fat to fuel the body's normal, everyday functions. When this happens, glucagon is secreted by the pancreas to break down stored glycogen in the liver into a more usable form, glucose. Ketones can be used by all tissue containing mitochondria, which includes muscle and the brain. Also supplementing with a fiber supplement is a good idea to make sure your plumbing doesn't get clogged. The brain can also call on protein to create more glucose for energy needs—a process called gluconeogenesis. 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). Back when I was in high school we relied on a combination of calipers (in the hands of an experienced user) and something called hydrostatic testing, where you are weighed in and out of water to calculate your percentage of body fat. It’s actually an easy problem if you can remember how to integrate the volume of an oval “cylinder” and you know the density of fat. Hence, in September 2009, I weighed 195 pounds, of which 156 was lean, 39 was fat, and my body fat (the number below) was 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. Doing in the “wrong” way can result in equal loss of fat and lean mass (or, worse yet, disproportionate loss of lean mass). 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. Without any loss of lean tissue, I had reduced fat mass to 13 pounds and body fat to under 8%. 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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