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Ketogenic Diet Raises Brain Energy (Press Release)
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Ketogenic Diet Raises Brain Energy (Press Release)
Source: Johns Hopkins Medical Institutions
Date: 2003-12-10 Atkins Diet May Reduce Seizures In Children With Epilepsy Along with helping some people shed unwanted pounds, the popular low-carbohydrate, high-fat Atkins diet may also have a role in preventing seizures in children with epilepsy, say researchers at the Johns Hopkins Children's Center. Related News Stories Ketogenic Diet Reduces Seizures In Many Children, Hopkins Researchers Find (October 1, 2001) -- Johns Hopkins neurologists report that a rigorously high-fat, low-carbohydrate diet not only reduces the number of seizures in children with severe seizure disorders, but also keeps the frequency of ... full story Controversial Atkins Diet May Be Beneficial For People With Epilepsy (February 1, 2005) -- Imagine that your child with epilepsy could have seizures less frequently, by eating more protein and less carbs. The first comprehensive review of possible dietary treatments of epilepsy has .... full story Very Low-carbohydrate Diets Work For Men And Upper Body Fat (November 15, 2004) -- Scientists say that low carbohydrate diets, like the Atkins and South Beach Diets, may actually be the best option for men who want to slim. New research, published this week in the Open Access ... full story Atkins Diet Shows Surprising Results, Researcher Says; One-year Study Shows Diet May Be As Effective And Safe As Conventional Diets (May 22, 2003) -- A 3-center study led by researchers at the Weight and Eating Disorders Program of the University of Pennsylvania School of Medicine reports the results of the first controlled trial of the Atkins ... full story In a limited study of six patients, including three patients 12 years old and younger on the Atkins regimen for at least four months, two children and one young adult were seizure-free and were able to reduce use of anti-convulsant medications. Findings of the study, scheduled for presentation today at the American Epilepsy Society Meeting in Boston, also showed that seizure control could be long-lasting on the diet, with the three patients continuing to be seizure-free for as long as 20 months. The researchers caution that because of the small number of study subjects, their look at the relationship between the Atkins diet and seizure control should not lead to its routine use in children with epilepsy, nor at this point should the Atkins diet be used to replace the ketogenic diet the rigorous high-fat, low-carbohydrate diet already proven to reduce or eliminate difficult-to-control seizures in some patients. The common elements in both diets are high fat and low carbohydrate foods that alter the body's glucose chemistry. The ketogenic diet mimics some of the effects of starvation, in which the body first uses up glucose and glycogen before burning stored body fat. In the absence of glucose, the body produces ketones, a chemical byproduct of fat that can inhibit seizures. Children who remain seizure-free for two years on the ketogenic diet often can resume normal eating and often their seizures don't return. The Atkins diet, while slightly less restrictive than the ketogenic diet, also produces ketones. "We just don't know yet how effective the Atkins diet is in reducing seizures or if it comes close to the benefits of the ketogenic diet, but our report raises new questions about the ideal level of calorie and protein restriction imposed by the ketogenic diet," said the study's lead author, Eric Kossoff, M.D., a pediatric neurologist at the Children's Center. "By learning more about how the Atkins diet works to control seizures, we should learn more about which patients may benefit best from either or both of these diets," he added. "It may be, for example, that some of those who can't tolerate the restrictiveness of the ketogenic diet could be helped with Atkins." In the short term, Kossoff says it's possible the Atkins diet could be used in selected patients as a "trial run" for individuals considering the ketogenic diet in the future. "Success on the Atkins diet may be a good indication of patient compliance and efficacy of the ketogenic diet," he adds. "Because the Atkins diet is easy to read and versions of it are available in paperback at bookstores, families can easily follow this kind of a strict, low-carbohydrate diet on their own for several weeks to determine if this is something they can adhere to." Also, because the Atkins diet was originally designed for weight loss, Kossoff says it is possible patients following the diet to reduce seizures may lose weight in the process. If that does occur, and a patient's weight has reached unhealthy levels, the patient should be instructed to increase calorie intake by eating more fats and proteins. In the Hopkins study, patients began with 10 grams of carbohydrates per day, more than the typical amount provided on the ketogenic diet, but fewer than used in the induction phase of the Atkins diet (20 grams/day). Carbohydrate intake was gradually increased for some patients. Five out of the six patients attained ketosis (the state of producing ketones) within days of starting the Atkins diet and maintained moderate to large levels of ketosis for periods of six weeks to 24 months. Kossoff says that Hopkins researchers will further examine the role the Atkins diet plays in the management of epilepsy in a larger clinical study of 20 children with epilepsy, which began in September 2003 and already has enrolled several patients. Co-authors of the current study were Gregory L. Krauss, Jane R. McGrogan, and John M. Freeman of the Department of Neurology at the Johns Hopkins Hospital. -- Ken "Buddhism elucidates why we are sentient." "Karma means that you don't get away with anything." "jbuch" wrote in message ... | The high-fat diet (Ketogenic Diet, KD) has long had medical uses, and | now there is beginning to be an understanding. | | Contact: Holly Korschun | | 404-727-3990 | | Emory University Health Sciences Center | | Ketogenic diet prevents seizures by enhancing brain energy production, | increasing neuron stability | | | WASHINGTON, D.C. -- Although the high-fat, calorie-restricted ketogenic | diet (KD) has long been used to prevent childhood epileptic seizures | that are unresponsive to drugs, physicians have not really understood | exactly why the diet works. New studies by a research team at Emory | University School of Medicine show that the diet alters genes involved | in energy metabolism in the brain, which in turn helps stabilize the | function of neurons exposed to the challenges of epileptic seizures. | This knowledge could help scientists identify specific molecular or | genetic targets and lead to more effective drug treatments for epilepsy | and brain damage. | | ,,,, | The ketogenic diet causes molecules called ketone bodies to be produced | as fat is broken down. Scientists have understood that these molecules | somehow cause a change in metabolism leading to a potent anticonvulsant | effect. According to some animal studies they also may limit the | progression of epilepsy. | | | | | | -- | 1) Eat Till SATISFIED, Not STUFFED... Atkins repeated 9 times in the book | 2) Exercise: It's Non-Negotiable..... Chapter 22 title, Atkins book | 3) Don't Diet Without Supplimental Nutrients... Chapter 23 title, Atkins | book | 4) A sensible eating plan, and follow it. (Atkins, Self Made or Other) |
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Ketogenic Diet Raises Brain Energy (Press Release)
Given the clear benefits of a ketogenic diet, fat-busting per se is
probably short-sighted. Nevertheless, here are some notes on CD36. I wonder how much in the way of ketogenic benefits stem from some sort of CD36 action. CD36 null mice have much less fatty acid uptake in heart, skeletal muscle and adipose tissues and less incorporation of fatty acids into triglycerides leading to an accumulation of diaglycerides; CD36 is heavily expressed in these organs [PMID 11478366] human cells recognize foreign antigens via the TLR system; CD36 scavenges potentially dangerous endogenous molecules from the body like oxidized and crosslinked proteins; CD36 may be a mediator in sterile inflammation and the TLR system may be involved as well; some TLR2 ligands related to bacterial infection are dependent on CD36 http://www.sciencedaily.com/releases/2005/03/050326002258/htm, [PMID 15690042] pregnant mice on a low-carb, high-fat diet ate fewer calories and had offspring which with half the liver triglycerides and higher levels of hepatic proteins like CD36, CPT-1 and PPARalpha http://www.sciencedaily.com/releases/2004/11/041123111459.htm a high unsaturated fat, high protein, low carbohydrate diet for pregnant rats dramatically lowered hepatic triglycerides and raised PPARalpha, CD36 and carnitine palmitoyltransferase-1 (CPT-1) in their adult female offspring [PMID 15319218] (hyperglycemia triggers overexpression of CD36 in kidney cells leading to chronic kidney disease after substances in diabetic blood bind to CD36 and trigger the death of these kidney cells http://www.sciencedaily.com/releases/2005/02/050223125732.htm); green tea catechins downregulate genes for PPARgamma, CD36, LXR-alpha, C-myc and upregulates transcription of PPARalpha and LDL-R (LDL receptor); this may be how green tea inhibits atherosclerosis [PMID 15022174] http://www.scientificamerican.com/ar...&articleID=000 AFE88-E770-1367-A6B083414B7F4945 November 14, 2005 Newsletters | RSS SCIENCE NEWS Potential Taste Receptor for Fat Identified French scientists have identified a protein receptor that resides in the taste buds and may be responsible for sensing fat. As such, this so-called fatty acid transporter, known as CD36, could be to blame for our love of high-fat foods--and could thus serve as a possible target for treatment of obesity. If the link bears out, CD36 would allow fat to join the five previously identified tastes that govern the experience of food: bitter, salty, sweet, sour and "umami," or savoriness (like the meaty goodness of soup stock). Researchers have long debated whether a sensor for fat existed, given that many animals display an innate attraction to fats. To determine whether CD36 -- a protein expressed in the taste buds -- might be the culprit, a team at the University of Bourgogne devised an experiment using mice that had been genetically modified to lack CD36. These mice, along with a group of wild mice were fed two solutions: one laced with fat and one containing xanthan gum to mimic fat's mouthfeel. Wild mice craved the fatty solution. The mice missing CD36, in contrast, showed no preference either way. In addition, neither group exhibited a change in either their desire for sugar or aversion to quinine, indicating that CD36's effect was limited to fats. Furthermore, removal of the CD36 gene in rats prevented their digestive tracts from preparing the various gastric juices necessary to digest fat. "Because expression of CD36 within the oral cavity and its effect on digestive secretions are conserved in mice and rats, it is likely that CD36 performs a basic function in the taste bud cells," Philippe Besnard and his fellow authors conclude in the current issue of the Journal of Clinical Investigation. The authors caution, however, that further studies are needed to determine whether CD36 is indeed the elusive fat sensor, how it signals fat to the taste bud, and, ultimately, why that prompts craving. "The sensory experience of food can be a primary reinforcer of intake," writes Nada Abumrad of Washington University in an accompanying commentary. "As more is learned about the specificity and mechanism of this receptor's function, it may be possible to devise strategies to treat some forms of obesity." --David Biello |
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Ketogenic Diet Raises Brain Energy (Press Release)
I keep hearing warnings from doctors that ketones are bad
for the heart, but I can't find any evidence for this. This widespread belief in medicine seems to come from studies of diabetics who have elevated ketone levels due to the same metabolic defects which pose a risk to their hearts. Since this old wives tale is making the circuit again, I thought I'd post the information I could find on the subject. FYI, diets like Atkins or South Beach are moderately ketogenic. Finally, I tacked on a comparison of high carb diets to low carb diets and what they did to cholesterol. As usual, the write assumes lowering cholesterol is a per se good thing. I wonder if the cholesterol-lowering effects of the high carb diet might partly explain why people with higher cholesterol levels live longer - they're eating more fats, have a higher levels of ketones in their blood and this makes their brains and other organs healthier by, among other things, protecting mtDNA. Anybody bothered to ever check mtDNA stability vs. cholesterol and ketone levels? (It would be useful if the authors broke high carb diets down according to glycemic index.) http://www.nytimes.com/aponline/nati...t-Matchup.html High Carbs Plus Protein Could Help Heart By THE ASSOCIATED PRESS Published: November 15, 2005 Filed at 9:38 p.m. ET CHICAGO (AP) -- Deciding what to have for a healthy breakfast just got a little easier. While a healthy high-carb diet has been shown to be good for you, replacing a few of the carbohydrates with a little protein like scrambled egg substitute or beneficial fats like olive oil margarine could be even better, helping further reduce heart disease risks, a study found. At dinner, this might mean instead of pasta, trying black bean tacos and multigrain pilaf with olive oil, the researchers said. They had volunteers try three variations of the same diet, all of them low in saturated fats and including plenty of fruits and vegetables. All three improved blood pressure and cholesterol readings after just six weeks, and adopting any of them would be beneficial, said lead researcher Dr. Lawrence Appel of Johns Hopkins School of Medicine. ''Most people aren't following anything close to any of these,'' he said, adding that the bottom line is: ''You can eat healthy in three different ways, and two of them are a bit better than the other.'' Appel presented the results Tuesday at an American Heart Association conference in Dallas. The study also appears in Wednesday's Journal of the American Medical Association. All participants tried each of the diets, eating meals prepared in a research kitchen and taking a few weeks' break before starting the next diet. The volunteers' average blood pressure started out borderline high -- 131 over 77. Systolic pressure -- the top number in blood pressure readings -- fell by an average of about 8 points while they were on the carb diet, 9.5 points on the protein diet and 9.3 points on the healthy fats diet. Levels of LDL cholesterol, the bad kind, measured 129 on average at the start; 100 is considered optimal. LDL levels fell an average of almost 12 points on the carb diet, about 14 points on the protein diet, and about 13 points on the healthy fats diet. Those reductions likely would translate into less heart disease if the diets were widely adopted, the researchers said. They estimated that for every 100 people with mild high blood pressure, there would be one less heart attack over 10 years for those on the protein or healthy fats diet, compared with the more carb-friendly diet. Appel said the high-protein diet also seemed to produce feelings of fullness and reduced appetite. ''These symptoms raise the intriguing possibility that if individuals were to follow these diets long-term, there may be some weight loss on the protein diet,'' he told conference participants. Dr. Timothy Gardner, a Delaware cardiologist, said at the meeting that the study was ''a tricky, difficult type of study to conduct, controlling all the factors, with very interesting results.'' A JAMA editorial about Appel's research, which was funded by the National Institutes of Health, questioned whether people in the real world would stick to the diets since they'd have to buy and prepare their own meals. ''Longer trials examining actual cardiovascular event outcomes will be needed to convince a skeptical public of the benefit of yet another unique and difficult-to-achieve dietary regimen,'' said editorial author Dr. Myron Weinberger of Indiana University. Rachel Johnson, a University of Vermont nutrition professor, said the results refine ''what we already know. It's not a huge about-face.'' ------ On the Net: JAMA: http://jama.ama-assn.org American Heart Association: http://www.americanheart.org Epilepsia. 2003 Apr;44(4):618-20. Related Articles, Links Selenium deficiency associated with cardiomyopathy: a complication of the ketogenic diet. Bergqvist AG, Chee CM, Lutchka L, Rychik J, Stallings VA. Division of Neurology, The Children's Hospital of Philadelphia, Department of Pediatrics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA. PURPOSE: The ketogenic diet (KD) is an efficacious treatment for intractable epilepsy, associated with infrequent side effects. The KD is known to be deficient in most vitamins and minerals and may be deficient in trace minerals. We report biochemical selenium deficiency in nine patients on the KD, including one who developed cardiomyopathy. METHODS: A whole-blood selenium level was obtained on the symptomatic patient after noting the patient's poor appearance on physical examination. Children already treated and children beginning the KD were then evaluated prospectively for selenium status by measuring whole-blood or serum selenium as part of routine laboratory evaluation every 3 months. RESULTS: The index case had no detectable whole-blood selenium. Cardiac physical examination and ECG were normal, but the echocardiogram revealed cardiomyopathy. Thirty-nine additional children had the selenium status evaluated. Eight had selenium levels below the normal range (six initially, and two developed low selenium levels on serial testing). They were referred for cardiology evaluations, which were normal. Selenium supplementation improved levels in all children. Low levels were seen in some children after only a few months of treatment. CONCLUSIONS: The nutrient adequacy of the currently used KD has not been fully evaluated. The nutrient content of KD with usual supplements may not meet Recommended Dietary Allowances (RDA) for selenium and may not provide other trace minerals in adequate amounts. At our center, selenium deficiency was found in 20% of the patients evaluated. Screening for selenium deficiency is suggested if the patient KD regimen does not meet or =75% of the RDA or if the child is symptomatic. Nutrient supplementation should provide adequate trace elements for children treated with the KD. The KD requires close monitoring of the overall nutritional status. Publication Types: * Case Reports PMID: 12681013 [PubMed - indexed for MEDLINE J Child Neurol. 2004 Jul;19(7):555-7. Related Articles, Links Lack of long-term histopathologic changes in brain and skeletal muscle of mice treated with a ketogenic diet. Rho JM, Sarnat HB, Sullivan PG, Robbins CA, Kim DW. Barrow Neurological Institute, Phoenix, Arizona 85013, USA. Although there is increasing awareness of adverse effects associated with use of the high-fat ketogenic diet, very little is known regarding its long-term clinical consequences, especially in relation to cardiovascular health. Recent reports have highlighted rare but significant cardiac problems in patients treated with the ketogenic diet. Given the inherent limitations in conducting detailed pathologic assessments in patients, we asked whether histologic changes might develop in the brain and skeletal muscle of mice fed a high-fat diet for 2 to 3 months. We found no evidence of gross morphologic or histochemical alterations in muscle or brain after administration of the ketogenic diet. Further, there was no abnormal lipid storage or mitochondrial enzymatic staining. Our data suggest that patients chronically treated with a ketogenic diet are not likely to develop a lipid myopathy or neuronal inclusions. PMID: 15526964 [PubMed - indexed for MEDLINE] CNS Drug Rev. 2005 Summer;11(2):113-40. Related Articles, Links KTX 0101: a potential metabolic approach to cytoprotection in major surgery and neurological disorders. Smith SL, Heal DJ, Martin KF. RenaSci Consultancy Ltd, BioCity, Nottingham, NG1 1GF, UK. KTX 0101 is the sodium salt of the physiological ketone, D-beta-hydroxybutyrate (betaOHB). This neuroprotectant, which has recently successfully completed clinical Phase IA evaluation, is being developed as an intravenous infusion fluid to prevent the cognitive deficits caused by ischemic foci in the brain during cardiopulmonary bypass (CPB) surgery. KTX 0101 maintains cellular viability under conditions of physiological stress by acting as a "superfuel" for efficient ATP production in the brain and peripheral tissues. Unlike glucose, this ketone does not require phosphorylation before entering the TCA cycle, thereby sparing vital ATP stores. Although no reliable models of CPB-induced ischemia exist, KTX 0101 is powerfully cytoprotectant under the more severe ischemic conditions of global and focal cerebral ischemia, cardiac ischemia and lung hemorrhage. Neuroprotection has been demonstrated by reductions in infarct volume, edema, markers of apoptosis and functional impairment. One significant difference between KTX 0101 and other potential neuroprotectants in development is that betaOHB is a component of human metabolic physiology which exploits the body's own neuroprotective mechanisms. KTX 0101 also protects hippocampal organotypic cultures against early and delayed cell death in an in vitro model of status epilepticus, indicating that acute KTX 0101 intervention in this condition could help prevent the development of epileptiform foci, a key mechanism in the etiology of intractable epilepsy. In models of chronic neurodegenerative disorders, KTX 0101 protects neurons against damage caused by dopaminergic neurotoxins and by the fragment of beta-amyloid, Abeta(1-42), implying possible therapeutic applications for ketogenic strategies in treating Parkinson's and Alzheimer's diseases. Major obstacles to the use of KTX 0101 for long term therapy in chronic disorders, e.g., Parkinson's and Alzheimer's diseases, are the sodium loading problem and the need to administer it in relatively large amounts because of its rapid mitochondrial metabolism. These issues are being addressed by designing and synthesizing orally bioavailable multimers of betaOHB with improved pharmacokinetics. PMID: 16007235 [PubMed - in process] Curr Atheroscler Rep. 2005 Nov;7(6):428-34. Related Articles, Links Benefits and hazards of dietary carbohydrate. Connor WE, Duell PB, Connor SL. Division of Endocrinology, Diabetes and Clinical Nutrition, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, L465, Portland, OR 97239, USA. Since the dawn of civilization, carbohydrate has comprised the largest source of energy in the diet for most populations. The source of the carbohydrate has been from plants in the form of complex carbohydrate high in fiber. Only in affluent cultures has sugar contributed so much of the total energy. When carbohydrate is consumed as a major component of a plant-based diet, a high-carbohydrate, low-fat diet is associated with low plasma levels of total and low-density lipoprotein cholesterol, less coronary heart disease, less diabetes, and less obesity. Very low-carbohydrate (ketogenic) diets may provide short-term solutions but do not lead to a long-term solution for most people. PMID: 16256000 [PubMed - in process] |
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