Candida Release Diet Increased reliance on aerobic glycolysis - TopicsExpress



          

Candida Release Diet Increased reliance on aerobic glycolysis and suppressed mitochondrial respiration are hallmarks of cancer (Warburg Effect). Therefore, one approach to decreasing tumour growth is to exploit the metabolic deregulation seen in tumours, which makes them rely preferentially on glucose as an energy source. In support of this concept, the high-fat ketogenic diet (KD) and caloric restriction, both of which reduce blood glucose, have been shown to reduce tumour proliferation in mouse astrocytoma that a KD may be useful therapeutic modality in patients. for CANDIDA RELEASE The ketogenic diet is designed to reduce the capacity of cancers or malignant cells to produce energy and thus induce either death of the cancer cell or reduce the rate of progression. As most cancer cells derive most of their energy from anaerobic glycolysis i.e. cancerous aerobic glycolytic cells can be only utilise carbohydrates, and have a limited ability to metabolise fats and proteins for energy production, any approach that inhabit the anaerobic glycolytic pathway will result in reduced energy production. The rate-limiting step of anaerobic glycolysis is the enzyme phosphofructokinase. Inhibition or modulation of this enzyme results in control of cellular energy production in cancer cells. Ketone bodies and citric acid have been found to inhabit the activity of this enzyme. The other enzyme system that is involved in cancer energy production is lactate dehydrogenase. This enzyme is modulated or inhabited by hyperthermia, improved oxygenation of caner cells and alkalinity. The KD increases the production of the ketone bodies (i.e. B-hydroxbutyrate (BHB and acetoacetate (ACA) which serves alternative fuels to normal cells. Most tumour cells use glucose as their energy source and are unable to metabolise ketone bodies for energy production due to altered or suppressed mitochondrial function. Aggressive tumours which have intact mitochondrial functional enzymes usually express increase levels of uncoupling protein. This results in reduced intracellular ATP. By supplying acetyl CoA and citrate, this diet-induced ketosis can further inhabit glycolytic ATP in tumours and thus reduce the energy needed for cancer growth. BIOCHEMICAL FUNTIONS OF KETOGENIC DIET The ketogenic diet introduces the following: 1. Reduces the growth of tumours and enhanced survival 2. Reduces reactive oxygen species (ROS) production in brain tumour tissue. 3. Alters the expression of genes involved in the cellular responsive to oxidative stress in tumour tissue, to a pattern seen in normal tissue. 4. Reduces cyclooxygenase 2 expression in tumour cells, which results in decreased metastatic and inflammation. 5. Protects the function of normal brain tissue during tumour treatment. 6. Effective for any cancer types containing genetically compromised metabolically- challenged tumour cells. 7. Fatty academia: Long chain fatty acids have been associated with apoptotic changes in a variety of tissues including cancer cells. The calorie restricted component of the diet contributes to it anti-tumour effects in the following ways. · Reduces circulating glucose levels and glycolysis, which tumour cells need for survival. · Induces anti-angiogenic, anti-inflammatory, and pro-apoptotic action in the experimental mouse (CT-2A Astrocytoma) and the human (U87-MG malignant glioma) brain cells. · Reduces secretion of insulin, insulin-like growth factors, and several inflammatory cytokines. · Increases mitochondrial biogenesis and energy efficiency through the production of nitric oxide (NO) by endothelial NO synthase (eNOS) · Protects genome integrity of preserve chromatin structure by the activation of DNA repair, ROS detoxification machinery, and the increased fidelity of DNA replication. · Increases cellular resistance to oxidative stress by reducing the accumulation of both nuclear and mitochondrial DNA damage produced by ROS. · Increases sirtuins (SIR:NAD+ dependent deacetylases) activity. The transition from glucose to ketone bodies for brain energy metabolism is the best under the natural conditions of calorie restriction. Restriction of calories in patients may be difficult to achieve, however, due to issues of compliance. Compliance may be better with KetoCal as this diet was designed for managing refectory human epilepsy under calorically restricted conditions. COMBINATION OF CALORIE-RESTRICTED AND KETOGENIC DIET (CRKD) Peroxisome proliferator activated receptor a (PPARa) is activated by nutrients (fatty acids and their derivatives) and influences these metabolic pathways acting antagonistically to oncogenic Akt and c-Myc activates. PPar a activity is induced by fasting and its molecular consequences overlap with the effects of calorie restriction and ketogenic diet (CRKD). CRKD induces increase of NAD + NADH ratio and drop on ATP/AMP ratio. The former is the main stimulus for enhanced sirtuin – protein deacetylase SIRT1 activity; the latter activates AMP-dependent protein kinase (AMPK). Both SIRT1 and AMPK exert their major metabolic activates such as fatty acid oxidation and block of glycolysis and protein, nucleotide and fatty acid synthesis, through the effector protein peroxisome proliferator activated receptor gamma 1 a captivator (PGC-1a), PGC-1a cooperates with PPAR a and their activates, and contributes to the anti-cancer effects of CRKD. The interplay between SIRT1, AMPK, PGC-1a, is the molecular basis of this anti-tumour dietary approach. COMPOSITION OF KETOGENIC DIET A keogenic diet may consist of 60% medium chain triglyceride (MCT) oil, 20-25% protein, 10% carbohydrate, and 5-10% other dietary fats. Alternatively, it may be taken as proprietary product KetoCal, which consists of 80% fat, 16.7% protein, 3.3% carbohydrate and 7.2Kcal/gm. In cancer patients exposure to omega 6 fatty acids present in safflower and sunflower oils should be restricted as they increase inflammation, decrease immunity and increase growth of cancer cells. Omega 3 fatty acids from fish oils and linseed oils are used in preference. At least 8-10% of fat must come from omega 3 oils. Inhibition or modulation of cyclo-oxygenase-2, PPAR and mTOR, enhances the effectiveness of this diet. (Refer to nutritional suggestions below) This diet increases the production of ketone bodies (acetone, acetoacetate, and beta-hydroxydutyrate), which modulate the activity of phosphofructokinase, side effects of the diet vary depending on the duration of strictness of the diet. Common symptoms range from: nausea, loss of appetite, hypoglycaemia, constipation, and intolerance to rapid onset of ketosis, poor fluid intake and possibility easy bruising. Biochemically, potassium, calcium and carnitine levels may fall. However, these are easily managed with appropriate supplementation such as: carnitine, antioxidants, fibre, buffers and multi-minerals. The effect of a ketogenic diet can be augmented by supplementing with citrates and alkalising buffers to reduce the acidity associated with the diet, and by improving oxygenation of the cancer and hyperthermia. The low calorie ketogenic diet should be followed for the minimum of 52 days, followed by a normal diet that is low in sugar and high in vegetables, moderate in fat and protein. Safety of Ketogenic Diet (KD) The KD is a high-fat, low carbohydrate diet that has been successfully used to treat medically refectory epilepsy for many decades, particularly in children and neurological disorders. Ketogenic diets are healthier because they promote a non-atherogenic liquid profile, lower blood pressure and diminish resistance to insulin with an improvement in blood levels of glucose and insulin. Such diets also have antineoplastic benefits, do not alter renal or liver functions, do not produce metabolic acidosis by Ketosis, have many neurological benefits in central nervous system, do not produce osteoporosis and could increase the performance in aerobic sports. Failure of Calorie Restricted Ketogenic diet Not all cancers respond to this diet. Genetic alterations in PIK3CA or PTEN can predict the response of tumours to calorie or dietary restriction (DR). The differential levels of P13K activation in tumours contribute to their differential sensitivities to DR, particularly during the early stages of carcinogenesis. The higher the activation the less sensitive is the tumour cell to dietary restriction. It is important to note that more advanced tumour stages, signalling pathways other than P13K may play key roles in meditating the effects of DR. Modulate P13K activity. FOODS TO AVOID: · All cereals and grain products except for specific fibre supplements. These include: breads, cakes, biscuits, crackers, doh nuts, chips, bagels, pizza, rice dishes, spaghetti, rice puddings, lasagne, linguine, muffins, macaroni, and pastries. · Sugary items: These include soft drinks, fruit juices, honey, jam, sugar, lollies, chocolate, sherbet, milkshakes, fruit cakes, marshmallows, pancake syrup, muesli, and jelly. · Potatoes are not aloud. This includes: sweet potatoes, white potatoes, yam or potato salad. · Fruits to be avoided are: apples, apple sauce, oranges, peaches, cantaloupe (rock melon), kiwi fruit, fruit juices, bananas, mangoes, pears, plums, prunes, raisins, dates, pineapple, nectarines, grapes, melons and berries. · Reduce carbohydrate content to 10-30 gm/day. FOODS TO EAT: · All red meats: all types of red meat. · All seafood: salmon, cod, mullet, perch, herrings, sardines, scallops, squid, octopus, and mackerel. · All fowl: chicken, duck, goose, turkey, ostrich, pheasant and quail. · Vegetables allowed: alfalfa sprouts, asparagus, avocado, bamboo shoots, broccoli, bok coy, cabbage, capers, cauliflower, celery, chicory, cucumbers, dill pickles in vinegar only, dandelion greens, eggplant, endive, fennel, garlic, kale, kohlrabi, lettuce, leeks, mushrooms, mustard greens, parsley, okra, green and red peppers, radishes, raw cob corn, salad greens, sorrel, spaghetti fruit, spinach, silver beet, string beans, summer squash, turnip, zucchini, tomato, watercress, zucchini, and artichoke. · Vegetables legumes high in carbohydrate include: Celeriac, chickpeas, cooked corn, and grains sprouted, horseradish, kidney beans, lima beans, parsnips, peas, popcorn and sunflower seeds. These should be restricted from the diet. They may be occasionally taken once per week. · Beans: soya, kidney, haricot, split peas, butter beans, green beans and purple beans. · Dairy products: cottage cheese, sour cream, camembert, cheese, edam cheese, feta cheese, mozzarella, jarlsberg cheese, parmesan cheese, Romano cheese, Swiss cheese, cream · Eggs: all types of eggs (organic) · Small amounts of beetroot, carrots (raw) onions and choco · Fruits: lemons, limes, loquat and fresh strawberries. · Nut and seeds: almonds, walnuts, pecans, sunflower seeds, and pumpkin seeds (all in moderation). · Oils and fats: medium chain triglycerides, butter, linseed oil, fish oil, lard, olive oil, sesame oil, coconut oil, ghee and copha. · Fluids: water (filtered), Chinese tea, soda water, mineral water, and herbal teas- chamomile tea. To flavour fluids, add freshly squeezed lemon or limejuice, or stevia can be added to add sweetness. The amino acid glycine can be added to food to give a sweet taste. · Spices: cider vinegar, garlic, curry, bouillon, salt, lemon juice, chilli, olives, mustard, pepper, onion powder, oil and vinegar salad dressing, peanut sauce, chives, herb spices- rosemary, thyme, bay leaf, coriander, turmeric, and lemon grass etc. Recipes for these food selections can be obtained from the internet under a search program ‘ketogenic diet recipes’ or ‘low carbohydrate recipes’. DIETARY PRINCIPLES A ketogenic diet is basically a high fat, moderate protein, very low carbohydrate diet. 1. Avoid margarine, but increase the consumption of cream, butter, coconut milk, olive oil, fish oil, medium chain triglyceride oil, fish, chicken, avocado, freshly make peanut better etc. 2. Restrict intake of vegetable oils that are rich in omega 6, e.g. canola, safflower and sunflower. 3. Carbohydrate-rich foods must be strictly avoided. 4. Maintain fibre intake with a high fibre supplement e.g. Fibre plus probiotic or ensure an adequate intake of salad type vegetables- cabbage, raw beetroot, lettuce, cucumber, celery, broccoli etc. 5. Ensure fluid intake is at least 2-4 litres daily. 6. Alkalize the body by supplementing with sodium bicarbonate/ citric acid buffer in water one hour after meals. 7. Supplement with a fat-soluble vitamins A, D, E and K. Trace element formula containing zinc, selenium, iodine, chromium and low dose multi B vitamin complex. 8. Support fatty acid metabolism with acetyl-l carnitine, at least 2 gm/day. 9. Supplement with pancreatic enzymes to improve digestion of fat. 10. Liver and bile support may also be of some benefit. Choline, glycine, taurine, cysteine, vitamin C supplementation, may be of benefit. The above dietary suggestions should be followed for at least 50-60 days to induce apoptosis or cancer cell death. Once the tumour is under control, the diet changes to a previous approach and is dependent on the type of tumour present. Patients with blood or immune based malignancy do ……. On a high protein, high fat diets, while patiens with …. Or soild tumours, tend to do better on a moderate …. Glycaemic index based diet. candidareelase
Posted on: Fri, 30 Aug 2013 10:56:33 +0000

Trending Topics



Recently Viewed Topics




© 2015