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CATEGORY: biology/metabolism TECHNICAL: **** SUMMARY: This document gives the rather technical/intimate details of how someone who is low-carb and ketogenic can sustain a weightlifting session and have the energy to do so start through finish. It's a pretty rough read for those uninterested in the biomedicine, so I'll give you the short version here. Your body accomplishes this task by using the "waste products" of active muscle exercise: lactate (which gives you that burning feeling) and pyruvate (another precursor to the glucose generation process) to synthesize new glucose in the liver. This new sugar is then sent back into the bloodstream for use by the active muscle. It's important to realize that amino acids are part of this process, so be sure to get enough protein in your diet as well as fats, or you may risk muscle loss (to the conversion process). Incidentally, you will also notice (as I have) that because of this glucose generation process - if you check for excess ketones in the urine stream (with ketostix) right after you train - you'll see that you're temporarily non-ketogenic. That is why it is a good idea to follow up a weight lifting session with a little easy, short aerobic work. Cycling, for example, can more rapidly remove the excess lactate from the working muscle and convert it back to muscle/liver glycogen. This not only reduces your post-workout soreness, but also drops your blood sugar and speeds you back into a ketogenic state. (and primes your muscles with stored glycogen for the next lifting session) ------------------------------------------------------------- Subject: The anabolic diet... Date: Sun, 4 Jun 1995 13:22:37 -0500 (CDT) Hello! I finally found the answer I was looking for regarding the anabolic diet. When people (my adv. nutrition teacher, biochemistry professor etc.) put me on the spot, I have reluctantly explained the diet based upon the manuals findings, which I explained were not technical enough, and had real difficulty convincing them. But now I finally found an answer that is technical enough, and explains the reasoning behind this ever so commonly asked question; "since weight training is anaerobic, where is your energy going to come from when you don't consume enough carbs, since glycolysis is the major pathway involved in anaerobic exercise?". Well I finally struck pay dirt. It took an inordinate amount of time, too much time in fact, and I am going to call Optimum Training Systems and request that they revise the manual or add an addendum in which this is explained more in depth. Like I said, you are going to be hard pressed when someone in the know starts battering away with technical questions, that the diet doesn't provide. Sure the manual tells you that dietary and body fat will be the fuel for your workouts along with the creatine from the red meat, but that doesn't cut it. Which finally leads me to this answer. Since anaerobic wt. training HAS to go through glycolysis, I thought that readdressing that pathway might lead me to an answer, and it did. As you know the 2 hormones insulin and glucagon work together, when carbs are present, insulin secretion from the pancreas increases, and times when carbs are low, glucagon secretion increases to supply carbs for energy. When going through glycolysis there are 3 regulatory steps, one of them involves the enzyme PFK-1 (phospofructokinase-1). It is one of the reactions that are catalyzed early in glycolysis, the third step If I recall correctly. Anyway, it seems that this enzyme PFK-1 is sensitive to levels of carbs in the blood. When carbs are low, as in the diet, glucagon is going to be chronically activated, which in turn will influence the enzyme PFK-1. When this happens, it tells the metabolic pathway that glucose just is not available, and therefore the reaction of glycolysis can not proceed in the normal fashion. THat is why it is a regulatory step. When this happens, glycolysis basically skips all the normal steps and proceeds to the end where pyruvate is formed. From there pyruvate can be converted (broken down) to lactate. Once lactate is formed from a reaction catalyzed be lactate dehydrogenase, lactate has no other metabolic fate than reconversion to pyruvate. Hence, lactate is commonly considered a metabolic dead end. Since lactate formation catalyzed by lactate dehydrogenase regenerates NAD+ from NADH, the pathway of glycolysis is complete, with NAD+ becoming available for glyceraldehyde 3 phosphate dehydrogenase reaction. Thus no net oxidation or reduction takes place during anaerobic glycolysis to lactate. The final product, lactate in glycolysis generates 2 mol ATP per mol of glucose consumed. Oxygen is not required in either case. In most cells, the majority of ATP is produced by oxidative phosphorylation, which is strictly an oxygen dependent process. Yet, in the cornea of the eye, for example, oxygen availability is limited by poor blood circulation. Anaerobic glycolysis meets the need for ATP in the abscence of sufficient oxygen for oxidative phosphorylation. When skeletal muscle is active, lactate and pyruvate are transported out of the muscle cells and carried via the circulatory system to the liver where lactate is converted to pyruvate by the action of hepatic lactate dehydrognease. Pyruvate can be further metabolized in various ways by the liver: a fraction of it is aerobically oxidized to Co2 via the Krebs cycle (citric acid cycle), and some of it is transaminated to alanine, which is used in protein synthesis. Pyruvate in liver cells can also be converted back to free glucose by gluconeogenesis. Liver is the principal organ responsible for regulating the supply of blood glucose to other cells of the body, including skeletal muscle cells. Thus, a portion of the metabolic burden of muscular contraction is borne by the liver, which metabolizes the by-products of muscle activity (lactate and pyruvate) and synthesizes blood glucose. This inter-organ metabolism, in which liver receives lactate and pyruvate and furnishes glucose for skeletal muscle, where glucose is glycolytically metabolized to generate ATP, is referred to as the Cori Cycle. Hope this reaches all the doubters out there who were not convinced the first time! Thanks! Jeffrey P. Krabbe Pre-Dietetics, Senior University of Nebraska, Lincoln :cool: TJ :cool:

Heh heh heh, it gets easier.. :grin: 1. a good multivitamin without iron 2. a good antioxidant supplement (extra C, E, beta carotine) 3. potassium 4. calcium 5. magnesium 6. zinc 7. iodine and for immuno enhancement: 8. flax seed oil 9. AFA blue-green algae Only if you want to overwork your kidneys and add waterweight you your frame. The extra weight leaves as soon as you quit taking the creatine. Used to. It's been taken down. I have been reposting the messages here, but took the last few weeks of due to the holidays. (everyone should eat badly over the holidays ) I'll ask my old web hoster/mistress if she can give me the raw files for rehosting.. :cool: TJ :cool:

Out of curiosity, what pilot jets does the factory jet kit come with for the 'Bird? :cool: TJ :cool:

I've heard that DynoJet uses a different numbering system for their jets than Honda does. That true? If so, anyone know where a conversion chart is located? I'm working on Jetting a bike and it ain't a Bird :wink: Thanks! :cool: TJ :cool:

Better/cheaper.. Gotta sniffer, like dynojet dynos.. :wink: http://www.aep.bigstep.com/digital.htm :cool: TJ :cool:

I've got the entire USDA nutrient database on CD if anyone wants it (15MB) Shoot me an e-mail with your postal address and I'll mail it to you for x-mas :cool: TJ :cool:

Seems like they might come in handy for tuning.. :cool: TJ :cool: http://knpowersports.com/airfuelmonitors.htm

1) Tires 2) My left nut, after having to buy my Corbin BeetleBags brand new TJ

I was looking at something like this: http://www.superchips.co.uk/bikes/indexfr.htm Aparently it gives fine ignition control to your bike -- a seemingly good idea for carby bikes that can be properly jetted but cannot make use of things like Power Commanders.. :cool: TJ :cool:

CATEGORY: biology/immune_sytem TECHNICAL: ** SUMMARY: This document is one that I have made reference, a number of times, to a few of you about. It is the original paper that discusses the adverse effects of sugar on the leukocytic index. As some of you may remember, you are generally not succeptable to viral attack or tumor growth if your immune rsponse is kept at high levels (more specifically, the strength and count of your NK cells). However, when exposed to sugars, the immune state is weakened considerably. Is it any wonder that we suffer from so many forms of cancer, and viral infections when the typical american diet is so high in refined, processed, carbohydrates? Most americans repeatedly supress their immune systems at regular intervals daily! ------------------------------------------------------------- Sugar and Immunity _________________________________________________________________ Leukocytic Index proves the devastating effect of refined carbohydrates on immunity. Many people have been asking for a mechanism for the depressed immunity seen in people who eat sugar and other refined carbohydrates. Many are known but the Leukocytic Index is an especially helpful one for many people to begin to take this health risk seriously. More than 20 years ago a large study was published about the effects of refined carbohydrates (of which sweets are the worst) on the leukocytic index. Our white cells are the most important factors in protecting us from invading organisms. The leukocytic index is a measure of how many organisms one white blood cell (WBC) can eat in an hour. Therefore an index of 10 means that that one WBC ate 10 organisms in THAT hour. The average LI (leukocytic index) in the USA--and remember, average is not as healthy as one can get--is about 13.9. Within 15 minutes, after an individual eats the amount of refined carbohydrates normally ingested in the evening meal --about 100 grams, the leukocytic index drops to about 1.4. Depending on the genetic susceptibility to this problem, it might be better or worse--this is just an average. Diabetics ALWAYS have a LI of less than 2. That means: the average person loses more than 90% of their immune function within 15 minutes of indulging in this poisonous substance. This deficiency lasts for about 2 hours after the stress occurs. What is routinely given intravenously during surgery? Glucose water! When Ringer's Lactate (which has no sugar) is used instead, the incidence of post operative infection is reduced by two thirds. The only reason I can think of for this kind of persistent ignorance is that there is no money in changing the thinking of operative routine. There is a lot more money in treating the infections that are created by the Allopathic Monopoly. Since this has been known for more than 20 years, don't you think it is time for this information to get out to the public? :cool: TJ :cool:

CATEGORY: diets/paleo TECHNICAL: ** SUMMARY: This is an interesting little document that I found quite a long time ago. It attempts to shatter the myth that neolithic humans (in Europe) were primarily plant eaters. This is significant when one considers the arguments made by vegans/vegetarians that human beings are, and have always been, primarily herbivores. Many on this list know that I staunchly believe that humans consumed a majority of animal based food and not vegetable foods. This does not mean I advocate a meat-only diet. It does, however, mean that I encourage the consumption of mostly fiberous veggies (and herbs, etc.), and getting a majority of calories from protein and fat sources. If this research proves to be correct, then it indicates something that is pretty important from an evolutionary point of view. Namely, that humans (of european origin/background) may not have had as much time to adapt to a grain based diet as expected. The previous estimate was about 20,000 years. This document argues otherwise (4,000 - 2,000 years). Should that be the case, then it's very unlikely we've had time to adjust to such a quick change in diet (from animal to grain). And, that adds fuel to the argument that grains are contributing significantly to the increase in diseases of degeneration so prominent today... ------------------------------------------------------------- British Archaeology, no 12, March 1996: Features _________________________________________________________________ Bone analysis suggests Neolithic people preferred meat, writes Mike Richards. `First farmers' with no taste for grain The Neolithic period is traditionally associated with the beginning of farming, yet in Britain - by contrast with much of the rest of Europe - the evidence has always been thin on the ground. Where are the first farmers' settlements? Where are the fields? The almost complete absence of this kind of evidence has led some archaeologists, over recent years, to question the view that people in Britain actually grew most of their food in the 4th and 3rd millennia BC. Now, a scientific study of Neolithic human bone seems to point in the same revisionist direction. The small-scale study - the first of its kind - of the bones of about 23 Neolithic people from ten sites in central and southern England, suggests that these `first farmers' relied heavily on animal meat for food, or on animal by-products such as milk and cheese, and that plant foods in fact formed little importance in their diet. The bones date from throughout the Neolithic, c 4100BC - c 2000BC. The study was based on the idea that our bodies are made up of organic and inorganic components derived from the foods we have eaten. There are a number of ways of tracing the original food source of some of our tissues, and one way is to look at the relative ratios of certain elements, known as `stable isotopes', in bone protein. These stable isotopes can tell us a number of things about what a person's diet has been for most of their life. One particular isotope can tell us whether humans were getting most of their food from plant or animal sources. Generally speaking, this is done by comparing human isotope values to animal isotope values. If the human values are more like that of a herbivore (eg, horses or cattle) they are eating a great deal of plant food, and if they are more like carnivores (eg, wolves or foxes), they are eating more meat. A number of human bones from the Iron Age and from Romano-British sites were also tested, and their isotope values were a little higher than those of herbivores. This is as we might expect, as there is little doubt that in these periods people practised relatively intense cereal agriculture, and only supplemented their diet with meat. The Neolithic results, however, were surprisingly different. They were as high, and sometimes even higher, than stable isotope values of carnivores. This suggests the Neolithic people had relatively little plant food in their diet and instead were consuming large amounts of meat. It could also mean they were eating a lot of animal by-products, like milk and cheese, as these are indistinguishable from meat itself using stable isotopes. So what, then, was the Neolithic economy based on? Animal remains from Neolithic sites are generally of domestic species (eg, cattle and pig) rather than wild, and cattle from Neolithic sites such as Hambledon Hill in Dorset are actually larger than the cattle typically found in the Iron Age. This evidence may suggest an animal-dependent economy - indeed, one in which animals were well treated and kept for a long time - and, as the Neolithic specialist Andrew Sherratt has suggested, the British Neolithic may have been characterised by a `secondary products revolution', with animal husbandry and an emphasis on animal milk and cheese, instead of by an `agricultural revolution' and the growing of crops. Grain and agricultural implements have, of course, been found at Neolithic sites in Britain. The isotope results do not rule out some limited grain production and consumption; but they suggest it did not form a significant portion of the diet. The sites where grain has been found generally seem to have been used mainly for ritual purposes, and it is possible (as archaeologists such as Richard Bradley and Julian Thomas have argued) that in Britain, on the edge of Europe, grain was grown, or even imported from the continent, only for ritual purposes. Agricultural implements may also have assumed a largely ritual significance. There are, however, potential difficulties with stable isotope analysis. The main concern is whether the animal stable isotope data used as a benchmark are accurate for the specific British Neolithic sites tested. In the study, we took `average animal values' from a large database, held at the Oxford Radiocarbon Accelerator Unit, covering all Europe over the past 10,000 years. It may be that there are regional variations in plant and animal isotope values of which we are, as yet, unaware. Research, however, continues - and if our preliminary results are confirmed, we may be able to scrap the notion of Neolithic agriculturalists in Britain once and for all. Mike Richards is a PhD student at the Research Laboratory for Archaeology in Oxford :cool: TJ :cool:

Cool, I hope you win it! That way you can put it in and try it out and give us a review :grin: :cool: TJ :cool:

Get ready for your first "sugar hangover". I'm surprised you're not comatose -- everytime I eat a ton of carbs after being keto for any period of time I immediately pass out and sleep for a few hours.. TJ

Pictures, pictures?? :cool: TJ :cool:

Sam's club down here was selling a really nice one for $50.0. I bought two and use them side by side to tote the 'Bird around. They have a combined capacity of 1/2 a ton.. :cool: TJ :cool:

Yep, nuthin there for my XX, my CBR 1000F or even my VTR 1000F :razz: TJ :razz:

Japanese tools are built with the same concepts of quality in mind as Japanese motorcycles.. Be it Ryobi, Makita, etc. :cool: TJ :cool:

CATEGORY: diets/lowcarb TECHNICAL: * SUMMARY: This document was written by an individual who was on another health/training list that I was a part of back in 1996. In this note, he describes (in detail) one of the earliest low-carb diets ever recorded, "the banting diet". The author does a really good job documenting the chronology of everything, and even discusses his own successes using the approach at the end. As you read through it, you will find suggested diet plans for the banting approach. Though I agree with low-carb diets in general, I would make the case that this is not an optimal approach. In my view, paleo-lowcarb is the only way to go. I will discuss that in the future as well as provide my exact diet for everyone's scrutiny. ------------------------------------------------------------- A few days ago I discovered this group while "surfing" and contributed an opinion in the "Dr. Atkins vs the World" thread. Basically, it pointed out that Dr. Atkins was a johnny-come-lately in the low-carbohydrate scheme of things. The low-carbohydrate diet seems to have originated with "A Letter of Corpulence", published in London in 1864 by a man named William Banting. It was so popular in the U.K. that one may still find in the Oxford English Dictionary the verb "to bant" as well as "banting" and "bantingism". My copy of the Oxford English Dictionary quotes an editor's response to a correspondent: Pall Mall Gazette - 12 June 1865 "If he is....gouty, obese, and nervous, we strongly recommend him to bant." So the low-carbohydrate way of eating predates calorie counting as a method of weight control, though it does not predate the earlier method, STARVATION, - poor ol' Henry VIII! There is a low-carbohydrate diet which works as swiftly as any proposed by Dr. Atkins, which does not involve placing a human being into artificial starvation, with the throwing off of ketones, and resultant straining of the kidneys. If you want to throw away those ketostix, or use them as coffee stirrers, read on. Dr. William D. Howe was a well-known medical doctor and a member of the Canadian parliament in Ottawa, representing the riding of Hamilton-South for the NDP (Socialist) party. In March of 1965 a column was written in "The Ottawa Journal" mentioning that fact that many formerly obese members of parliament were looking slim- and-trim these days, thanks to a method of weight control devised by Dr. Howe, and the diet was given. This casual mention brought a flood of mail. In two months Dr. Howe had mailed out 1500 copies, the Ottawa Journal's files had been stripped of clippings, and the national radio (C.B.C.) had done a 15 minute report on it. On Monday, May 3, 1965 and Tuesday, May 4th, the Ottawa Journal reprinted the diet along with a number of articles concerning it. Since I have the clippings (and would never part with them) I am excerpting the relevant material here: <<OPEN QUOTE - Ottawa Journal, May 3, 1965>> You May Eat: Meat, even fat meat Milk and cream Fish, cheese and eggs Butter and margarine Leafy vegetables such as lettuce, cabbage, spinach Stem vegetables such as asparagus, celery, broccoli Coffee & tea with cream and saccharin/sweetener You Must Eat: Vitamin C - 100 mg daily in unsweetened tablet form (inexpensive at drug store). Some form of vegetable oil such as corn, taken straight or splashed on salads. (1 tbsp) You Must not Eat: Bread Any dessert Seed vegetables such as peas & beans Root vegetables such as beets, parsnips, turnips, potatoes Or anything containing sugar, starch, or flour. Dr. Howe: "In 2 months I cut from 220 to 172 and trimmed my waist 11 inches" Murdo Martin (NDP MP for Timmins): "Down I came in 10 weeks from 268 to 227, with 7 inches and 7 notches off my belt line." Eric Winkler (Conservative MP): "I pared down from 226 pounds to 193 in 6 weeks." It is important to realize with this diet that quantity is not the, or even a factor. The diet eliminates almost all carbohydrates, which most of us eat in large proportions. Carbohydrates come in the form of sugar, starch and flour. The logic of this diet is that our bodies are unable to use surplus carbohydrates and therefore they are converted to fat and stored -- usually around the waist. We lose the fat and the fat only, while building up muscle, blood and other tissues with no loss of energy, no failure of drive or a lessening of zest for living. The diet is self limiting -- when the fat is gone, you stop losing weight and remain constant at your natural and correct level. "I tell you", says Martin enthusiastically, "this diet works. What's more, you feel like a million bucks on it - lots of energy, drive to burn - and you don't go around, as on most diets, feeling like a grizzly bear." "I swear on it," says Mr. Winkler with conviction, "this diet does it, not only painlessly but pleasantly. The only fault I found with it, I went down so fast I couldn't get my suits taken in quickly enough to match the belt-line Dr. Howe's "Eat & Drink Up Diet" is so short, so simple, some people suspect there must be more to it. There really isn't. It's all there under 3 headings: You May Eat You Must Eat You Must Not Eat It covers broadly all foods. <<CLOSED QUOTE - The Ottawa Journal, May 3, 1965>> The following day, responding to requests for suggested menus, the following was published: <<OPEN QUOTE - The Ottawa Journal, May 4, 1965>> Breakfast: Tomato Juice, liquid or jellied consomme, sauerkraut juice or avocado. Bacon or ham and eggs, all you can eat. Coffee, tea or milk. Lunch: Martini or Scotch & water, etc. *if desired*. Any cold meat: Beef, ham, turkey, lamb, chicken, pork, salami, bologna, veal, tongue, liver, lean or fat it doesn't matter. Salad with an oil & vinegar dressing or blue cheese (*not* Thousand Island Dressing). Lettuce, cress, parsley, green & red peppers, shredded cabbage, kale, dandelion greens, tomatoes, asparagus... (any leafy vegetable). Dinner: Shrimp or lobster cocktail. Avocado or tomato stuffed with fish or fowl. Any soup, including cream soups, so long as no rice, barley or macaroni. Any stem or leafy vegetable - asparagus, brussels sprouts, cabbage, cauliflower, celery, collards, endive, kale, lettuce, mushrooms, parsley, peppers, sauerkraut, spinach, squash, tomatoes, turnip/beet greens. Cheese of any kind. *Sugarless* ice cream, sherbets or gelatins. Coffee or tea with cream. Milk. Dr. Howe emphasizes that this diet is for healthy people only. You don't have to stint, but don't go overboard either. Eat & drink enough for comfort and health, but no more. "If you're healthy, you won't anyway" says Dr. Howe. Dr. Howe stresses that if a person is under medical or psychiatric care, the diet is for his own personal physician and not Dr. Howe to prescribe. Dr. Howe's "Eat & Drink Up Diet" has been criticized by some as having something of a resemblance to one which has been published in California as "The Drinking Man's Diet", and this has been criticized as a diet which will leave you fat and drunk. Dr. Howe points out that the Drinking Man's Diet permits fruit and even seed vegetables. Dr. Howe rules these out as being too heavily loaded with fat making carbohydrates. <<CLOSED QUOTE - The Ottawa Journal, May 4, 1965>> Notes: Dr. Howe allows one to have a can of cream soup, or tomato soup, when desired, so long as they contain NO rice, pasta, potatoes, etc. There is some carbohydrate in these soups, but nowhere near enough to sabotage the diet. You may use unsugared strawberries in desserts. You may use sugar-free soda pop. Milk has 12 gms. of carbohydrate per glass - scientifically speaking. Almost none of these carbohydrate are usuable by the vast majority of humans as they are in the form of lactose, milk sugar, which very few people can metabolize well, if at all. Hence, drink up. Try not to use a lot of yogurt, or acidophilus milk, or any dairy product which has been treated with a bacteria which breaks lactose down into a "digestible" form. Yogurt is not off the menu, just don't eat more than a cup a day or so. Sour cream is not a problem, as it is made from full- fat cream and thus is low in lactose to begin with. Do NOT use "Calorie-wise" dressings, or anything labelled "light". Use full-fat dressings such as Ranch, Blue Cheese, Caesar, etc. Look on the bottle, if they have a carbohydrate count of 1 gm/serving. or less, use with abandon. If you do so, you will have fulfilled your oil requirement in the "You Must Eat" category. Whisky and hard liquor are allowed. Dry red or white wine may be taken with meals - be sure is has a sugar count of 3 or less (or says "dry" or "very dry" on the label. LASTLY: And MOST important. Do NOT mix apples and oranges so to speak. Do NOT take a part of this diet and a part of that diet. Low- carbohydrate diets are not as "forgiving" as low-calorie diets. Do THIS diet or DON'T do it. Don't mix and match, it is too confusing. If you follow this diet you will lose a pound a day or so, if you add a chocolate bar, a bran muffin, or a potato to the menu ALL THOSE FAT GRAMS become AVAILABLE to the body for metabolization. One slip can ruin your whole day. It isn't worth it: nothing tastes as good as thin feels. My Personal Story: In 1965 I was 17. I was 323 lbs. of misery. 6'1". I was so desperate to lose weight and "fit in" that I used to take the bus to the last stop on the line and try to walk the 10 or 15 miles back to my home. I was never able to make it. I had been told, without solicitation, that I should "turn the fat into muscle by exercise" by a wafer-thin cousin... On Saturday, May 1st, 1965 I read on the front page of the newspaper that "Dr. Howe's Diet" would be reprinted on Monday. When I read the diet it seemed to be doable. The first week I lost an impressive amount of weight (I don't remember exactly how much). By October I remember that I was down 100 pounds. It took about 5 or 6 months until I finally hit 190 lbs., largely because my social life had improved to the point where I was "out with the gang" instead of watching television. A teenager eats frenchfries, burgers and pizza when in company, even in 1965. 31 years later I am still at 190 lbs. Once one has been overweight, it is a lifelong struggle, no matter WHICH diet one chooses. I have gained as much as 30 lbs. back before dieting. I have done Weight Watchers and bought the Susan Powter tapes. I did this largely because I was constantly told by thin friends (some of whom have since passed on) that a high-fat, low-carb diet was dangerous. I am the healthiest person I know. No diet is suitable for all people. If you think you'd like to try this diet, go to it! P.S.: As far as desserts go... try a Bavarian Cream using an envelope of sugar-free gelatine, made and removed from the refrigerator when partially set. Mix in a cup of cream which has been whipped separately and sweetened with Sweet & Low. Return to refrigerator until fully set. Each it all in one sitting if you like. Yum! Orange Jello Bavarian is my favourite. Or, how about baking an egg custard? Use artificial sweetener and chill. Cover with freshly whipped cream if liked. Use full-fat milk for the custard, I find cream too cloying. :cool: TJ :cool:

I've seen some have increased total cholesterol numbers on low-carb diets. However, it's mostly because HDL (good) increases.. Not because of LDL (bad). Get your blood work numbers from your doc. I wanna see 'em. To be honest though, the triglyceride is a better indicator of heart disease. One, predominant, reason for this kind of action is reduced fiber in low-carb diets. You need to make sure you eat enough raw veggies and raw/unsalted nuts to keep fiber intake up. That's the only way we get rid of excess cholesterol (via bile acids..) Also, make sure you're getting plenty of antioxidant vitamins. This includes vit. C, E, and beta carotene. I usually take 2-3g of C daily.. :cool: TJ :cool:

Cholesterol is _NOT_ and indicator for heart disease. There are many people with high cholesterol who never develop heart disease and also people with very low cholesterol who have it. (long story) What was your triglyceride count? What is your blood pressure? :cool: TJ :cool:

Probably not.. My guess is that you may get a little bit of gastro-intestinal distress the next day, though. Specially if you've been low-carb for a while. Generally these things work by inhibiting enzyme production.. But hey, you could prolly get some wicked farts that way -- if you've got someone you want to offend for fun :cool: TJ :cool:

To be honest, I would avoid these like the plague. They allow sugars to pass the entire length of the intestine without being properly handled by the correct enzymes. The net effect is that bacteria in the digestive tract have a large amount of substrate to feed on, etc. I think that those pills could lead to things like intestinal cancer, chrone's disease, IBS, etc. if used over any significant period of time. Just my $0.02 :cool: TJ :cool:

CATEGORY: diets/ketogenic TECHNICAL: *** SUMMARY: This document is part one of a lengthy technical document on Cyclical Ketogenic Diets (CKD's). It was written by a friend of mine who, at the time, was a member on another mailing list of people (mostly athletes) who used CKD's for fat-loss, or to increase muscle gain in the gym. This work is sort of like a treatise on the whole topic of CKD's. It discusses what ketones are, what ketosis is, and the effects that they have on your body. It's a fairly technical document but a good read none the less. If you read through it, you'll get an overall picture of how your hormones respond to low-carb diets, and why low-carb diets aid in fat loss. He's also very complete, and gives both positives and negatives (as he sees them). Bear in mind, though, that there have since been many new studies that prove the efficacy of ketogenic diets. I just wanted to show you this because it sort of lays it out in a fairly easy to understand manner. I don't exactly agree with everything he states here, but the jist is on target. ------------------------------------------------------------- Surviving and Thriving on a Low Carb Diet Beyond Atkins, Di Pasquale and Duchaine by David Greenwalt B.Sc. There is currently a great debate over which diet is best with special emphasis on high fat/low carb or high carb/low fat. Each group makes "spot" claims and neither really covers the issues which really matter. What are these issues? 1. What is your goal? A. Fat loss? B. Muscle hypertrophy? C. Endurance improvements? D. Longevity? 2. What foods do you like? A. Are you a vegetarian? B. Do you rarely eat fresh fruits and vegetables? C. Do you like fish? D. Do you like to cook? E. Are you married or single and does your spouse like to cook? 3. Do you plan on staying on this diet forever? 4. Are you going to use the diet temporarily for any number of reasons? Many of the arguments which begin between rigid dieting rivals are ghost-like, in that neither side knows, or cares, what the goals are of the other. I, speaking personally, do not know a very large, muscular vegetarian. An argument can be made that vegetarianism is healthiest, however, from purely an observational perspective, I don't want to look like any vegetarian I know or have ever seen. My goals, as a bodybuilder, are to be as big and lean as I can be genetically and naturally. At this point, a vegetarian and I are most likely polar opposites. We must define our goals if we are to intelligently discuss diets because simply talking about calories in, calories out or arguing over diets which are supported in scientific literature as health-giving versus diets purported to be more anabolic is assanine. It's almost like saying "I like apples. Well, I like Ferrari automobiles." One has little to do with the other. There are so many diets for sale it can be bewildering to most people. While all of these diets cause dietitians to shake their heads in most cases, the personal bioindividuality isn't taken into consideration. Take a recent example in which a relative of mine was counseled on a weight problem by a physician (M.D.). My relative was told to eat low fat, high carb, fruits and veges and eat fish at least twice a week because of the benefits of the essential fatty acids in the fish. This advice is patented medical standard protocol for anyone overweight and might be very good for a majority of the population. Problem: My relative hates fish and so do I for that matter. It is because of our individual likes and dislikes that so many diets are made available. Most are effective in their own right but many are imbalanced and do not include a wide variety of foods. The Registered Dietitians (RD) of America push the Food Guide Pyramid. The Atkins followers push the low carbohydrate diet. Others push high protein or low protein, fasting, grapefruit only, soup only, no fruits, etc. etc.. All may serve a purpose and all may be valid but until we know about goals and individual sensitivities like intolerance to certain foods, allergies, medical conditions and personal likes and dislikes, there can be no intelligent discussion about which diet is better. This paper is an attempt to clear up the disinformation which exists regarding the low carbohydrate diet which causes ketonuria and ketonemia. Whether we're talking about an Atkins (low carb everyday) or Di Pasquale (low carb 5 1/2 days, med. carb 1 1/2 days) they both cause considerable ketosis. There are those who follow a low carb diet and have done so for more than a year. Atkins' book gives several examples of individuals who have chosen to make low carb a part of their life style (5). A certain, small percentage of epileptic children who suffer from intractable seizures and don't respond well to drug therapy are purposely placed and medically supervised on a low carb (herein called Ketogenic Diet) for periods of two years or more (1). A key difference between an epileptic child and a healthy bodybuilder consuming similar foods is fluid intake. A ketogenic diet is closely monitored for an epileptic child because water intake is restricted. This is because the ketone bodies, which are synthesized in high quantities on a ketogenic diet, are actually the medicine for the child. Epileptic children wouldn't respond as well if the "medicine" was being flushed down the toilet in large quantities as the kidneys filtered them with super consumption of water. A non-epileptic, otherwise healthy adult does not have the same goal as the epileptic child. Ketones are not medicine. They are an energy source but not medicine to the healthy bodybuilder. They are a byproduct of the diet which we want to excrete if in excess (We'll cover some biochemistry later). There are those who believe that the world nearly stops when benign dietary ketosis is caused with a ketogenic diet. Scare tactics such as "The Kreb's cycle collapses due to insufficient carbohydrate intake", there will be more "bruising" of blood vessels because of higher fat traffic on a ketogenic diet, increased risks of morbid obesity and increased coronary heart disease lipid factors, and finally the great myth that we must have hundreds of grams of carbohydrates per day to fuel the brain and other tissues which require glucose for energy. Some of these claims are simply false and others are completely unsubstantiated in current medical journals. What must be taken into consideration, before wild claims are made, are the ratios of the nutrients consumed and making sure that whether it's an epidemiological study or small 10 person study, were the study participants consuming a diet which is the same as those following a typical ketogenic diet consisting of 70% fat, 20% protein and 5% carbohydrate? In nearly any case which examines fat intake and increased risks of CHD and obesity, the fat intake is coupled, arm-in-arm with high dietary carbohydrate ingestion or at least substantially higher than the ketogenic 5% we're discussing in this paper. The scare tactics, like the ones above, are used by the ill-advised and ignorant who feel their diet is best. There is no cookie cutter "best". There is no "one size fits all." For these reasons we can only discuss physiology, biochemistry and scientific literature reviews which are pertinent to humans following identical diets. Rat studies may be better than nothing but not much better. In-vitro studies are only a place for scientists to start, not a place for pragmatists to review. In this paper I'll cover how a ketogenic diet works to support life and activity and I'll also discuss how a ketogenic diet may even be beneficial for some individuals. The research I have conducted for this paper has led me to recommend a ketogenic diet for the following individuals under the following circumstances: 1). Medically supervised epileptic children who don't respond to standard drug therapy; 2). Dieting bodybuilders in precontest dieting phases, up to 12 weeks in duration; 3). Strength phase athletes who want to incorporate more meat without a large weight increase or any weight increase; 4). Type II diabetics (non-insulin dependent) 6-12 weeks, with carbohydrates brought back in slowly and in measured quantities; 5). Anyone, who is otherwise healthy, but overweight and not happy with the mirror may want to consider giving this diet a try for 6-12 weeks then bring back in carbohydrates slowly and in reduced/measured quantities. Yes, every class is temporary and it is believed, by this writer, that a low carbohydrate, non-ketogenic diet would be the goal, eventually, for anyone following a current ketogenic diet because ketosis is not a normal, everyday, physiological state and was not intended to be from a physiology standpoint. With all of this said let's begin. What is a ketogenic diet and why would anyone want to modify their current eating regimen to adapt to and follow a ketogenic diet? First, let me say that the ketogenic diet dates back to biblical times and in more modern times of the 20th century, the ketogenic diet has been studied extensively with more research warranted even so (1). The word ketogenic reveals the basic identity of the metabolic process in humans of ketone (keto) production (genic). So we've produced ketones. What does this mean and how are ketones used as ready substrates to fuel anabolic and catabolic reactions, or better stated, how are ketones used to fuel metabolism? Ketones are a byproduct of fatty acid catabolism and this process of breaking down triglycerides into glycerol and fatty acids is known as lipolysis. Lipolysis is a normal physiological event occurring at times when the body is utilizing fat as a fuel source and thus, breaking down stored triglycerides and mobilizing free fatty acids and glycerol for further catabolism into our body's absolute source of energy, ATP. Lipolysis is activated during normal calorie-restrictive dieting conditions and partially explains the reason we lose body fat during hypocaloric periods or when we've created a net calorie deficiency when activity, such as exercise, coupled with our basal metabolic rate creates a greater need for calories than we are providing through our diet. Ketone production is an indicator that lipolysis has been activated and you are now, at least partially, burning fats for fuel. A ketogenic diet, as you might expect, is a diet which promotes lipolysis as a chief energy source, in preference to dietary glucose, the principal carbohydrate utilized by the body after breaking down polysaccharides into the monosaccharide glucose. If lipolysis is the goal of a ketogenic diet for otherwise healthy individuals, what is the best way to accomplish this? To give ourselves a reference point and provide the baseline for comparison, I present the highly touted pyramid of healthy eating. The food guide pyramid, as many of you have seen, is representative of what mainstream dietetics in 1996 want the majority of the American population to consume on a daily basis for health, vigor and longevity. The base and foundation of the pyramid suggests 6-11 servings of bread, cereal, rice and pasta with the following other food groups and servings providing the remaining calories in a given day: vegetables 3-5 servings, fruits 2-4 servings, milk, yogurt and cheese 2-3 servings, meat, poultry, fish, dry beans, eggs and nuts 2-3 servings, and last but not least fats, oils and sweets are to be used sparingly. Upon visual observation of the actual pyramid represented you can see the food groups are arranged with the foods which should be consumed in greater quantities at the bottom, and which are representative of a strong, solid foundation on which to build (2). When you are eating a ketogenic diet we turn everything upside down, except that turning the pyramid upside down only provides an unstable pivot point which the pyramid couldn't possibly be supported by. What we really must do to represent the ketogenic diet appropriately is move the food groups and provide for a solid base, consisting of fats and oils as the foundation to build upon. With a ketogenic diet, fats and oils are indeed representative of the greatest proportion of the macronutrient organic molecules; lipids, proteins, carbohydrates and nucleic acids eaten on a daily basis. There's a good chance, as you sit there right now that you're in a serious state of denial and many walls have already been put up doubting the efficacy of this diet. I mean, after all, isn't it fat that makes us fat? How could we possibly even maintain our current weight, let alone lose weight with a diet which works off a structure of fats first, protein second and carbohydrates third? Fat has been portrayed as an evil villain. I mean, remember the traditional pyramid? Fats and oils are to be used sparingly! Fat-free this and fat-free that. It's all good. It's all O.K. if it's fat-free. Not true and even potentially dangerous for some people who don't metabolize sugars properly. In spite of the plethora of enzymes and metabolites in each cell, metabolism is not random. Rather, it is highly regulated. If each of the possible metabolic reactions were to occur at a fixed rate all of the time, organisms would be incapable of reacting to changes in their environment. For example, the intake of energy may be sporadic (e.g. meals), yet organisms expend energy continuously. Metabolism must therefore be regulated so that an organism can respond efficiently to the availability of energy or food. When there is no intake of food but a continued need for energy expenditure, metabolic fuels are mobilized from storage depots at a rate sufficient to supply cells with oxidizable substrates. Humans, for example, can survive periods of starvation as long as five to six weeks when provided with water. A very obese adult could probably endure a fast of more than a year, but physiological damage and even death could result from the accompanying extreme ketosis after this amount of time (7) (Remember, we're not starving, we're eating everyday). Keep in mind that any organism responds not only to external demands but also to genetically programmed instructions. The responses of organisms to changing demands may involve alterations in many pathways or only a few and may occur on a time scale ranging from less than a second to hours or longer. Briefly, and very simplified, this is what occurs when a normal, otherwise healthy person eats a typical meal consisting of 55% carbohydrates, 30% fats, 15% protein- in other words, the "ideal diet". Lipids are catabolized into fatty acids, carbohydrates to monosaccharides and proteins are broken down into amino acids. Absorption of macromolecules is primarily achieved in the small intestine and the macromolecules are used to fuel glycolysis, the kreb's cycle and the electron transport system, with carbohydrates being burned preferentially to fats and proteins as an energy source. As long as glucose is plentiful and insulin is present, glucose fuels the human machine and fats are burned primarily as a fuel source only when carbohydrates are insufficient or the body perceives an insufficiency, as is the case in diabetes mellitus. A ketogenic diet has been compared to a fasting/starvation diet because in many ways, the metabolic pathways responsible for energy production are similar in both. There is one striking difference which should be very obvious, however, between a fasting/starvation diet and the diet presented here. FOOD! We are neither fasting nor starving with a ketogenic diet and in fact we are consuming, in some degree, all three of the major energy-producing organic macromolecules which are, once again, lipids, proteins and carbohydrates. To better illustrate how the body could possibly survive and even thrive on such a diet it should be understood that individuals who may benefit the greatest from a diet of this type are individuals who don't process sugars properly, as is the case in Type II, Noninsulin dependent, Adult-Onset Diabetes, and individuals who are at greater risk for coronary heart disease due to complications associated with morbid obesity. Briefly, Noninsulin dependent diabetes is usually associated with obesity and insulin secretion may be normal. Circulating levels of insulin may even be elevated, thus the problem is not a shortage of insulin, but insulin resistance resulting from decreased sensitivity, poor responsiveness, or both. Chronic hyperglycemia (high blood sugar) is the result. A drop in insulin production is often observed in individuals as time passes and currently there is strong evidence to support a tiring of the pancreas from chronic insulin output. A drop in insulin production is often observed in individuals with NIDDM as time passes. NIDDM affects about 5% of the population or approximately 12,500,000 people nationwide. Chronic hyperglycemia can lead to a number of complications including cataracts, sclerotic lesions in blood vessel walls, and general ill health associated with obesity The aim of all regimens for the management of diabetes is control of blood glucose levels. Dietary modifications are often sufficient to control NIDDM and this type of diabetes may even disappear with moderate weight loss and a program of exercise (3). If obesity begets NIDDM and NIDDM begets obesity then we can begin to realize the seriousness which surrounds a diet which may help control blood glucose levels and which promotes the dissolving of fat. The health risks of overfatness are so many that it has been declared a disease: obesity. Besides diabetes and hypertension, other risks threaten obese adults. Among them are high blood lipids, cardiovascular disease, sleep apnea, osteoarthritis, abdominal hernias, some cancers, varicose veins, gout, gallbladder disease, respiratory problems, liver malfunction, complications in pregnancy and surgery, flat feet and even a high accident rate. Moreover, after the effects of diagnosed diseases are taken into account, the risk of death from other causes remains twice as high for people with lifelong obesity as for others. An estimated 25 percent of U.S. adults are overweight to a degree that incurs such risks (2). As I stated before, a ketogenic diet is compared to a fasting diet because of similar metabolic reactions for utilizing fatty acids and protein as principle energy substrates when glucose levels are low. So, in very simplified form, this is what happens when we change from a typical "fed state" in which carbohydrates are plentiful and the fasting or ketogenic state in which carbohydrates are restricted. In the absorptive phase, lasting from 2-4 hours after a meal, the level of glucose in the blood rises. Glucose is rapidly taken up by the liver, skeletal muscle and the brain. If the level of glucose in the blood rises above the ability of the kidney to reabsorb filtered glucose, the excess is lost to the urine, as is the case with hyperglycemia and diabetes. High blood glucose triggers the release of insulin, which has many physiological effects including stimulation of glycolysis (utilization of glucose to form 2 ATP and 2 pyruvic acid molecules), fatty acid synthesis and protein synthesis as well as inhibition of glycogenolysis (breaking down glycogen to glucose), gluconeogenesis (conversion of noncarbohydrate sources to glucose), fatty acid oxidation (cleaving long chain fatty acids 2 carbons at a time into shorter fatty acids), ketogenesis (producing ketones) and proteolysis (breaking down proteins). Glucagon, which acts only on liver, has effects that are in general, opposite those of insulin. Insulin levels are high in the fed state (a state generally associated with food consumption containing carbohydrates); glucagon levels are high in the fasted state (or states in which glucose levels are low such as the ketogenic diet). Lipids entering the body during the absorptive phase are packaged in chylomicrons (a transporter for lipids). Triglycerides in chylomicrons are delivered to peripheral tissues (peripheral tissues are defined as any tissue which is not the liver, indicating the liver's central role in metabolism and filtration of toxins). Triglycerides are hydrolyzed outside the cell and fatty acids are taken up, esterified (relinked with glycerol) and stored (3). Stored lipid represents the body's most plentiful source of potential energy. Relative to other nutrients, the quantity of lipid available for energy is almost unlimited. The actual lipid fuel reserves in a typical young adult male amount to about 90,000 to 110,000 kcal (23,800kJ) of energy. In contrast, the carbohydrate energy reserve is about 2% of this total, or approximately 2000 kcal (8400kJ) (6). Dietary amino acids arrive at the liver during the absorptive phase. These amino acids are either catabolized, used for protein synthesis or permitted to pass unaltered to peripheral tissues. Oxidation of the amino acids in liver generates a large amount of ATP, much of which is immediately consumed by the pathways of gluconeogenesis and urea synthesis, which remove the carbon and ammonia, respectively, generated by amino acid catabolism. In the transition into early starvation or initial ketogenic dieting, the absorption of dietary glucose slows, the levels of insulin drops and the level of glucagon rises. The liver responds to the hormonal changes by breaking down glycogen and releasing glucose. Low levels of insulin are also accompanied by an increase in the rate of lipolysis in adipose tissue and an increase in the release of free fatty acids into circulation. In addition to gluconeogenesis there is another revelation that may come as a shock to some of you. When choice is available, most tissues use fatty acids as fuels before ketone bodies, and BOTH BEFORE GLUCOSE (3). This means that glucose is used only when it is abundant and other fuels are scarce. Fatty acids are used in preference to glucose even though the concentration of circulating glucose is always much higher than the concentration of free fatty acids. The glucose-fatty acid cycle, first proposed by Philip Randle, explains how the preference for glucose or fatty acids is determined by metabolic conditions. Operation of the glucose-fatty acid cycle requires that low concentrations of glucose correspond to greater fatty acid availability. As I've stated earlier, low availability of glucose results in decreased levels of insulin. Less insulin means that lipolysis inhibition in adipose tissue has been lifted and the availability of free fatty acids rises. The glucose-fatty acid cycle contributes to the maintenance of blood glucose levels by sparing the oxidation of glucose in peripheral tissues. This pattern of fuel use is usually observed only when the availability of glucose is low, such as after liver glycogen stores are exhausted, but the cycle predicts that any rise in the level of circulating fatty acids will decrease glucose use. The glucose-fatty acid mechanism suppresses the use of glucose when fatty acids are available; when glucose is low, insulin is low, release and catabolism of fatty acids is high, and products of fatty acid catabolism (NADH, acetyl CoA and citrate) inhibit glucose degradation and spare the use of glucose. Other cycles of metabolism which assist in sparing glucose when glucose levels are low include the Cori cycle which regenerates ATP from lactate produced in muscle tissue. The lactate generated is returned to liver for conversion back to glucose. The glucose-alanine cycle interconverts glucose to alanine in muscle and then back to glucose once again in liver. Amino acids are the major gluconeogenic precursors initially and one key difference between starvation or fasting and an eucaloric ketogenic diet is that during starvation the use of endogenous amino acids requires degradation of body proteins and accompanying loss of protein function. With a ketogenic diet copious amounts of dietary proteins are being consumed everyday. As you will see, the body strives to maintain protein homeostasis and particularly, the precious intracellular proteins. When given the choice, it is the belief of this writer that the body will utilize dietary proteins during this initial gluconeogenic activity, although some body proteins may initially be sacrificed through the actions of various hormones until adaptation has occurred. Protein turnover is continuous and the two processes comprising turnover, synthesis and degradation, approximately balance one another in the healthy adult. Whole-body turnover in humans is correlated to ones' metabolic mass. Daily turnover of protein is calculated to be approximately 4.6g/kg body weight. For the average 70-kg male, turnover of whole-body protein would approximate 320 g daily (7). Individual body proteins, however, vary in their turnover rate; the half-life of a protein can range from only a few minutes to several months. Furthermore, neither the turnover rate of an individual protein nor that of total body protein remains constant. The rate of synthesis and degradation can be influenced by a variety of factors related to nutrition, including immediate food intake, previous diet, and overall nutrition status. Some have postulated that during a ketogenic diet we will continuously show accelerated proteolysis of intracellular proteins and muscle for gluconeogenesis which is the opposite of what any athletic individual wants to do. During the initial stages of a ketogenic diet the catabolism of muscle tissue may occur for a brief period until the body has adapted to the diet and the use of fatty acids and ketones as primary fuel substrates. Protein degradation rates decrease concurrently so that even in chronic starvation, which the low carb diet is not, daily losses of nitrogen become quite small. For example, a person fully adapted to starvation can survive at a cost of 3 to 4 g of his or her body protein per day. This new priority is justified by the vital physiological importance of body proteins. Proteins that must obviously be conserved for life to continue include antibodies, needed to fight infection, enzymes, which catalyze life-sustaining reactions and hemoglobin for the transport of oxygen to tissues. The protein sparing shift at this point is from gluconeogenesis to lipolysis, as the fat stores, and if following a ketogenic diet, dietary fats, become the major supplier of energy. This shift to fat breakdown also releases a large amount of glycerol, which becomes the major gluconeogenic precursor, rather than amino acids (7). The principal mechanism of adjustment to starvation is a change in hormone balance. Decreased insulin activity, coupled with increased synthesis of counterregulatory hormones such as glucagon, epinephrine and norepinephrine promotes fatty acid mobilization from adipose tissue, production of ketones and the availability of amino acids for gluconeogenesis. Initially, in starvation or fasting and possibly preadjustment to a ketogenic diet, glucocorticoids are important in gluconeogenesis because they promote catabolism of muscle protein to provide substrates for gluconeogenesis. We must remember that proteolysis of muscle tissue may occur on a ketogenic diet in the early preadjustment stages, however, ketogenic dieters are not starving and the initial increased catabolism of body proteins will not continue for longer than as little as a few days or perhaps up to a few weeks. Ketogenic dieters are still consuming lipids, proteins and carbohydrates on a daily basis and are not starving. An increased adjustment to starvation (or a ketogenic diet) is characterized by a decrease in the secretion of glucocorticoids, however (7). As fasting or starvation (or a ketogenic diet) continues, tissues continue to use fatty acids and glucose for energy, but also begin to use ketones formed in the liver from fatty acid oxidation. A decrease in protein catabolism and gluconeogenesis occurs concurrently with the brain's and other tissues' adaptation to ketones as a source of energy. Glutamine metabolism in the kidney increases as starvation continues and acidosis occurs. Within the kidney, glutamine catabolism generates ammonia, which serves to help correct the potential for acidosis (7). Once again, a difference between the ketogenic diet and starvation is acidosis. Acidosis is well regulated in individuals who are not starving and even in those who are, however, a discussion of protein and amino acid turnover should include renal glutamine metabolism which is also a regulator of blood pH. As carbohydrates continue to remain low and the body is forced to use fatty acids, proteins and glycerol via gluconeogenesis for fuels, fatty acids are converted to ketone bodies, which, unlike fatty acids, can cross the blood-brain barrier and serve as fuel for the brain, further sparing the use of glucose. Less use of glucose at this state means less What we've clearly shown thus far, is that the body is adaptive and utilizes many complex mechanisms to not only spare glucose for organs which absolutely require it like the kidney medulla, the retina, red blood cells and parts of the brain, but also regenerates necessary glucose from non carbohydrate sources. If further evidence is necessary to convince any doubters that a low carbohydrate diet can not only sustain life but provide a great abundance of energy for daily activities, exercise and even intense exercise, I'll provide the following scenario: In humans, in the fed state (which as I mentioned before is generally associated with carbohydrate ingestion), the brain requires about 120 grams of glucose per day and all other glycolytic tissues require about 60 grams per day. Total glucose necessary per day during intermediate starvation is reduced to approximately 110-120 grams per day (3). The body, at this stage, is already making adjustments for reduced carbohydrate availability. As ketone bodies become more readily available, they can substitute as an energy source in tissues which would normally otherwise utilize glucose as a fuel source. What tissues can utilize ketone bodies for energy? (1) The brain (2) Muscle (3) The Kidneys (4) Small intestine The sparing effect of ketone bodies on glucose when a eucaloric diet is still being utilized, ensures that peripheral tissues will have the glucose they need to function efficiently. During intermediate starvation and potentially, during initial ketogenic dieting, about 40-50 grams of the 110-120 grams of glucose used per day are accounted for by the activity of the Cori cycle (if you'll think back, the Cori cycle was a cycle of glucose regeneration from glucose to lactate in muscle and then back to glucose again in the liver). In starvation, lipolysis of adipose tissue will contribute between 15 and 20 grams of glucose per day and remains fairly constant during starvation. We can conclude that lipolysis of adipose tissue as well as fatty acid oxidation of dietary lipids with a ketogenic diet will produce glucose in at least as great a concentration as starvation. So far we've created approximately 70 grams of glucose via the Cori cycle and lipolysis with another 40-50 grams of glucose needed to fill the bank and provide peripheral tissues with glucose to operate effectively. How do we get the remaining glucose we absolutely must have during intermediate starvation or preadjustment ketogenic dieting? Gluconeogenesis from amino acids is quite high, even in the absorptive phase when carbohydrates are present. During starvation, proteolysis of peripheral tissues increases to provide gluconeogenic precursors at the liver. During the ketogenic diet protein is consumed in copious amounts, thus thwarting the debilitating effects of losing precious cellular proteins and muscle protein. The production of 100 grams of glucose requires the breakdown of about 175 grams of amino acids. During starvation this cannot last long as even a small amount of lost protein to provide energy is accompanied by loss of functional capacity (3). Once again, we're not starving, we're eating generous portions of lipids, proteins and minimal carbohydrates. A typical 180 pound bodybuilder, for instance, will consume approximately 180-360 grams of protein per day depending on training philosophy and ideas about the benefits in general of consuming additional protein as a bodybuilder. There is even stronger evidence to suggest that endurance athletes may benefit from increased protein consumption (even more so than bodybuilders) and they may in fact be consuming large amounts of protein from their diet as well. I cannot speak for them, however (4). We've already exceeded the minimal necessary amounts of glucose to keep peripheral tissues functioning efficiently and we haven't even eaten any carbohydrates yet. Let's not forget that most ketogenic diets don't advocate abstinence from carbohydrates completely and that most bodybuilders or dieting individuals following a ketogenic diet will consume between 30 and 50 grams of carbohydrates per day. We've already shown that glucose will be plentiful and available to fuel tissues which require it but let's review thus far how it was accomplished. (1) A reduction in carbohydrate intake has reduced insulin production, although insulin in normal, healthy individuals is present at all times in blood, albeit, in lower concentrations during low carbohydrate ingestion. (2) A lowering of insulin has lifted the inhibition on lipolysis and lipolysis is now stimulated. If calories are insufficient to maintain BMR plus activity then adipose tissue and dietary fatty acids will effectively be used to generate energy via the beta oxidation of free fatty acids and gluconeogenesis of glycerol, the back bone of stored triglycerides. In either case, hypocaloric or eucaloric dieting, lipolysis will be enhanced and the choice of fuels will be determined by calories consumed with preference given to dietary lipids first and adipose tissue second. (3) The glucose-fatty acid cycle dictates that when carbohydrate is low, fatty acids can serve as a preferred fuel source, thus, lowering the need for glucose. (4) The Cori cycle recycles glucose by converting glucose into lactate within muscle and then a reconversion of lactate in the liver back to glucose takes place, thus completing the cycle. (5) The glucose-Alanine cycle is similar to the Cori cycle except that glucose is converted into pyruvate within muscle once again and then to Alanine, also within muscle, which is transported to the liver for reconversion into glucose. (6) The body has adapted to the reduction in glucose and is ready and willing to utilize ketone bodies as a fuel source in certain tissues. (7) We are still eating some carbohydrates every day! As starvation or the ketogenic diet continues, lipolysis continues to release considerable amounts of fatty acids, which are taken up by the liver. Fatty acids enter the mitochondria, where they are partially oxidized. The citric acid cycle in liver can absorb only a fraction of the acetyl CoA produced by beta oxidation, and most is converted to the ketone bodies beta-hydroxybutyrate and acetoacetate. Ketone bodies that are taken up and metabolized by tissues spare the use of glucose, just as glucose is spared by the operation of the glucose-fatty acid cycle. As ketone bodies initially become available, they provide up to 50% of the energy requirement of skeletal muscle. The most important overall effect, however, of the use of fatty acids and ketone bodies as alternatives to glucose, is that, as I stated in previous pages, less demand for glucose means that less proteolysis of muscle protein is required to supply the gluconeogenic pathway. Ketone bodies are acidic, water soluble short chain fats and if left to accumulate in an uncontrolled fashion could have devastating effects on our central nervous system. Excess ketones are filtered and diluted ( as they are water soluble) and excreted in urine. Our body also has very capable buffering systems in place, (one previously mentioned is the use of renal glutamine metabolism to create ammonia) to accept the extra hydrogen ions released in the blood which prevent wild fluctuations in blood pH. An excellent example of buffer capacity is found in the blood plasma of mammals, which has a remarkable constant pH of 7.4. Consider the results of an experiment that compares the addition of an aliquot of strong acid to a volume of blood plasma with a similar addition of either physiological saline or water. When 1.0ml of 10 M HCL (hydrochloric acid) is added to 1000ml of physiological saline or water that is initially at pH 7.0, the pH is lowered to 2.0. However, when 1.0 ml of 10 M HCL is added to 1000 ml of blood plasma at pH 7.4, the pH is again lowered, but only to 7.2- impressive evidence for the effectiveness of physiological buffering (3). The pH of the blood is primarily regulated by the carbon dioxide(CO2)-carbonic acid(H2CO3)-bicarbonate(HCO3) buffer system. The buffer capacity of blood depends upon equilibria between gaseous carbon dioxide(which is present in the air spaces of the lungs), aqueous carbon dioxide(which is produced by respiring tissues and dissolved in blood), carbonic acid, and bicarbonate. When the pH of blood falls due to a metabolic process that produces excess hydrogen ions, the concentration of carbonic acid increases momentarily, but carbonic acid rapidly loses water to form dissolved carbon dioxide(aqueous), which enters the gaseous phase in the lungs and is expired as carbon dioxide (gaseous). An increase in the partial pressure of carbon dioxide in the air expired from the lungs thus compensates for the increased hydrogen ions. This system of pH regulation effectively neutralizes the excess hydrogen ions, however, it does so at the cost of depleting the blood bicarbonate. A bicarbonate repletion mechanism exists in the kidney and requires the amino acid glutamine (3). Conversely, if the pH of the blood rises, the concentration of bicarbonate increases transiently, but the pH is rapidly restored as the breathing rate changes and the reservoir of carbon dioxide(gaseous) in the lungs is converted to carbon dioxide (aqueous) and then to carbonic acid in the capillaries of the lungs. Again, the equilibrium of the blood buffer system is rapidly restored by changing the partial pressure of carbon dioxide in the lungs (3). One point which must be addressed when discussing the effects of buffering systems and the acidic nature of ketone bodies is the incorrectly assumed potential for ketoacidosis in individuals who still have the ability to secrete normal amounts of insulin from the pancreas. In diabetics, who are vivid negative examples of what can go wrong with the integration of metabolism and metabolic regulation (homeostasis) for the continuance of life, ketoacidosis and metabolic acidosis are very real and serious problems which must be taken into consideration by those individuals. In diabetics, who are already at risk for chronic hyperglycemia, diuresis leads to a dehydration compounded by increased insensible water loss due to hypernea of metabolic acidosis. Metabolic acidosis results from the excessive ketogenesis occurring in the liver. Peripheral circulatory failure, a consequence of severe hemoconcentration leads to tissue hypoxia with a consequent shift of the tissues to anaerobic metabolism. Anaerobic metabolism raises the concentration of lactic acid in the blood, thereby worsening the metabolic acidosis. The ketonuria along with glucosuria associated with acidosis causes an excessive loss of sodium from the body; loss of this extracellular cation further compromises body water balance. A net loss of potassium, the chief intracellular cation, accompanies increased protein catabolism and cellular dehydration, both of which characterize uncontrolled diabetes (7). In non-insulin dependent diabetics or the overweight but healthy individuals who are utilizing a ketogenic diet this cascade of events, which eventually may lead to coma or death, does not occur. If it did, we'd have a lot of very sick or dead dieters to deal with and in all actuality we wouldn't be writing this paper because the diet would not be as "trendy" as it has become. Why then, don't type II diabetics or normal but overweight individuals succumb to the hazards of ketoacidosis or metabolic acidosis? The answer lies in the body's innate ability to maintain homeostasis. With a ketogenic diet we are mobilizing large amounts of free fatty acids which are producing ketone bodies in large quantities. Ketone bodies are acidic. If we agree thus far in this paragraph then let's elucidate the reason we aren't all dropping like flies. When plasma ketone concentrations reach 4-6mmol, insulin release from the pancreas is stimulated. This blunts (but does not normalize) lipolytic activity in the fat cell such that plasma free fatty acid (FFA) levels are fixed at about .7-1.0mmol - sufficient to allow moderate production of aceto-acetate and 3-hydroxybutyrate by the liver, but insufficient to allow maximum rates of production required to develop ketoacidosis. In type I diabetics subjects the protective ketone-insulin feedback loop cannot operate because of beta-cell failure in the Islets of Langerhans. As a consequence, plasma FFA reach much higher concentrations, driving ketone production to maximal rates, thereby leading to the ketoacidotic state (8). Another, perhaps more obvious advantage, is our ability as human beings to utilize common sense. Since the kidneys are going to help us flush unused ketones then we can help our kidneys do their job by drinking a lot of distilled water everyday. At least one gallon of distilled water should be consumed everyday when individuals are following a ketogenic diet or any diet for that matter. I've spent a lot of time covering the basic metabolic pathways associated with a ketogenic diet consisting of 75% lipids, 20% proteins and 5% or less carbohydrate. There are those who profess to have all the answers and shriek at a diet which promotes such a high fat consumption and, in the beginning, nearly excludes certain food groups. There are great differences between this type of diet and someone who is ill with Insulin Dependent Diabetes Mellitus. A normal person produces insulin but may not regulate blood glucose levels and uptake very efficiently due to many factors. An Insulin Dependent Diabetic does not produce insulin, or very much, and has lost much of the control that healthy, but overweight individuals possess. You may be curious about exactly what foods are acceptable for this diet. In general: All meat, all fish, all fowl, all shellfish, all eggs, almost all cheeses, vegetables of 10% carbohydrate or less, cauliflower, tomatoes, spinach, sauerkraut, broccoli, brussels sprouts, spices, sugar free beverages, fats and oils, nuts and seeds in moderation, peanut butter in moderation and water as the principle dietary solvent (5). Final recommendations and general guidelines for anyone following a ketogenic diet: Generally speaking, when individuals are strictly following the initial dieting changes which accompany this diet they are lacking in various vitamins, minerals and fiber. While there is great controversy over whether fiber is of vital importance for life-long health and cancer prevention, this writer believes fiber should be sought and not avoided. Because I have made initial recommendations that anyone following this diet will not be on it in its strict form for more than 12 weeks there are some simple ideas which I think are important; (1) Drink at least one gallon of distilled water every day, (2) While carbohydrate intake will most likely be limited to 30-50 grams per day it is important to make the carbohydrates you do eat of a fibrous nature. Vegetables which are high in fiber and nuts can help balance the carbohydrate/fiber issue. They are also a rich source of vitamins and minerals. I suggest not eating any carbohydrate that contains greater than a 3:1 ratio of carbs to fiber grams. In other words, if the package of nuts you're eating has 6 grams of carbs, it should also contain 2 grams of fiber or more. Assuming the eggs and other products you're going to be eating that contain trace amounts of carbs equals no more than 6 grams of carbs per day, you will have between 24 and 44 grams of carbs left to consume. In these carbs you should strive to eat those which contain the 3:1 ratio of carbs to fiber. In this way you'll get between 8 and 15 grams of fiber everyday. You may also want to take a carbohydrate-free fiber supplement, available at any health food store, if your fiber intake is less than the range above. Additionally, if your bowel movements are less than one per day, after two weeks of adaptation to the diet, you may want to consider adding in a fiber supplement as well. (3) Take a complete multi-vitamin and mineral supplement everyday to prevent any possibility of vitamin and mineral deficiencies, (4) Optionally, take free-form glutamine in supplemental form for optimal intestinal, skeletal muscle and renal functioning. The walk-away message from this paper is an understanding that lipolysis is the process of dissolving fat and there is "no lipolysis without ketosis and no ketosis without lipolysis" (5) and how this diet differs substantially from a starvation diet and doesn't cause metabolic acidosis in normal insulin producing individuals. We aren't going to die by placing our bodies in a state of benign dietary ketosis while we get our blood sugar under control and lose excess weight in the process. In fact, we may actually see an improvement in energy, health and mental stability in the absence of wild fluctuations in blood sugar. Eventually, you will want to bring in other food groups and carbohydrates, however, if you're carbohydrate sensitive, you will want to bring them in slowly and in measured quantities, not exceeding the carbohydrate levels which your body can efficiently process without laying down fat and without causing wild fluctuations in blood sugar. In the meantime, many people will enjoy a reduction in bodyfat with an exceptionally little amount of lean mass lost in the process, as well as an increase in perceived energy and perhaps, for the first time in many years, a stabilization of blood sugar. References: 1. Spalding, K, Amorde, MS RD, (J Am Diet Assoc, Nov. 96, pp.1134) 2. Cataldo, Debruyne, Whitney, "Nutrition and Diet Therapy", 1995 3. Moran, Scrimgeour, Horton, Ochs, Rawn "Biochemistry" 2nd Ed., 1994 4. Wolinsky, Ira, Hickson, James "Nutrition in Exercise and Sport", 2nd Ed., 1994 5. Atkins, Robert MD "Dr. Atkins New Diet Revolution", 1995 6. Mcardle, Katch, Katch "Exercise Physiology", 1996 7. Groff, J, Sareen, G, Hunt, S "Advanced Nutrition and Human Metabolism", 2nd Ed, 1995 8. Rifkin, Porte "Diabetes Mellitus: Theory and Practice", 1990 MORE READING ON KETOGENIC DIETS Wing RR; Vazquez JA; Ryan CM Cognitive effects of ketogenic weight-reducing diets Int J Obes Relat Metab Disord, 19:11, 1995 Nov, 811-6 Gumbiner B, etal Effects of diet composition and ketosis on glycemia during very-low-energy-diet therapy in obese patients with non-insulin-dependent diabetes mellitus Am J Clin Nutr, 1996 Jan Amari A, et al Achieving and maintaining compliance with the ketogenic diet J Appl Behav Anal, 1995 Fall Nebeling LC, et al Effects of a ketogenic diet on tumor metabolism and nutritional status in pediatric oncology patients: two case reports. J Am Coll Nutr, 1995 Apr Nebeling LC, et al Implementing a ketogenic diet based on medium-chain triglyceride oil in pediatric patients with cancer. J Am Diet Assoc, 1995 June Baron JA, et al A randomized controlled trial of low carbohydrate and low fat/high fiber diets for weight loss Am J Public Health, (1986 Nov) 76(11):1293-6 Alford BB et al The effects of variations in carbohydrate, protein, and fat content of the diet upon weight loss, blood values, and nutrient intake of adult obese women. J Am Diet Assoc (1990 Apr) 90(4):534-40 Rabast U, et al Loss of weight, sodium and water in obese persons consuming a high or low carbohydrate diet. Ann Nutr Metab (1981) 25(6):341-9 Lambert EV, et al Enhanced endurance in trained cyclists during moderate intensity exercise following 2 weeks adaptation to a high fat diet. Eur J Appl Physiol (1994) 69(4):287-293 McCargar LJ, et al Dietary carbohydrate-to-fat ratio: Influence on while-body nitrogen retention, substrate utilization, and hormone response in healthy male subjects. Am J Clin Nutr (1989 Jun) 49(6):1169-78 Lopez A, et al Some interesting relationships between dietary carbohydrates and serum cholesterol. Am J Clin Nutr (1966 Feb) 18(2):149-153 Kasper H, et al Letter: Behavior of body weight under a low carbohydrate, high fat diet. Am J Clin Nutr (1975 Aug) 28(8): 800-1 Kasper H, et al Response of body weight to a low carbohydrate, high fat diet in normal and obese subjects. Am J Clin Nutr (1973 Feb) 26(2):197-204 Young CM, et al Effect of body composition and other parameters in obese young men of carbohydrate level of reduction diet. Am J clin Nutr (1971 Mar) 24(3):290-6 Hodges RE, et al Dietary carbohydrates and low cholesterol diets: effects on serum lipids on man. Am J Clin Nutr (1967 Feb) 20(2):198-208 Krehl WA, et al Some metabolic changes induced by low carbohydrate diets. Am J Clin Nutr (1967 Feb) 20(2):139-148 Rosen JC, et al Mood and appetite during minimal-carbohydrate and carbohydrate-supplemented hypocaloric diets. Am J Clin Nutr (1985 Sep) 42(3):371-9 Tremblay A, et al Diet composition and postexercise energy balance Am J Clin Nutr (1994 May) 59(5):975-9 Phinney SD, et al Capacity for moderate exercise in obese subjects after adaptation to a hypocaloric, ketogenic diet. J Clin Invest (1980 Nov) 66(5):1152-61 Yang MU, et al Composition of weight lost during short-term weight reduction. Metabolic responses of obese subject to starvation and low-calorie ketogenic and nonketogenic diets. J Clin Invest (1976 Sep) 58(3):722-30 Council on Foods and Nutrition A critiquie of low-carbohydrate ketogenic weight reduction regimens. A review of Dr. Atkins' diet revolution. JAMA (1973 Jun 4) 224(10):1415-9 Vazquez JA, et al Protein sparing during treatment of obesity: ketogenic versus nonketogenic very low calorie diet. Metabolism (1992 Apr) 41(4):406-14 Newbold HL Reducing the serum cholesterol level with a diet high in animal fat. South Med J (1988 Jan) 81(1):61-3 Kuroshima A, et al Effect of a high-fat diet on metabolic responses to exercise. Jpn J Physiol (1975) 25(5):575-84 Rabast U, et al Comparative studies in obese subjects fed carbohydrate-restricted and high carbohydrate 1,000 calorie formula diets. Nutr Metab (1978) 22(5):269-77 Golay A, et al Similar weight loss with low or high carbohydrate diets. Am J Clin Nutr (1996 Feb) 63(2):174-8 Kundu SK, Judilla Am Novel solid-phase assay of ketone bodies in urine. Clin Chem (1991 Sep) 37(9):1565-9 Fery F, et al Hormonal and metabolic changes induced by an isocaloric isoproteinic ketogenic diet in healthy subjects. Diabete Metab (1982 Dec) 8(4):299-305 Kather H, et al Influences of variation in total energy intake and dietary consumption on regulation of fat cell lipolysis in ideal weight subjects. J Clin Invest (1987) 80(2):556-72 Giorski J. Muscle triglyceride metabolism during exercise. Can J Phys Pharm (1992) 70(1):123-31 Symons JD, et al High-intensity exercise performance is not impaired by low intramuscular glycogen. Med Sci Sports Exerc (1989) 21(5):550-7 Evans WJ, et al Dietary carbohydrates and endurance exercise. Am J Clin Nutr (1985) 41(5):1146-54 Mitchell GA, et al Medical aspects of ketone body metabolism. Clin Invest Med (1995) 18(3):193-216 Rabast U, et al Dietetic treatment of obesity with low and high carbohydrate diets. Intl J Obesity (1979) 3(3):201-211 Liu VJ, et al Chromium and insulin in young subjects with normal glucose tolerance. Am J Clin Nutr (1982) 25(4):661-67 Rickman F, et al Changes in serum cholesterol during the Stillman diet. JAMA (1974) 228:54 Fontbonne A, et al Coronary heart disease mortality risk: plasma insulin level is a more sensitive marker than hypertension or abnormal glucose tolerance in overweight males: the Paris prospective study. Intl J Obesity (1988) 12:557-65 Coulston AM, et al Deleterious metabolic effects of high-carbohydrate, sucrose-containing diets in patients with non-insulin dependent diabetes mellitus. Am J Med (1987) 82:213-20 Coulston AM, et al Original articles: persistence of hypertriglyceridemic effect of low-fat high-carbohydrate diets in NIDDM patients Diabetes Care 1989 12(2):94-101 Stout, RW. Hyperinsulinaemia- a possible risk factor for cardiovascular disease in diabetes mellitus. Horm Met Res (1985) 15:37-41 Tremblay A, et al Nutritional determinants of the increase in energy intake associated with a high-fat diet Am J Clin Nutr (1991) 53:1134-37 McGill HC The relationship of dietary cholesterol to serum cholesterol concentration and to atherosclerosis in man. Am J Clin Nutr (1979) 32:2664-2702 Willett WC, et al Relation of meat, fat and fiber to the risk of colon cancer in a prospective study among women. NEJM (1990) 323(24):1664-72 Willett WC, et al Original article: dietary fat and the risk of breast cancer. NEJM (1987) 316(1):22-28 Macquart-Moulin G, et al Case control study on colorectal cancer and diet in Marseilles. Intl J Cancer (1986) 38(2):183-91 Haenszel W, et al A case-control study of large bowel cancer in Japan. J National Cancer Institute (1980) 64(1):17-22 Tuyns AJ, et al Colorectal cancer and the intake of nutrients: oligosaccarides are a risk factor, fats are not. A case-control study in Belgium. Nutrition and Cancer (1987) 10(4):181-96 :cool: TJ :cool:

MUUUUUUAAAAAHHH HA HA HA HA!! Then my work here is done.. :wink: TJ :wink:

Ding Bathroom's done Ding Bathroom's done DING Bathroom's done DING Bathrooooooom's doooooooone.... TJ