Please Scroll Down to See Forums Below That's why fonz made the textbook statement.Unfortunately,science isn't always 100% dead on when it comes to real world results,particularly in respect to athletes.For how many years did we see abstracts from the scientific community supporting 'supposed facts' that anabolics did not increase muscular performance/size?Sometimes it becomes important to not stand so rigidly behind what is on paper,and listen to what is occurring from real life experience.I think the wisest policy is to use both as your finale weighing scale.Too many athletes have reported remarkable results with various ALA products to discount what they're saying based on what a particular research paper or two has concluded.Science is constantly shifting and evolving,and what may be law at one moment can completely change in the next.
ALA for athletes
- Thread starter swimmar
- Start date
What, that ALA increases glycogen synthase and glycogen storage? Did they perform muscle biopsies on themselves and then do an assay for those two things?
If people want to spend their money on ALA and they think it works I think that's great. My objective here is to add a little science to the nonstop ALA hype that swamps this board. Hopefully some people might be able to use that science to help weigh the undocumented claims about ALA, and learn a little about how the body works in the process.
swimmar
New member
nandi12 said:
But you are saying that since there has been no studies that show that ALA improves glycogen synthase and glycogen storage, that ALA does not improve glycogen synthase and glycogen storage.
Yes, it has never been shown. That's no reason to then state, without any reservation, that it...
Again, the absence of proof of a statement does not lead to the statement being false. Something along the lines of "If ALA decreases .... and increases ...., then this would happen" would be appropriate.
quartermiler
New member
nandi12, not to flame or anything... but some people here cant break down what all your saying because it is too complicated, like you copy and pasted it from a book or something. You are very knowledgable, but try to break it down into lamen's (spelling?) terms for some of us, lol. Once again, dont mean to flame or anything.
macrophage69alpha
New member
1. ala and r-ala increase glycogen stores.. if you wish to dispute show some CONCLUSIVE evidence otherwise... because ALL evidence, both clinical and anecdotal, use points to this.
2. ala is not an "anti-diabetic" drug.. it is a naturally occuring vitamin and produced in vivo by humans (well at least r-ala is)..
3. reduction of plasma insulin is GOOD.... note that the person above who was having trouble using fat was using ala (if from an older batch was likely proportionately higher in s-ala).. increased plasma insulin is VERY BAD for fat loss.. from several stand points.. including gh and LPL..
4. Nandi.. your research is good but your application shows limited experience.. as well as gross underestimation of both insulin resistance in the population and effects of higher plasma insulin levels.
5. to address the ketotic issue..
ALA, among other things, will give FALSE POSITIVES with sodium nitroprusside (the reagent in ketostix)
2. ala is not an "anti-diabetic" drug.. it is a naturally occuring vitamin and produced in vivo by humans (well at least r-ala is)..
3. reduction of plasma insulin is GOOD.... note that the person above who was having trouble using fat was using ala (if from an older batch was likely proportionately higher in s-ala).. increased plasma insulin is VERY BAD for fat loss.. from several stand points.. including gh and LPL..
4. Nandi.. your research is good but your application shows limited experience.. as well as gross underestimation of both insulin resistance in the population and effects of higher plasma insulin levels.
5. to address the ketotic issue..
ALA, among other things, will give FALSE POSITIVES with sodium nitroprusside (the reagent in ketostix)
Quartermiler, one thing I seldom do is cut and paste. I may quote passages from relevant studies or post abstracts, but if you spent some time on the boards where I am either a mod or administrator, you would see how I lash into people who cut and paste.
Would you be happier if instead of trying to explain things using what I consider minimal terminology from basic physiology and metabolism I said simply "IMO ALA sucks and all the crap you read about it here is just that: crap". If I simply said "There is no evidence that it works except in type 2 diabetics" members like swimmar would say "the absence of proof of a statement does not lead to the statement being false".
Is there proof that creatine will increase my IQ, make me rich, and make me more attractive to women? No. To quote once again swimmar's logic: "the absence of proof of a statement does not lead to the statement being false". So should I assume creatine may actually do these things until proven otherwise? I don't think so. That is not how science works.
If a person has type 2 diabetes I have no doubt that by improving overall glucose uptake by increasing the effectiveness of the GLUT 4 transport system, both oxidative (burning for fuel) and nonoxidative (storage as glycogen) glucose disposal will increase. Is there evidence that ALA has this effect in the estimated 75% of the population that is not insulin resistant or has type 2 diabetes? No. As swimmar pointed out, this does not mean it doesn't happen. Should I assume it works and spend my money on it. No, but that is me.
My original point in this whole thread was that in people for whom ALA works, namely type 2 diabetics, by virtue of increasing pyruvate dehydrogenase there is a substrate shift from fat burning to carb burning by increasing the flux of pyruvate into the citric acid cycle.
Swimmar also was wondering about using ALA to induce ketosis. As I pointed out earlier, ketosis and the production of ketone bodies are a byproduct of gluconeogenesis, your liver's attempt to increase the supply of blood glucose for the brain. Another way ALA works to lower blood sugar is to slow gluconeogenesis (1). The liver powers the gluconeogenesis process by burning fat. Less gluconeogenesis means less fat burning. All this is part of ALA's strategy to more effectively use the carbs you eat.
But as Fonz and Huck would say, sometimes you have to ignore the science and go with your feelings.
And as far as my limited experience goes, I have been doing science both in academia and the private sector for almost 25 years now. As far as evidence goes that ALA does not work, here is an abstract showing no effect no non diabetic rats. Macro, Huck, or Fonz, can you produce a study showing that ALA works in those who do not have type 2 diabetes?
J Appl Physiol 2002 Jan;92(1):50-8
Effects of exercise training and antioxidant R-ALA on glucose transport in insulin-sensitive rat skeletal muscle.
Saengsirisuwan V, Perez FR, Kinnick TR, Henriksen EJ.
Muscle Metabolism Laboratory, Department of Physiology, University of Arizona, College of Medicine, Tucson, Arizona 85721-0093, USA.
We have recently demonstrated (Saengsirisuwan V, Kinnick TR, Schmit MB, and Henriksen EJ, J Appl Physiol 91: 145-153, 2001) that exercise training (ET) and the antioxidant R-(+)-alpha-lipoic acid (R-ALA) interact in an additive fashion to improve insulin action in insulin-resistant obese Zucker (fa/fa) rats. The purpose of the present study was to assess the interactions of ET and R-ALA on insulin action and oxidative stress in a model of normal insulin sensitivity, the lean Zucker (fa/-) rat. For 6 wk, animals either remained sedentary, received R-ALA (30 mg. kg body wt(-1). day(-1)), performed ET (treadmill running), or underwent both R-ALA treatment and ET. ET alone or in combination with R-ALA significantly increased (P < 0.05) peak oxygen consumption (28-31%) and maximum run time (52-63%). During an oral glucose tolerance test, ET alone or in combination with R-ALA resulted in a significant lowering of the glucose response (17-36%) at 15 min relative to R-ALA alone and of the insulin response (19-36%) at 15 min compared with sedentary controls. Insulin-mediated glucose transport activity was increased by ET alone in isolated epitrochlearis (30%) and soleus (50%) muscles, and this was associated with increased GLUT-4 protein levels. Insulin action was not improved by R-ALA alone, and ET-associated improvements in these variables were not further enhanced with combined ET and R-ALA. Although ET and R-ALA caused reductions in soleus protein carbonyls (an index of oxidative stress), these alterations were not significantly correlated with insulin-mediated soleus glucose transport. These results indicate that the beneficial interactive effects of ET and R-ALA on skeletal muscle insulin action observed previously in insulin-resistant obese Zucker rats are not apparent in insulin-sensitive lean Zucker rats.
(1) Biochem J 1984 May 1;219(3):773-80
Inhibition of gluconeogenesis in rat liver by lipoic acid. Evidence for more than one site of action.
Blumenthal SA.
Would you be happier if instead of trying to explain things using what I consider minimal terminology from basic physiology and metabolism I said simply "IMO ALA sucks and all the crap you read about it here is just that: crap". If I simply said "There is no evidence that it works except in type 2 diabetics" members like swimmar would say "the absence of proof of a statement does not lead to the statement being false".
Is there proof that creatine will increase my IQ, make me rich, and make me more attractive to women? No. To quote once again swimmar's logic: "the absence of proof of a statement does not lead to the statement being false". So should I assume creatine may actually do these things until proven otherwise? I don't think so. That is not how science works.
If a person has type 2 diabetes I have no doubt that by improving overall glucose uptake by increasing the effectiveness of the GLUT 4 transport system, both oxidative (burning for fuel) and nonoxidative (storage as glycogen) glucose disposal will increase. Is there evidence that ALA has this effect in the estimated 75% of the population that is not insulin resistant or has type 2 diabetes? No. As swimmar pointed out, this does not mean it doesn't happen. Should I assume it works and spend my money on it. No, but that is me.
My original point in this whole thread was that in people for whom ALA works, namely type 2 diabetics, by virtue of increasing pyruvate dehydrogenase there is a substrate shift from fat burning to carb burning by increasing the flux of pyruvate into the citric acid cycle.
Swimmar also was wondering about using ALA to induce ketosis. As I pointed out earlier, ketosis and the production of ketone bodies are a byproduct of gluconeogenesis, your liver's attempt to increase the supply of blood glucose for the brain. Another way ALA works to lower blood sugar is to slow gluconeogenesis (1). The liver powers the gluconeogenesis process by burning fat. Less gluconeogenesis means less fat burning. All this is part of ALA's strategy to more effectively use the carbs you eat.
But as Fonz and Huck would say, sometimes you have to ignore the science and go with your feelings.
And as far as my limited experience goes, I have been doing science both in academia and the private sector for almost 25 years now. As far as evidence goes that ALA does not work, here is an abstract showing no effect no non diabetic rats. Macro, Huck, or Fonz, can you produce a study showing that ALA works in those who do not have type 2 diabetes?
J Appl Physiol 2002 Jan;92(1):50-8
Effects of exercise training and antioxidant R-ALA on glucose transport in insulin-sensitive rat skeletal muscle.
Saengsirisuwan V, Perez FR, Kinnick TR, Henriksen EJ.
Muscle Metabolism Laboratory, Department of Physiology, University of Arizona, College of Medicine, Tucson, Arizona 85721-0093, USA.
We have recently demonstrated (Saengsirisuwan V, Kinnick TR, Schmit MB, and Henriksen EJ, J Appl Physiol 91: 145-153, 2001) that exercise training (ET) and the antioxidant R-(+)-alpha-lipoic acid (R-ALA) interact in an additive fashion to improve insulin action in insulin-resistant obese Zucker (fa/fa) rats. The purpose of the present study was to assess the interactions of ET and R-ALA on insulin action and oxidative stress in a model of normal insulin sensitivity, the lean Zucker (fa/-) rat. For 6 wk, animals either remained sedentary, received R-ALA (30 mg. kg body wt(-1). day(-1)), performed ET (treadmill running), or underwent both R-ALA treatment and ET. ET alone or in combination with R-ALA significantly increased (P < 0.05) peak oxygen consumption (28-31%) and maximum run time (52-63%). During an oral glucose tolerance test, ET alone or in combination with R-ALA resulted in a significant lowering of the glucose response (17-36%) at 15 min relative to R-ALA alone and of the insulin response (19-36%) at 15 min compared with sedentary controls. Insulin-mediated glucose transport activity was increased by ET alone in isolated epitrochlearis (30%) and soleus (50%) muscles, and this was associated with increased GLUT-4 protein levels. Insulin action was not improved by R-ALA alone, and ET-associated improvements in these variables were not further enhanced with combined ET and R-ALA. Although ET and R-ALA caused reductions in soleus protein carbonyls (an index of oxidative stress), these alterations were not significantly correlated with insulin-mediated soleus glucose transport. These results indicate that the beneficial interactive effects of ET and R-ALA on skeletal muscle insulin action observed previously in insulin-resistant obese Zucker rats are not apparent in insulin-sensitive lean Zucker rats.
(1) Biochem J 1984 May 1;219(3):773-80
Inhibition of gluconeogenesis in rat liver by lipoic acid. Evidence for more than one site of action.
Blumenthal SA.
Last edited:
swimmar
New member
quartermiler, the concepts aren't terribly difficult, it helps to have another web browser open so you can do a google search on any familar terms.
But "The enzyme pyruvate dehydrogenase, which converts pyruvate to acetyl coenzyme A which enters the citric acid cycle for complete oxidation, is defective in type 2 diabetes" was just a little too much. Yeah, it's great that you can throw all these technical terms around. Impressive. It's also akin to walking into a high school calculus class and start spouting off stuff on Irrotational and Solenoidal Fields if they are just beginning integration. If nandi12 were on sci.med, it would be different.
But "The enzyme pyruvate dehydrogenase, which converts pyruvate to acetyl coenzyme A which enters the citric acid cycle for complete oxidation, is defective in type 2 diabetes" was just a little too much. Yeah, it's great that you can throw all these technical terms around. Impressive. It's also akin to walking into a high school calculus class and start spouting off stuff on Irrotational and Solenoidal Fields if they are just beginning integration. If nandi12 were on sci.med, it would be different.
serge
New member
READ AND LEARN
KETOSIS FOR NEWBIES
by Beowulf
Even if you are just taking up this ridiculous hobby, you know doubt have heard of a ketogenic diet. It should be noted that ketogenic diets are, well, an unrelenting bitch from hell intent on destroying you and stealing your newly acquired rocket car (typically reserved for "gold" level AE writers). So, since you are familiar with ketogenic diets do you really know how they work? Do you know what to expect? The intent of this article is to answer these, no doubt, burning questions.
If you are uninterested in the science of things this is not section for you. However, if you want to learn the "why" in addition to the "how" part of the equation, I would recommend that you keep reading. In a normal dietary situation (in the presence of carbohydrates) your body uses glucose as its primary fuel source. Every one is happy. Your brain has sufficient glucose to function at 100%, your muscles have bountiful glycogen stores, and your kidneys are not having to put in overtime to remove urea from your blood. The body only requires 50 grams of carbohydrates per day to avoid going into ketosis. That is only two hundred kcalories a day from carbs (one gram of carbs = four kcalories). This is rather remarkable considering that your brain all by its lonesome utilizes 140-150 grams of carbohydrate in a day.
In the absence of carbohydrates, or with a very restricted carbohydrate intake, your body thinks it is starving to death. You could even be hypercaloric (more calories consumed than spent) and your body would still think that it is starving. In reality, your brain is starving. Did you ever wonder why bodybuilders who misuse insulin die? Failure to consume adequate carbohydrate and the usage of insulin will result in the effective removal of all the glucose in the bloodstream. The insulin drives it into muscle and fat. The end result is that the brain just runs out of gas and one goes into a coma or dies.
Enter your friend and mine: ketosis. In the absence of carbohydrates the body still has to have glucose to operate. This is because the CNS (Central Nervous System) prefers to use glucose for fuel. It will only use ketone bodies for fuel once blood plasma concentrations are extremely high, primarily because ketone bodies don't pass through the blood brain barrier all that well. There are two substances in the body that we will be concerned with that can convert to glucose: glycerol and protein. Lactate can also be converted to glucose, but this is not of terrible importance for our purposes.
Glycerol has a three-carbon skeleton and that is what the krebs cycle is looking for. Once protein is broken down into its constituent amino acids it enters the krebs cycle at different places. Some of these intermediaries are three carbon molecules and some will eventually become pyruvate itself. You see, pyruvate has a three carbon skeleton as well so by stripping off all the crap and starting from the three carbon skeleton up, two glycerols or pyruvates can be run essentially backwards through glycolisis (the formation of two three carbon pyruvates from one six carbon glucose) to form one six carbon molecule of glucose.
Where does the gycerol come from? A fat is constructed from three fatty acids and, you guessed it, a gycerol. Since fatty acids cannot be run backwards through glycolisis, something has to be done with them when they are stripped of their glycerol. The fatty acids are chemically modified into acetyl CoA (trust me, this process far outreaches the scope of this article) which progresses through the Krebs cycle, or citric acid cycle. A good number of these acetyls are metabolized completely and produce ATP. However, a considerable portion of these do not proceed all the way through the krebs cycle. There is excess acetyl CoA generated from the oxidation of fat because the Krebs cycle only works so fast (however, it really is remarkably fast). This extra acetyl CoA is packaged by the liver as ketones. The liver is the only place in the body that produces ketones.
Ketones are funny things. Their primary purpose is, of course, to serve as a fuel source. Ketones feed what glucose would ordinarily feed. The thing is that once blood ketone concentrations rise to a certain point they can no longer be efficiently utilized by the body and certain cells in your body just don't use them all that well. The end result is that they are removed from the bloodstream and end up in your urine. You are essentially peeing calories. This is a novel theme because your body is an ancient and incredibly efficient machine. It almost never wastes anything.
Another interesting thing to note is most nutritional experts will tell you that a ketogenic diet WILL cause muscle wasting. However, as bodybuilders we know that ketogenic diets are notorious for their muscle sparing properties. What gives here? In the author's humble opinion it all has to do with weight training. Compare a normal sedentary individual with resistance trainee. Are they both going to use protein for fuel? You bet. Are they going to equal amounts of protein for fuel? Doubtful. A sedentary individual will never need as much dietary protein to repair the microtrauma incurred from everyway events like walking and standing upright as a trained person would require to repair the catastrophic (by comparison) microtrauma resulting from a hard day of squats. Bodybuilders simply need that protein for things other than fuel. I concede the fact that protein is going to be used to make glucose. The brain absolutely positively must have glucose and we should be glad to spare some protein so that we don't slip into a coma or die. However, I simply don't buy the notion that a disproportionate amount of protein to fat is going to be utilized. The body will do what it has to do to stay alive first, but after that, it has a miracullous way of healing itself.
It is important to note that in order for protein to be used as a fuel source, its constituent amino acids must be deaminated. This means that the amino group is cleaved off of the amino acid. The problem arises because this amino group contains a nitrogen and that nitrogen reacts to form ammonia in your cells. Needless to say, ammonia in your cells is some serious shit. This ammonia makes its way to the liver, where it is converted to urea. Urea is toxic as well and excess levels can lead to gout (uric acid poisoning), however, it is not as toxic as it predecessor. Urea is eventually filtered out of the blood by the kidneys and excreted in urine. This is important because when urea concentrations rise you must urinate more in order to expel the potentially toxic product. Also, due to the higher concentration of urea in the blood you have to urinate much more frequently. This, in combination with the fact that glycogen stored in muscles actually exists in a 1:3 ratio with water and when the glycogen leaves so does the water, can spell trouble. .If you do not drink an increased amount of water, you will become dehydrated.
Part of the reason that the Atkins diet became so popular so quickly in the mainstream is because dieters can lose weight very rapidly during the first week of the diet. They could also lose weight very rapidly if we were to administer a diuretic and they didn't diet. Essentially the same thing is happening.
While ketosis is a really nifty trick, it is important to remember that energy expenditure is the real determinant in weight loss. If you cut carbs and are still in a hypercaloric state, guess what, you are going to gain weight. If you are in ketosis and you are in a hypercaloric state, you will more than likely gain weight. Ketosis is not a ticket to eat all you want. You are still subject to the law of energy conservation.
Another consideration should be that your body really does prefer glucose as a fuel source to ketones (I am can't stress this point enough). Being as such, the tissues that don't use ketones for fuel well are going to give you problems in the form of decreased performance. This is a major problem because two of the tissues that don't fare well on ketones are the brain and skeletal muscle.
The brain will find a way to function, let there be no doubt, but it will not function at full capacity. Things will seem a little hazy. You will more than likely not notice this because everything slows down, even the conscious perception which would enable you to notice it. While potentially troubling, this is not a huge problem. Reaction times will be longer for certain, but probably not to the point of compromising safety in most situations.
The inability to use ketones as a fuel source of skeletal muscles will get your attention. You will go to the gym and perform like shit. You will miss your heaviest lifts and you will feel shame. Obviously, the rules are altered a considerable deal by simultaneous usage of AAS and implementation of a ketogenic diet but if you are training clean, you will have to fight through some piss poor training sessions. This is the beauty of diets such as Bodyopus, The Anabolic Diet, and Animabolics. They allow for a carb up period after a given time and, as a result, you won't feel, for lack of a better term, so flat.
While most of the other side effects primarily afflict special populations with either liver or kidney damage, another side effect is universal. You see, fiber has a way of hiding itself in foods that contain carbohydrates. Fiber is the primary reason for peristalisis, or the contraction of your bowel to move food toward the toilet. This is a very nice way of saying that you will more than likely become very very badly constipated if you don't use a fiber supplement to keep the plumbing flowing. I can speak from personal experience on this one. You will find yourself in the bathroom making deals with the almighty. Sayings like, "Dear Lord, if you let me take this dump I swear that I will bake cookies for the church bake sale" or "Dear Lord, if I don't make it through this, give the paramedics the intelligence to come up with a good story to tell my mother like I died saving a bus full of orphans or something like that....." will become part of your daily restroom regimen.
I have never met anyone who was not completely miserable while on a ketogenic diet. You are starving your body and it is really, really pissed at you. You will experience carb cravings the lacks of which no one but Oprah has experienced. It will be entirely unpleasant. The smell of bread will instantly transform you into a frothing rabid beast. It will be bad. However, if you stay the course you will be rewarded with body recomposition that is more radical than any other nutrition plan known to man. Is it possible to lose weight with carbs? You bet. Remember, caloric expenditure is the key to weight loss. Do I think that ketogenic diets are more effective at striping off adipose and sparing muscle? I do.
KETOSIS FOR NEWBIES
by Beowulf
Even if you are just taking up this ridiculous hobby, you know doubt have heard of a ketogenic diet. It should be noted that ketogenic diets are, well, an unrelenting bitch from hell intent on destroying you and stealing your newly acquired rocket car (typically reserved for "gold" level AE writers). So, since you are familiar with ketogenic diets do you really know how they work? Do you know what to expect? The intent of this article is to answer these, no doubt, burning questions.
If you are uninterested in the science of things this is not section for you. However, if you want to learn the "why" in addition to the "how" part of the equation, I would recommend that you keep reading. In a normal dietary situation (in the presence of carbohydrates) your body uses glucose as its primary fuel source. Every one is happy. Your brain has sufficient glucose to function at 100%, your muscles have bountiful glycogen stores, and your kidneys are not having to put in overtime to remove urea from your blood. The body only requires 50 grams of carbohydrates per day to avoid going into ketosis. That is only two hundred kcalories a day from carbs (one gram of carbs = four kcalories). This is rather remarkable considering that your brain all by its lonesome utilizes 140-150 grams of carbohydrate in a day.
In the absence of carbohydrates, or with a very restricted carbohydrate intake, your body thinks it is starving to death. You could even be hypercaloric (more calories consumed than spent) and your body would still think that it is starving. In reality, your brain is starving. Did you ever wonder why bodybuilders who misuse insulin die? Failure to consume adequate carbohydrate and the usage of insulin will result in the effective removal of all the glucose in the bloodstream. The insulin drives it into muscle and fat. The end result is that the brain just runs out of gas and one goes into a coma or dies.
Enter your friend and mine: ketosis. In the absence of carbohydrates the body still has to have glucose to operate. This is because the CNS (Central Nervous System) prefers to use glucose for fuel. It will only use ketone bodies for fuel once blood plasma concentrations are extremely high, primarily because ketone bodies don't pass through the blood brain barrier all that well. There are two substances in the body that we will be concerned with that can convert to glucose: glycerol and protein. Lactate can also be converted to glucose, but this is not of terrible importance for our purposes.
Glycerol has a three-carbon skeleton and that is what the krebs cycle is looking for. Once protein is broken down into its constituent amino acids it enters the krebs cycle at different places. Some of these intermediaries are three carbon molecules and some will eventually become pyruvate itself. You see, pyruvate has a three carbon skeleton as well so by stripping off all the crap and starting from the three carbon skeleton up, two glycerols or pyruvates can be run essentially backwards through glycolisis (the formation of two three carbon pyruvates from one six carbon glucose) to form one six carbon molecule of glucose.
Where does the gycerol come from? A fat is constructed from three fatty acids and, you guessed it, a gycerol. Since fatty acids cannot be run backwards through glycolisis, something has to be done with them when they are stripped of their glycerol. The fatty acids are chemically modified into acetyl CoA (trust me, this process far outreaches the scope of this article) which progresses through the Krebs cycle, or citric acid cycle. A good number of these acetyls are metabolized completely and produce ATP. However, a considerable portion of these do not proceed all the way through the krebs cycle. There is excess acetyl CoA generated from the oxidation of fat because the Krebs cycle only works so fast (however, it really is remarkably fast). This extra acetyl CoA is packaged by the liver as ketones. The liver is the only place in the body that produces ketones.
Ketones are funny things. Their primary purpose is, of course, to serve as a fuel source. Ketones feed what glucose would ordinarily feed. The thing is that once blood ketone concentrations rise to a certain point they can no longer be efficiently utilized by the body and certain cells in your body just don't use them all that well. The end result is that they are removed from the bloodstream and end up in your urine. You are essentially peeing calories. This is a novel theme because your body is an ancient and incredibly efficient machine. It almost never wastes anything.
Another interesting thing to note is most nutritional experts will tell you that a ketogenic diet WILL cause muscle wasting. However, as bodybuilders we know that ketogenic diets are notorious for their muscle sparing properties. What gives here? In the author's humble opinion it all has to do with weight training. Compare a normal sedentary individual with resistance trainee. Are they both going to use protein for fuel? You bet. Are they going to equal amounts of protein for fuel? Doubtful. A sedentary individual will never need as much dietary protein to repair the microtrauma incurred from everyway events like walking and standing upright as a trained person would require to repair the catastrophic (by comparison) microtrauma resulting from a hard day of squats. Bodybuilders simply need that protein for things other than fuel. I concede the fact that protein is going to be used to make glucose. The brain absolutely positively must have glucose and we should be glad to spare some protein so that we don't slip into a coma or die. However, I simply don't buy the notion that a disproportionate amount of protein to fat is going to be utilized. The body will do what it has to do to stay alive first, but after that, it has a miracullous way of healing itself.
It is important to note that in order for protein to be used as a fuel source, its constituent amino acids must be deaminated. This means that the amino group is cleaved off of the amino acid. The problem arises because this amino group contains a nitrogen and that nitrogen reacts to form ammonia in your cells. Needless to say, ammonia in your cells is some serious shit. This ammonia makes its way to the liver, where it is converted to urea. Urea is toxic as well and excess levels can lead to gout (uric acid poisoning), however, it is not as toxic as it predecessor. Urea is eventually filtered out of the blood by the kidneys and excreted in urine. This is important because when urea concentrations rise you must urinate more in order to expel the potentially toxic product. Also, due to the higher concentration of urea in the blood you have to urinate much more frequently. This, in combination with the fact that glycogen stored in muscles actually exists in a 1:3 ratio with water and when the glycogen leaves so does the water, can spell trouble. .If you do not drink an increased amount of water, you will become dehydrated.
Part of the reason that the Atkins diet became so popular so quickly in the mainstream is because dieters can lose weight very rapidly during the first week of the diet. They could also lose weight very rapidly if we were to administer a diuretic and they didn't diet. Essentially the same thing is happening.
While ketosis is a really nifty trick, it is important to remember that energy expenditure is the real determinant in weight loss. If you cut carbs and are still in a hypercaloric state, guess what, you are going to gain weight. If you are in ketosis and you are in a hypercaloric state, you will more than likely gain weight. Ketosis is not a ticket to eat all you want. You are still subject to the law of energy conservation.
Another consideration should be that your body really does prefer glucose as a fuel source to ketones (I am can't stress this point enough). Being as such, the tissues that don't use ketones for fuel well are going to give you problems in the form of decreased performance. This is a major problem because two of the tissues that don't fare well on ketones are the brain and skeletal muscle.
The brain will find a way to function, let there be no doubt, but it will not function at full capacity. Things will seem a little hazy. You will more than likely not notice this because everything slows down, even the conscious perception which would enable you to notice it. While potentially troubling, this is not a huge problem. Reaction times will be longer for certain, but probably not to the point of compromising safety in most situations.
The inability to use ketones as a fuel source of skeletal muscles will get your attention. You will go to the gym and perform like shit. You will miss your heaviest lifts and you will feel shame. Obviously, the rules are altered a considerable deal by simultaneous usage of AAS and implementation of a ketogenic diet but if you are training clean, you will have to fight through some piss poor training sessions. This is the beauty of diets such as Bodyopus, The Anabolic Diet, and Animabolics. They allow for a carb up period after a given time and, as a result, you won't feel, for lack of a better term, so flat.
While most of the other side effects primarily afflict special populations with either liver or kidney damage, another side effect is universal. You see, fiber has a way of hiding itself in foods that contain carbohydrates. Fiber is the primary reason for peristalisis, or the contraction of your bowel to move food toward the toilet. This is a very nice way of saying that you will more than likely become very very badly constipated if you don't use a fiber supplement to keep the plumbing flowing. I can speak from personal experience on this one. You will find yourself in the bathroom making deals with the almighty. Sayings like, "Dear Lord, if you let me take this dump I swear that I will bake cookies for the church bake sale" or "Dear Lord, if I don't make it through this, give the paramedics the intelligence to come up with a good story to tell my mother like I died saving a bus full of orphans or something like that....." will become part of your daily restroom regimen.
I have never met anyone who was not completely miserable while on a ketogenic diet. You are starving your body and it is really, really pissed at you. You will experience carb cravings the lacks of which no one but Oprah has experienced. It will be entirely unpleasant. The smell of bread will instantly transform you into a frothing rabid beast. It will be bad. However, if you stay the course you will be rewarded with body recomposition that is more radical than any other nutrition plan known to man. Is it possible to lose weight with carbs? You bet. Remember, caloric expenditure is the key to weight loss. Do I think that ketogenic diets are more effective at striping off adipose and sparing muscle? I do.
