You've got to be able to kill stuff to survive and that means muscle. Yes and no. Although it's wonderful to imagine Paleolithic man taking down wild animals with his bare hands like in all the "Tarzan" movies, it's more likely that man used his bigger brain to outfox animals when it came to hunting.
Our brains are staggeringly large relative to our bodyweight than those of other animals; most likely we used our brains to compensate for relatively less muscle mass.
So while a modicum of muscle was necessary for survival, and our ancestors are thought to have had more muscle than the average American couch potato which isn't really saying much , excessive muscle mass was probably a liability. Sure, you need enough to get around and get food but anything more than that is basically dead weight. In the wild, with the possible exception of impressing a potential mate, an 18 inch arm wouldn't have been much of a benefit.
If anything, it might have slowed down your spear-throwing a bit. In contrast to fat, muscle requires a lot of energy to build, requires a lot of energy to sustain, and doesn't provide much energy when it is broken down.
Even then, your body will happily break it down when you diet. My point is that you run into an equally difficult set of adaptations occurring when you try to push your muscle mass beyond a certain point.
Our physiology reflects this which makes things really suck for folks who want to be bigger and leaner. In short, we're fighting against millions of years of evolution and adaptation to reach our goals of bigger and leaner. Usually, the body wins. They are called pro bodybuilders. There are a few reasons why the images in the majority of the magazines aren't very relevant to the rest of us.
First and foremost, pro bodybuilders or athletes in general have better genetics than the rest of us. They are the genetic elite. This isn't some type of personal grouse or whine, simply a statement of fact and reality. If you had their genetics, you wouldn't be reading this book. If you look at pro bodybuilders in their early stages, they are still typically leaner and bigger than the normal individual.
From a physiological standpoint, they probably have higher than average testosterone levels and don't overproduce cortisol. Thyroid levels are probably optimal or close to it, helping to naturally optimize metabolic rate, fat burning and protein synthesis. They have good skeletal muscle insulin sensitivity and tend to put calories into muscle more effectively i. They probably have fewer fat cells than most people and that fat is evenly distributed although even female pros have problems with lower bodyfat.
When they diet, they don't have as many problems with metabolic slowdown. Their evenly distributed fat comes off easily and, since they can use fatty acids easily for fuel, they don't lose as much muscle when they diet. All of these factors contribute to their success. We can contrast that to the average individual who could have any number of potential metabolic defects that prevents them from reaching their desired goals.
Testosterone might be on the low side of normal, cortisol production is elevated, thyroid or nervous system output may be low meaning a lower than optimal metabolic rate. Skeletal muscle insulin sensitivity is low which means that excess calories get pushed towards fat cells more effectively.
When these folks diet, the brain tends to overreact, lowering metabolic rate which probably wasn't optimal to begin with. Fat loss slows to a crawl. Difficulties mobilizing bodyfat, along with problems with testosterone and cortisol, lead to increased muscle loss.
I could keep going but you get the idea. I'm not just telling you this to depress you; consider it more of a reality check to make you aware of what is and isn't possible. My point is that pro bodybuilders hell, pro athletes of any sort are the genetic elite. You are not like them and they have advantages naturally that you don't. Most importantly, trying to mimic what they do, or expecting their results, can only lead you down an endless path of frustration.
And then there are drugs All professional bodybuilders and most athletes use drugs. Anyone who says differently is lying or trying to sell you something. Again, this isn't a grouse or whine, but rather a statement of fact.
Couple better than average genetics with enough drugs and you get professional bodybuilders. You are not one of them, you will not be one of them. No amount of wishful thinking can change that. Even if you had access to all of their drugs, there's no guarantee you'd get as big; it's likely that one of the genetic advantages that professional bodybuilders have is a high sensitivity to the drugs that they do take. Anyone who tells you that the various bodybuilding drugs anabolic steroids, insulin, clenbuterol, etc.
Usually they have an all-natural supplement or steroid replacement to sell you in the first place I just have a book. I'd be lying if I told you that anything you'll read in this book could take you to the development level of even the worst pro. It can't. Without both their genetics and their drugs, it simply can't be done. To go above your genetic potential requires drugs.
The sooner you come to terms with this, the better off you'll be. The fact is that drugs, even the relatively simple testosterone, can take you to a level of development otherwise unachievable by any natural training, diet and supplement methods. At even moderate doses, testosterone allows you to sidestep your normal physiology and reach a higher level. It raises the "setpoint" of how much muscle you can carry; it reduces your fat mass at the same time.
Once you introduce all the other drugs endemic to pro-bodybuilding, you get a physiology that is unattainable in non-drug using individuals. Still not convinced? A single example should help to make my point. Testosterone levels are typically bottomed out some studies even find castrate levels, which is why a lot of natural contest bodybuilders can't get their dick hard, not that they have a sex drive in the first place , thyroid levels are bottomed out, IGF-1 levels are bottomed out, sympathetic nervous system output is way down meaning decreased caloric and fat burning, appetite is through the roof, cortisol is through the roof, on and on it goes.
Your body is turning off every system metabolic, reproductive, immune, etc. Contrast that to a dieting professional bodybuilder. With the choice of the right drugs, he can eliminate pretty much all of the above problems. Anabolic steroids replace natural testosterone, synthetic thyroid replaces what the body is no longer making, injectable insulin, GH, and IGF-1 fix the insulin, GH and IGF-1 problem, clenbuterol replaces sympathetic nervous system output, appetite suppressants can deal with appetite and anti-cortisol drugs deal with the cortisol problem.
That's only a partial drug list, by the way. Again, my point in explaining this isn't so much to give you a metaphorical kick in the nuts before we get started; it's to explain the basic realities of the situation. One of the worst things that a natural athlete or bodybuilder can hope to do is to emulate the pros in terms of their results, training or diet.
Pro athletes and bodybuilders have at least two major advantages that you don't have: genetic and drugs. Hoping that you can achieve what they achieve or, even worse, trying to use their approach to do it, is destined for failure.
But all is not lost. One of the goals of the UD2 is to mimic, to as great a degree as possible, some of the processes that occur normally in the genetic elite. By using specific nutritional and training practices, the occasional supraphysiological level of supplements and even the occasional drug, we can duplicate some of what's going on.
Either you can't wait to get into the nuts and bolts of this diet, or you're still not convinced. I mean, you can open any of the muscle magazines or should we call them supplement catalogs?
So how come I'm right and they're wrong? As I said in chapter 1, the biggest problem with the standard advice is simply that it is generally so standard. Most bodybuilding writers, nutritionists and gurus are more concerned with maintaining the status quo, maybe refining it a bit, than going out on a limb and suggesting something new and radical. So let's look at the status quo and see why it won't ultimately let you achieve your goal again, if it did, you wouldn't have gotten or even needed this book.
The standard prescription to do what I've described more muscle, less bodyfat is usually a fairly standard moderate to high carb, moderate to high protein, and low to moderate fat diet depending on the personal philosophy of the magazine and the writer in question.
High fiber, clean carbs, lots of quality protein, fats seem to be the most variable although everyone is finally getting onto the healthy fat bandwagon like they should have done years ago. Couple that with weight training and cardio and magic will happen, right?
Well, sort of. Most people remember those wonderful beginner days, when muscle gain and fat loss come without too much effort. It's true, beginners can pull off what seems like a magical body composition transformation without much difficulty.
Folks coming back from a layoff or injury, where they typically gain fat and lose muscle, can do this too. Muscle memory allows the muscle to be regained while the fat is coming back off. As people become more advanced, gaining more muscle, or reaching lower bodyfat levels, this trick becomes more and more difficult until the point that it is more or less impossible.
You usually end up either having to focus purely on muscle gain accepting that some fat will come with it or fat loss accepting that you'll lose some muscle. Bulking and cutting phases, basically. Personally, I don't have that kind of patience. I've always wanted a faster solution even if it was more complicated. Even without trying to gain muscle while you're losing fat, simply losing fat without losing muscle is problematic.
Getting to those levels without muscle loss isn't too much of a problem but getting leaner tends to cause muscle loss at faster and faster rates.
The usual advice is to up protein which only works up to a point or lose fat so abysmally slowly 0. Maybe with less cardio, or slightly different training, but the same nonetheless.
Once again, past the beginner stage, lifters find that putting on muscle at any sort of appreciable rate without drugs anyhow usually means gaining some bodyfat as well. Then there's the folks who want to lean out significantly while gaining muscle or strength at the same time. As I said above, this is pretty easy in beginners, folks who are very fat, or those coming back from a layoff. For everybody else, it's more difficult, approaching impossible. For short periods, the UD2 will let you do it.
Defining the problem again If you go around into any commercial gym, you typically see folks in a lot of different conditions. There are typically some big but fat guys, some small but lean guys, some small and fat guys, and a few big and lean guys. But, unless you belong to a gym with a large bodybuilder contingent, the last group tend to be few and far between. The question is why? Why is it so difficult to get both big and lean at the same time? It's almost as if the body can do one or the other well, but not both, which really isn't far from the truth.
Related to that, why is it so difficult to lose fat and gain muscle at the same time? Or to gain muscle without gaining fat at the same time? Hell, even losing fat without losing muscle is difficult enough. To answer the question of why things are so difficult, let's start simple and move towards more complex explanations, since that will lead us to an understanding of how to solve the problem.
The simplest answer I could give, I've already discussed in the last chapter and in my last book: evolution. On top of that, once you're past puberty, your body is far more concerned with homeostasis remaining the same than with anything else.
To one degree or another, it tends to defend your bodyweight and bodyfat percentage at a certain level which appears to be programmed in the brain.
You can change that set point to some degree with training and diet, but your body always strives to maintain the status quo more than anything else. But both of those are really just statements of the amazingly obvious, without really telling us much. So let's move a level deeper and start to get into the physiology of why accomplishing our goals is so difficult. That will lead us towards the solution. For example, study after study has shown that combining heavy strength training with heavy endurance training compromises the overall results.
Strength training sends the muscle an adaptive signal to become bigger and stronger and more efficient at using glucose for fuel; endurance training send a signal to become more energy efficient which typically means smaller because smaller muscle fibers can get energy more readily and use more fat for fuel.
End result is that the body can't do both optimally and you get less than stellar results when you try to do both. How does this apply to losing fat and gaining muscle?
In short, they have different and, in fact, mutually exclusive requirements. That is, gaining muscle and losing fat require different scenarios in terms of nutrition, hormones, etc. In fact, the specific requirements for gaining muscle are also the reason that you tend to gain fat at the same time. Similarly, the requirements for fat loss are part of the reason along with your body's adaptations that you will lose muscle at the same time.
I'll discuss this in detail next chapter. Synthesizing new tissue whether muscle or fat requires energy and that energy can't just magically appear. Synthesizing new muscle tissue is especially costly, at least when compared to synthesizing new fat.
While it's wonderfully idyllic to think that the calories for muscle growth will magically be generated from burning fat, it rarely happens that way, at least not without powerful repartitioning drugs like clenbuterol. Which makes a rather nice segue into the next chapter. At its simplest, partitioning refers to where the calories go into muscle or fat cells when you eat more of them or come from from muscle or fat cells when you eat less of them.
Unfortunately, we don't live in an ideal universe. As I mentioned early in this book, some hapless individuals will lose as much as one pound of muscle for every pounds of fat that they lose when they diet. Typically, those same individuals will put on about the same amount of fat and muscle when they gain weight.
Thus is the balance of the universe maintained. More genetically advantaged individuals tend to put more calories into muscle meaning less into fat when they overeat and pull more calories out of fat cells and less out of muscle when they diet. They stay naturally lean and have few problems dieting. Once again, you aren't one of them, or you wouldn't be reading this book.
When talking about calorie partitioning, researchers refer to something called the P-ratio. Essentially, P-ratio represents the amount of protein that is either gained or lost during over or under feeding. So a low P-ratio when dieting would mean you used very little protein and a lot of fat.
A high P-ratio would mean that you used a lot of protein and very little fat. It looks like, for the most part, P-ratio is more or less the same for a given individual: they will gain about same amount of muscle when they overfeed as they lose when they diet.
P-ratio can vary between individuals, of course, but for any given person, it appears to be relatively constant. So what controls P-ratio? As depressing as this is, the majority of of the P-ratio is out of our control; it's mostly genetic. Supraphysiological amounts of certain compounds supplements and, of course, drugs, can also affect the P-ratio. Exercise is perhaps the most significant weapon we have in battling with our body and affecting P-ratio.
So what are the main determinants of calorie partitioning? Hormones are crucially important. High testosterone levels tend to have positive partitioning effects more muscle, less fat while chronically high levels of cortisol have the opposite effect less muscle, more fat. Thyroid and nervous system activity affect not only metabolic rate but also fat burning. Thyroid also affects protein synthesis. Optimal levels of these hormones not only mean better fat loss and less muscle loss when you diet but better muscular gains and less fat gain when you gain weight.
Unfortunately, levels of these hormones are basically "set" by our genetics; the only way to change them significantly is with supplements or drugs. Another factor controlling P-ratio is insulin sensitivity which refers to how well or how poorly a given tissue responds to the hormone insulin. High insulin sensitivity means that a small amount of insulin will generate a large response; insulin resistance indicates that it takes more insulin to cause the same effects to occur.
Now, insulin is a storage hormone, affecting nutrient storage in tissues such as liver, muscle and fat cells. In that same ideal world, we'd have high insulin sensitivity in skeletal muscle as this would tend to drive more calories into muscle and poor insulin sensitivity in fat cells making it harder to store calories there.
This is especially true when you're trying to gain muscle. By limiting the muscle's use of glucose for fuel, insulin resistance not only spares glucose for use by the brain, but also increases the muscles use of fatty acids for fuel.
In addition to hormonal advantages, it's likely that the genetic elite have high skeletal muscle insulin sensitivity. They store tremendous amounts of calories in their muscles, which leaves less to go to fat cells. Their bodies also don't have to release as much insulin in response to food intake.
In contrast, individuals with poor skeletal muscle insulin sensitivity tend to overproduce insulin, don't store calories in muscle well this is part of why they have trouble getting a pump: poor glycogen storage in muscle cells and tend to spill calories over to fat cells more effectively.
So what controls insulin sensitivity? As always, there are a host of factors. One is simply genetic, folks can vary 10 fold in their sensitivity to insulin even if everything about them is the same.
Another is diet. Diets high in carbohydrates especially highly refined carbohydrates , saturated fats and low in fiber tend to impair insulin sensitivity.
Diets with lowered carbohydrates or less refined sources , healthier fats fish oils and monounsaturated fats like olive oil and higher fiber intakes tend to improve insulin sensitivity.
Another major factor is activity which influences insulin sensitivity in a number of ways. The first is that muscular contraction itself improves insulin sensitivity, facilitating glucose uptake into the cell.
Glycogen depletion remember this, it's important improves insulin sensitivity as well. So what else controls the P-ratio? As it turns out, the primary predictor of P-ratio during over- and underfeeding is bodyfat percentage. The more bodyfat you carry, the more fat you tend to lose when you diet meaning less muscle and the leaner you are, the less fat you tend to lose meaning more muscle.
The same goes in reverse: naturally lean but not folks who have dieted down individuals tend to gain more muscle and less fat when they overfeed and fatter individuals tend to gain more fat and less muscle when they overfeed. There are a few easy answers. One is that bodyfat and insulin sensitivity tend to correlate: the fatter you get, the more insulin resistant you tend to get and the leaner you are the more insulin sensitive you tend to be.
A second is that, the fatter you are, the more fatty acids you have available for fuel. In general, when fatty acids are available in large amounts, they get used. This spares both glucose and protein. By extension, the leaner you get, the more problems you tend to have; as it gets harder to mobilize fatty acids, the body has less to use. Since there is less glucose available because you're dieting this increases the reliance on amino acids protein for fuel.
The original Ultimate Diet advocated medium chain triglycerides a special type of fatty acid that is used more easily for fuel than standard fats and this can be a good strategy under certain circumstances. I'll mention some other options later on in the book. But that's not all. It turns out that bodyfat percentage is controlling metabolism to a much greater degree than just by providing fatty acids. Research over the past 10 years or so has identified fat cells as an endocrine tissue in their own right, secreting numerous hormones and proteins that have major effects on other tissues.
Perhaps the most important, and certainly the one most talked about is leptin, but that's far from the only one. Tumor necrosis factor-alpha, the various interleukins, adiponectin and other compounds released from fat cells are sending signals to other tissues in the body which affect metabolism.
Without getting into all of the nitpicky details many of which haven't been worked out yet , I just want to talk a little about leptin if you read my last book, this will all be familiar ground. Leptin, the short course Leptin is a protein released primarily from fat cells although other tissues such as muscle also contribute slightly. Leptin levels primarily correlate with bodyfat percentage, the more fat you have the more leptin you tend to have note: different depots of fat, visceral versus subcutaneous, show different relationships with leptin.
At any given bodyfat percentage, women typically produce times as much leptin as men. In addition to being related to the amount of bodyfat you have, leptin levels are also related to how much you're eating. After that initial rapid drop, there is a slower decrease in leptin related to the loss of bodyfat that is occurring. In response to overfeeding, leptin tends to rebound equally quickly much faster than you're gaining bodyfat.
In contrast to what you might think, it looks like leptin production by fat cells is mainly determined by glucose availability you'd think it was fat intake. Basically, leptin represents two different variables: how much bodyfat you're carrying and how much you're eating. That is, it acts as a signal to the rest of your body about your energy stores.
I'll come back to this in a second. Like most hormones in the body, leptin has effects on most tissues in the body. Leptin receptors have been found all over the place, in the liver, skeletal muscle, in immune cells; you name a site in the body and there are probably leptin receptors there.
There are also leptin receptors in the brain but I'll come back to that below. For now, let's look at a few of the effects that leptin has on other tissues in the body. In the liver, leptin tends to reduce insulin secretion from the beta-cells. In skeletal muscle, leptin promotes fat burning and tends to spare glucose and therefore amino acid use.
In fat cells, leptin may promote fat oxidation as well as making the fat cell somewhat insulin resistant. Leptin also affects immune cell function, decreasing leptin impairs the body's ability to mount an immune response.
Now you know at least part of the reason you tend to get sick more when you diet. On and on it goes. An entire book could and should be written about leptin.
Leptin and the brain Now, I want you to think back to the first couple of chapters of this book, where I talked about the evolutionary reasons it's so hard to get extremely lean. To your body, becoming too lean is a very real threat to your survival. From a physiological standpoint, that means that your body needs a way to "know" how much energy you have stored. As you may have guessed, or known from my last book, leptin is one of the primary signals along with many others including ghrelin, insulin, peptide YY and other as of yet undiscovered compounds that signals the brain about how much energy you have stored and how much you're eating.
All of these hormones send an integrated signal to a part of the brain called the hypothalamus that "tell" it what's going on elsewhere in your body. Changes in levels of these hormones causes other changes in various neurochemicals such as neuropeptide-Y NPY , corticotrophin releasing hormone CRH , pro-opiomelanocortin POMC and several others to occur. These neurochemicals regulate metabolic rate, hunger and appetite, hormones and a host of other processes.
So when you restrict calories, causing changes in all of the hormones and neurochemicals mentioned above, and a number of physiological processes change, mostly for the worse. This results in lowered levels of thyroid and testosterone.
Cortisol levels go up as does hunger and appetite. You get the idea. What you end up seeing is an all purposes systems crash when you try to take bodyfat to low levels. I should note that these processes are occurring to one degree or another during all diets, they simply become more pronounced at the extreme low levels of bodyfat. Ideally, the opposite effects should occur when you raise calories. However, for reasons I detailed in my last book, the system is asymmetrical: falling leptin and changes in all of the other hormones has a much larger impact on the body's metabolism than raising leptin does unless you're raising it back to normal.
So the body ends up fighting weight loss to a far greater degree than weight gain. Generally speaking, people find that it a lot easier to get fat than to get lean. Of course, there are exceptions, folks who seem to resist obesity or weight gain altogether.
Research will probably find that they are extremely sensitive to the effects of leptin and other hormones , so when calories go up, they simply burn off the excess calories without getting fat.
Most of us aren't that lucky. Rather, like insulin sensitivity discussed above, researchers will probably find that leptin sensitivity is a huge factor influencing how changes in caloric intake affect metabolism. Someone with good leptin sensitivity will tend to stay naturally lean and have an easy time dieting; folks with worse leptin sensitivity leptin resistance won't.
You might be thinking that the quick and dirty solution would be leptin injections. Using bromocriptine or other dopamine agonists seem to fix at least part of the problem by sending a false signal to the brain by making it think leptin levels are normal.
Recent studies that have given injectable leptin to dieters show that the fall in leptin is one of the primary signals in initiating the adaptation to dieting. However, unlike in rats, injecting leptin into humans doesn't fix all of the problems. This is because, in humans, there is more of an integrated response to both over and underfeeding.
To understand this better, I want to take a snapshot of what happens when you either reduce or increase calories. Dieting So you decide to diet, reducing carbs, calories or both.
Vary rapidly, blood glucose and insulin levels are going to be reduced. This is good as it releases the "block" on fat mobilization. Additionally, catecholamine release typically goes up at least initially , further increasing fat mobilization from fat cells. This causes blood fatty acid levels to increase. This is also good, as it tends to promote fat burning in tissues such as liver and muscle. The increase in blood fatty acid levels also has the short-term effect of causing insulin resistance.
As I mentioned, this is a good thing on a diet since it spares glucose and helps promote fat oxidation. So far, so good, right? Unfortunately, along with these good effects, a lot of bad things start to happen. I already described many of the central adaptations above: changes in leptin, ghrelin, Peptide YY and certainly other hormones "tell" your brain that you're not eating enough.
This causes changes in the various neurochemicals stimulating a number of negative adaptations. I want to note that the response is not immediate, there is a lag time between the changes in all of these hormones and the body's response. There are also many other adaptations which occur when you diet, so let's look at some of those.
First and foremost, the drop in leptin directly affects liver, skeletal muscle and fat cell metabolism, mostly for the worse. While the drop in insulin mentioned above causes better fat mobilization, it causes other problems. One is that testosterone will bind to sex-hormone binding globulin SHBG better, lowering free testosterone levels this is in addition to the drop in total testosterone.
As well, insulin is anti-catabolic to muscle, inhibiting muscle breakdown. The increase in cortisol that occurs with dieting enhances protein breakdown as well as stimulating the conversion of protein to glucose in the liver. Additionally, a fall in energy state of the muscle impairs protein synthesis although it increases fatty acid oxidation.
The mechanism behind this is more detail than I want to get into here. But the combined effect of these processes is that protein synthesis is decreased and breakdown is accelerated; this causes muscle loss. On top of that, high blood fatty acid levels tend to impair the uptake of T4 inactive thyroid into the liver. There are also changes in liver metabolism that impair the conversion of T4 to T3 active thyroid. Both of these processes cause decreased blood levels of T3. There is some evidence that high blood fatty acid levels causes tissues to become resistant to thyroid hormone itself this is part of why just taking extra thyroid on a diet doesn't fix all of the problems.
After the initial increase, there is also a drop in nervous system output that can occur in as little as days after you start a diet. Along with the drop in thyroid, insulin and leptin, this explains a majority of the metabolic slowdown that occurs. The change in liver metabolism and the reduction in insulin also impairs the production of IGF-1 from GH. All of these adaptations serve two main purposes.
The first is to slow the rate of fat loss, as this will ensure your survival as long as possible. Related to that, the body tends to shut down calorically costly activities. This includes protein synthesis, reproduction and immune function; there's little point keeping any of these functioning when you're starving to death. The second is to prime your body to put fat back on at an accelerated rate when calories become available again.
As I mentioned earlier, this makes perfect evolutionary sense, even if it presents a huge pain in the ass to us. I haven't even mentioned the hunger and appetite issue which is a topic worthy of an entire book. The combination signal sent by leptin, ghrelin, insulin, glucose, and a host of other hormones cholecystokinin, glucagon-like peptide 1 and 2, bombesin and many many others are all involved in both hunger and appetite. The changes that occur with dieting tend to make both shoot through the roof: you tend to get and stay hungry, thinking about food nearly constantly.
Bodybuilders and athletes may have unbelievable food control but it still sucks being hungry constantly when you try to diet. Ok, enough about dieting, what about overfeeding? Overfeeding To a great degree, most of the adaptations that occur with dieting reverse when you overeat.
Actually, that depends a lot on the situation. As I mentioned above, the body as a whole tends to defend against underfeeding better than it does against overfeeding which is why it's generally easier to gain weight than to lose it.
Studies where leptin has been increased above normal i. There are a couple of theories as to why this might be the case. Another possibility is related to something I alluded to above: leptin sensitivity and resistance.
It's thought that people have varying degrees of leptin resistance which means, in essence, that they don't respond as well to leptin as they should. On top of this, when leptin levels go up, it appears to stimulate resistance to itself. That is, when leptin gets and stays high, it causes you to become resistant to its effects.
Both explanations for the failure of high leptin levels to defend against weight gain make good evolutionary sense. Your body doesn't want to be lean but it doesn't really mind getting fat. This is because, during our evolution, being fat was never a risk, while being lean was. If anything, getting fat was a benefit which is why our bodies tend to be so good at it. It's only in modern times when people can get and, more importantly, stay fat for extended periods, that being fat is a problem.
Ten thousand years from now, perhaps we will evolve defenses against being fat. This is what would happen if you were extremely sensitive to leptin and does happen in a small percentage of individuals. Leptin can induce resistance to itself in only a few days of overeating.
But we're not really talking about raising leptin above normal here, we're talking about reversing or preventing the drop that occurs with dieting. In that situation, many of the above adaptations to dieting will reverse to one degree or another. What degree will depend on how lean you are, how long you diet, and how long you overeat. So now you increase your calories and carbs. Let's look at some of what happens when you do so. First there are all of the central adaptations that occurred during dieting, that will reverse to some degree while overfeeding.
However, I do want to get rid of belly fat, so this is good read. He mentioned UD2. I have not read the book but the way OP has described, he has included exercise routine along with diet. Why would you do that? Everybody likes their own exercise routine, some more lifting, some more cardio. It should not matter! For me simple diet rules work much better than some rigid diet cast in stone. Keep track of overall calories and macros.
There is no try. Originally Posted by snigam. Originally Posted by qft. So what do you think of "the other book"? Any new interesting points in that book? Isn't that a little much? Obsessed is just a word the lazy use to describe the dedicated. I have not finished the book yet, so I won't pass a judgement. Let's just say I did not get a "ah.. If you have been reading forums and other articles, you will feel like you already know most of this stuff.
There is some interesting read about fat metabolism, biochemistry, etc, if you are interested in that kind of details. Half of the book I have read feels more like a research paper like Tom Venuto has reviewed Of course, he recommends his UD2. Fair enough. I will edit it out. Feel free to delete. Well, I don't put it past BN, but I know a lot of members here also frequent his board at bodyrecomposition.
He's a very nice guy IMO that helps everyone who reads his book. Shit like this is why Dante, the maker of DC training took down his stickies and doesn't answer any questions really about DC training except for his paying trainees.
Thanks for editing that out Slayer. I'm leaving the thread up so everyone can see the level of respect we have for him and his work here at this site. Gotta agree on this.
Lyle is a good shit, and the book is only 20 beans. He had the best intensions in this i'm sure. I do it for me and no one else, its just part of who I am. RoryL's Stats. What needed to be said has already been said. Not a good idea EricT's Stats. Just sucks that if someone goes the ebook route instead of a book publication, that people will pirate it and he'll end up losing out on a lot of profits that could've been made. To view links or images in signatures your post count must be 10 or greater.
If you act sanctimonious I will just list out your logical fallacies until you get pissed off and spew blasphemous remarks.
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