It’s taken me a while to get here, but we are finally going to address the real way in which your body actually loses body fat, and why 90% of the diets out there are just plain wrong!! It’s funny when most of the diets that are based on some form of calorie restriction, i.e. #IIFYM make the contention that the only reason why “eating clean” works is because they incidentally create a calorie deficit. The irony of these comments is that it is actually the other way around. Confused? Read on... To make sense of it, I’m going to have to talk a little about how your fat cells actually work. This being a blog post I obviously can’t go in to the detail that explains everything, but at least you will hopefully grasp the basic concepts. The main thing I hope you will get out of this is one key concept. Your fat cells can’t count calories. Contrary to what most people believe, your fat cells are not just a storage dump for the excess calories you ate last Saturday night for dinner. They are actually classified as an endocrine organ. In simple terms your fat cells actually release hormones and also respond to different hormones. Think of your fat cells as one big organ spread all around your body, and the hormones they release can influence a number of things, including your metabolism and appetite. But, I digress... The first concept to understand is that your fat cells are actually in a constant state of flux. This means that fat is constantly being broken down and rebuilt. At the end of the day, if more fat gets stored than released, you will get fatter. Conversely, if more fat gets released than stored, you will lose fat. What you should be mainly concerned with then is, what factors influence this state of flux? The second key concept is this: it is a few key enzymes that govern the rate of how much fat gets trapped inside the fat cell and how much fat gets let free. Free fatty acids (or FFA) can easily travel in and out of a fat cell. But, handcuff 3 of these to what is known as a glycerol backbone, and now the molecule is too big to escape. You have effectively handcuffed and locked fat inside the fat cell and your fat cell will get bigger (i.e. you get fatter). If, however, you unlock these fatty acids from the glycerol backbone, they can then run free and escape the fat cell (you will lose fat). This is what scientists call the FFA / TAG cycle. There are two main enzymes responsible for this process. LPL is the main one that “handcuffs” fat inside the fat cell. Switch this enzyme on and you will store more fat. At the other end of the spectrum is another enzyme called HSL, this “unlocks” fatty acids from their glycerol backbone and releases the FFA out in to the wild. In simple terms LPL = bad , HSL = good. If these enzymes influence the state of flux, your next question should be, what switches these enzymes on and off?? The third key concept: The main thing that switches these enzymes on and off is actually...hormones! And the most powerful hormone that influences this state of flux is Insulin. Insulin activates LPL and signals your body to store more fat. More than this, insulin also acts as a powerful inhibitor to HSL. This is why if you have constantly elevated levels of insulin it is pretty much impossible to drop body fat. When you think in terms of insulin resistance, obesity and type II diabetes you can start to appreciate the power that this has. This is also the main reason that why, for any given calorie intake, a lower carbohydrate version will work better than a higher carbohydrate version when it comes to body composition. This has also lead researchers to give a higher protein / lower carbohydrate diet the term #metabolicadvantage. At the other end of the hormone spectrum, the main antagonist to insulin is actually adrenalin. Adrenalin switches on HSL and signals your body to strip body fat. This is one of the main reasons why HIIT has been found to have more favourable effects on body composition than low intensity cardio. So, notice in all of the discussion on what influences whether a fat cell gets bigger or smaller we didn’t mention one critical little word? That’s right, we didn’t mention calories! When it comes to stripping body fat #caloriesdontcount. Your fat cells don’t know and don’t care what a calorie is. Insulin is actually the main regulator of your fat cell, not calories. The only reason why calorie restricting diets work is because they incidentally influence this state of flux. Not the other way around. That is why calorie restriction only works up to a certain point before metabolism starts slowing down and this is why eating pizza is not the same as eating chicken breast when it comes to body composition. Now, notice I haven’t discussed anything about #insulinsensitivity #glucosetolerance #nutrienttiming #workoutnutrition or any individual differences in metabolism. These are all factors that influence the above as well, I’m just sticking to basic principles at the moment. The best diet for stripping body fat while maximising lean muscle gains is therefore one that simultaneously influences everything discussed above as well as the post that discussed protein intake and muscle protein synthesis. Before all you haters write in crying bu$$*^t and defiantly defending calorie counting to death, just think back to a time when we thought that the only way to build more muscle was to create a calorie surplus. We now know that the rules that govern protein synthesis are a little more involved than just calories in vs calories out. Maybe it’s about time we started accepting the rules that govern fat loss don’t play by those same rules either. To summarise, your fat cells aren’t regulated on a basis of looking at how many “calories” you just ingested. What’s more important is the hormonal and metabolic influence of the foods you just ate as well as the hormonal and metabolic state of your body at the time of feeding. If any of you are interested in reading about this further, I have a book that will hopefully be released in the next couple of months called Calories Don’t Count. I will keep you updated on its release date.
Posted on: Tue, 15 Oct 2013 06:37:56 +0000
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