So what about body fat?
When people talk about body fat, what they mean are triglycerides which are stored in your fat cells (there is also some stored in your muscles, called intramuscular triglyceride, but it is a tiny amount compared to what's stored on your fat butt or stomach). An average individual may have 30 billion fat cells which are composed of about 90% triglyceride stored as one big droplet. The remaining 10% is water and the enzymatic machinery which controls cellular metabolism. Now, not all fat cells on your body are the same. Researchers have identified at least 4 different "types" of bodyfat, although we can actually make at least one further distinction. First is essential bodyfat, which exists in small quantities (about 3% of the total in men, and 9-12% of the total in women) in the brain, spinal cord, etc. You can't lose it, and if you did you'd be dead. The amount of essential bodyfat sets the ultimate lower limit for bodyfat percentage. So that should be 3% for men and 9% for women. I should note that you will occasionally see claims of bodyfat percentages less than 3% for men or less than 9% for women. It's not that the folks are lying, so much as the fact that the measurement methods being used aren't as accurate as they need (or are claimed) to be. We don't need to worry about essential fat in this book. Like I said, you can't lose it and even if you could, you'd be dead.
A second type of fat is brown fat which is a specialized type of fat that actually burns up the other types of fat, producing heat in the process. In contrast to white fat (all the other types), which is primarily triglyceride with a little bit of other stuff, brown fat is made up mainly of mitochondria (the powerhouse of the cell), with very little triglyceride. The high mitochondrial content makes brown fat ideal for burning fatty acids for heat. The problem is, while animals have a lot of brown fat (they need it to keep body temperature up against the cold and such), humans lose most of their brown fat once they move past the baby stage of life. We can pretty much ignore it for the rest of this book. You should also question any supplements that claim to cause fat loss via brown fat activation; it will probably work wonderfully in your pet hamster or mouse but that's about it. Next up is visceral fat. This is a type of fat that surrounds your internal organs. In excess it gives you a pregnant look because it makes your gut stick out. Visceral fat has a number of different characteristics from subcutaneous fat (which I'll discuss next chapter) which has some consequences for both health and dieting. Men tend to have more visceral fat than women as testosterone and cortisol tends to promote its growth. Women who use anabolic steroids, or who have higher than normal testosterone for whatever reason, tend to accumulate visceral fat as well. By the time men reach the 12-15% bodyfat range, it is unlikely that they will carry much visceral fat unless they have been using androgens. The type of fat most dieters are concerned with is subcutaneous fat which is found under the skin. In men, subcutaneous fat tends to accumulate around the midsection and low-back; in women, it tends to be on the hips and thighs. This occurs under the influence of the hormones testosterone/cortisol and estrogen/progesterone in men and women respectively. This is why kids before puberty have the same bodyfat patterns and kids after don't. In fact, when researchers pump sex-change patients up with hormones, they see a shift in bodyfat: men take on female bodyfat patterns and vice versa. Women who don't go on hormone replacement after menopause (meaning they produce no estrogen) tend to lose the fat in their hips and thighs and gain it in their stomach area. As I've mentioned, some lucky individuals have more even fat distributions and still look ok even when they're carrying a lot of fat; they are simply smooth all over. If you're reading this book, odds are you aren't one of them. We (not the researchers) can subdivide subcutaneous fat into two types: normal and stubborn. Normal fat is just normal subcutaneous fat that comes off without too much effort. A little calorie cutting, a little cardio, and it comes off without too much trouble. Stubborn fat is the other kind, that stuff that goes on first, and comes off last, if it ever comes off at all. Stubborn fat is generally ab and low back fat for men and hip and thigh fat for women. There are reasons that stubborn fat is so stubborn that you'll learn about soon. Now that you know the basics of both dietary fat metabolism and bodyfat, let's get into the details of how fat is burned off and how we can optimize the process.
Chapter 6: Fat cell metabolism
The ultimate goal of a diet is to lose bodyfat of course so let's look at the processes controlling that. That means examining the steps involved in mobilizing fat from fat cells and burning them off. First, let me elaborate on what it means to lose or "burn" bodyfat. What this means is that the fat stored in your fat cells is removed from those cells and converted to energy elsewhere in the body. Most tissues in the body (there are a few exceptions such as the brain) can use fatty acids for fuel, but the main ones we are interested in are skeletal muscle and the liver. I want to mention that even though the brain can't use fatty acids directly, it can use ketones which are made from fatty acid metabolism in the liver. Let's look at the mechanisms underlying the process of fat loss. Although the process can be further subdivided, we are only interested in three major steps of fatty acid metabolism: mobilization, transport, and oxidation (burning).
Step 1: Mobilization
The first step in burning off bodyfat is getting it out of your fat cells. You might even argue that this is the most important step since, if you can't get it out of the fat cell, you can't burn it off. Recall from last chapter that bodyfat is primarily stored triglyceride, with a small amount of water and some enzymatic and cellular machinery. Mobilizing bodyfat requires that we first break down the stored triglyceride into three fatty acids and a molecule of glycerol. The rate limiting step in this process is an enzyme called hormone sensitive lipase (HSL). So what regulates HSL? Although a number of hormones such as testosterone, cortisol, estrogen, and growth hormone have modulating effects on HSL activity (mainly increasing or decreasing total levels of HSL in the fat cell), the only hormones that we need to be concerned with in terms of HSL activity are insulin and the catecholamines. The primary inactivator of HSL is the hormone insulin and it only takes very tiny amounts (depending on insulin sensitivity) to have an effect. Even fasting insulin levels are sufficient to inactivate HSL by nearly 50%. Small increases in insulin (from either protein or carbohydrate intake) inactivate HSL further. Additionally, the mere presence of triglycerides in the bloodstream (via infusion or by just eating dietary fat by itself) also inhibits HSL activity so this isn't as simple as just blaming insulin. One way or another, any time you eat, HSL is going to be inactivated, either by the increase in insulin from protein or carbs or the presence of fat in the bloodstream from eating fat.
The primary hormones which activate HSL are the catecholamines: adrenaline and noradrenaline. Adrenaline is released from the adrenal cortex, traveling through the bloodstream to affect numerous tissues in the body. This means that blood flow to fat cells has an impact on how much or how little adrenaline will reach fat cells. Noradrenaline is released from nerve terminals which interact directly with the cells. More technically, both insulin and the catecholamines affect levels of cyclical AMP (cAMP) in the fat cell which is what really determines how active HSL is. When cAMP levels are low, HSL activity is also low and fat breakdown is low. When cAMP levels are high, HSL activity is high and fat breakdown increases. Insulin lowers levels of cAMP and the catecholamines, in general, raise levels of cAMP (I'll explain this statement in a second). The higher the level of cAMP, the more active HSL is and the more bodyfat that gets broken down and released from the fat cell. It should be clear that, from a fat loss standpoint, we want high levels of cAMP.
A tangent: all about adrenoreceptors
To understand some of the cryptic remarks above, I need to back up a bit and explain how the catecholamines send their signals. All hormones work through specific receptors and the catecholamines are no different, they have their own specific receptors called adrenoreceptors. There are two major classes of adrenoreceptors: beta and alpha, which are found all over the body. This includes the brain, liver, skeletal muscle, fat cells, heart, blood vessels, etc.; you name it and there are probably adrenoreceptors there. Now, there are at least 3 (and maybe 4) different beta receptors called, imaginatively: beta-1, beta-2, beta-3, and beta-4 (or the atypical beta-3). Alpha-adrenoreceptors come in at least two flavors, alpha-1 and alpha-2. There are additional subtypes of each adrenoreceptor but this is more detail than we really need. Tangentially, beta-3 receptors (and drugs called beta-3 agonists) became a huge research project when it was found that beta-3 activation caused major fat loss in animals; it was hoped that the drugs would work in humans as well. Unfortunately, beta-3 receptors are found primarily on brown fat cells which, as I said, animals tend to have lots of and humans don't. The main receptors we need to worry about in human fat cells are alpha-2 receptors and beta-1 and beta-2 receptors, both of which actively bind the catecholamine hormones. When catecholamines bind to beta-1,2 receptors, they increase cAMP levels, which increases fat breakdown. Great. However, when the catecholamines bind alpha-2 receptors, they decrease cAMP levels which decreases fat breakdown. Not great. But it means that catecholamines, which I told you were fat mobilizers, can actually send both fat mobilizing and anti-fat mobilizing signals: by binding to either alpha- or beta-receptors.
So why does this matter? Different areas of bodyfat have different distributions of alpha-2 and beta-2 adrenoreceptors. For example, women's lower bodyfat (hips and thighs) have been found to have 9 times as many alpha-2 receptors as beta-2 receptors. Some research indicates that men's abdominal fat is similar, with more alpha-2 than beta-2 receptors. Now you know part of why its so difficult to reduce these stubborn fat areas; with a greater number of alpha-2 receptors to bind catecholamines, it's that much more difficult to stimulate fat breakdown in those fat cells. Other factors affect adrenoreceptor function as well. Androgens and thyroid tend to increase the sensitivity of beta-2 receptors to the catecholamines. This may be part of why men (who have higher androgens and higher thyroid, on average) lose fat more easily. The factors controlling alpha-2 adrenoreceptor function aren't as well elucidated.
Step 2: Blood flow and transport
So imagine a situation where insulin is low and the catecholamines are high, causing stored triglyceride to be broken down (the technical word is hydrolyzed) to glycerol and free fatty acids (FFAs). Both enter the micro-circulation around the fat cells. The glycerol can be used for a lot of different things, including glucose production in the liver, but we can ignore it for now. The FFAs
are what we're interested in. Some of the FFA will simply get stored back in the fat cell (a process called re- esterification). What doesn't get restored may either sit in the bloodstream as a free fatty acid or bind to albumin (a protein made in the liver). So now we have albumin-bound FFAs sitting in the circulation surrounding the fat cell Since the FFA can't be burned there, it has to be transported away from the fat cell; this depends on blood flow to and from the fat cell. As with insulin sensitivity and adrenoreceptor ratios, fat depots differ in terms of blood flow. Visceral fat, for example, has an extremely high blood flow relative to other fat depots. This is on top of being extremely sensitive to the catecholamines, and relatively resistant to the effects of insulin. Visceral fat is mobilized fairly easily and, because of this, it generally goes away the fastest (especially with exercise). Relative to visceral fat, abdominal (and probably low-back) fat has less blood flow, is less sensitive to the fat mobilizing effects of the catecholamines, and more sensitive to insulin. This makes it more stubborn than visceral fat. Hip and thigh fat is, by far, the worst; it has the lowest blood flow, is the least sensitive to the catecholamines and the most sensitive to insulin. So now we have yet another reason that stubborn fat is stubborn: poor blood flow which makes transporting the mobilized fatty acids away more difficult. Actually, it isn't entirely true that blood flow to stubborn fat cells is always slow. In response to a meal, blood flow to stubborn fat increases readily; at all other times, blood flow to stubborn fat is slow. Basically, it's easier to store calorie in stubborn fat than to get it back out. Studies show that women tend to have preferential increases in blood flow to their hips and thighs after a meal; the old wives’ tale about fatty foods going straight to the hips turns out to be true after all. Men tend to send more to visceral fat (which is actually easy to mobilize) and more of it sits around in their bloodstream; this makes it easier to lose bodyfat but is one reason men are more prone to heart attacks. But the point is made, poor blood flow to stubborn fat cells is yet another reason dieting to sub-average bodyfat levels is difficult. So how might we improve blood flow to and from fat cells? Blood flow to fat cells improves during fasting and, although we can't fast completely (too much muscle loss), we can mimic the condition with a low-carbohydrate/ketogenic diet. This fits in with our goal of lowering insulin in the first place and turns out to have an extra advantage that I'll discuss in a later chapter. As it turns out, thyroid levels affect blood flow to fat cells significantly. Low thyroid (which is common among women and, I suspect, among genetically average men) decreases blood flow to fat cells and normal or even high thyroid levels improve it. Short of using thyroid medication (a replacement dose of perhaps 25-100 mcg), there's not much we can do here. However, aerobic exercise improves blood flow to fat cells in addition to burning calories, so that's a possible solution. Some studies show that exercise can overcome the normally low blood flow. Considering their problems with lower bodyfat, this might explain the observation that female bodybuilders need to do more cardio than men to get ripped. There are also alpha- and beta-adrenoreceptors on the walls of the circulatory system which control whether or not the blood vessels constrict (slowing blood flow) or dilate (increasing it). As with fat cell metabolism itself, alpha-adrenoreceptors tend to decrease adipose tissue blood flow while beta-adrenoreceptors tend to increase it. Other hormones such as nitric oxide, prostaglandins and adenosine also affect adipose tissue blood flow and it appears that the fat cell regulates its own blood flow to a great degree. In general, if you can get fat breakdown to occur, various hormones which are produced tend to increase blood flow (to get the FFAs away from the fat cell).
нормално ако се држат со паузи.Гледано во еволуцијата на човекот овошје имало само пролет/лето во другите периоди целовреме биле базирани на високо/протеинска диета пред да се воведе земјоделието.Не велам дека сите житарици се лоши,некој реагира супер на бел леб некој не.Се зависи до човекот и до неговиот метаболизам.
