How to Destroy Fat Cells
A persons bodyfat percentage represents the number of fat cells multiplied by the size of each cell. The goal of most diets is to shrink those cells to their bare minimum. They are bound to fail, as they only address one side of the bodyfat equation. The number of adipose, or fat, cells is an insuperable threshold, as each adipocyte has a minimal size. For success, especially longterm success, a diet should not only attempt to reduce the size of each cell but also to get rid of as many of them as possible.
The Anabolic Competition Hypothesis
Bodybuilders typically divide the year into two distinct seasons: the off-season, in which the goal is to eat as much as possible to gain mass, and the competition season, in which the goal is to trim down the newly accumulated fat. Many have abandoned that strategy, however, because it failed to produce the kind of ripped physique the judges look for. Some competitors still do it, but I wouldn’t want to know what they’re using to shed the fat.
A healthier approach is to watch your diet year-round. The idea is to look good all the time, not just a few months of the year. The processes of gaining muscles and gaining fat have one thing in common: they’re both due to anabolic actions. One stores excess fat; the other stores excess proteins. Research shows that the body’s capacity to gain muscle is limited, while its ability to gain fat seems almost limitless.
There may be a competitive relationship between the two types of anabolism. in other words, the process of gaining fat may weaken the anabolic drive that builds muscle by competing against it. That theory is well illustrated by the following example. A group of rats received antibodies to adipocytes-meaning substances that kill fat cells-over four days. The results were stunning. Six months after the four-day treatment almost half the fat cells had disappeared, which was reflected by a dramatic fat loss even though food intake was unchanged or increased. So there was a profound long-lasting effect. Here’s the clincher though: The treated rats packed on more muscle mass than the placebo group over the six months, despite their being completely sedentary.
The treatment didn’t affect muscles directly, as it acts on adipocytes exclusively. Consequently, whenever the possibility of fat gains is removed, the food you eat can only help you pack on more muscle, and when fat gain is possible, muscle gain is not as great. That’s the anabolic competition hypothesis: The more fat you accumulate, the more you compromise your ability to pack on muscle.
The effect of repartitioning agents like clenbuterol may be partly due to that phenomenon. By preventing any fat gain, they may redirect the anabolic drive toward the muscle by means of an intracellular mechanism that’s still not well understood. That may explain why nobody can say exactly how clerthuterol works in animals. It may also provide clues to the drug’s lack of anabolic effect in humans. The doses needed to stop any possible fat gains when you’re on a high calorie diet may be far too high for humans to bear.
The Human Model:
I wouldn’t be surprised if some bodybuilders have already tried adipocyte antibodies, but if they have, the information isn’t yet available to me. In the short term the competition theory seems to be logical in terms of animals and appears to be safe for them, but who knows what might happen with humans? The major obstacle is finding specific antibodies for human adipocytes. Maybe in 10 to 20 years this will be a method of treating obesity. You’ll be able to eat whatever you want, and you’ll stay lean while gaining muscle.
The days of the bodybuilding gyms may be numbered.
Meanwhile, we do have a human model with which to test the competition theory. People who have congenital lipodystrophy are born with almost no fat cells. They are exceptionally lean, and some have very good musculature. The extra muscle mass is due to hyperplasia, which is an increase in the number of muscle fibers. In fact, one large and very lean famous female bodybuilder and wrestler does have lipodystrophy. It enables her to stay lean year-round. In case you’re wondering, you cannot catch this illness. It’s something you’re born with it.
Imagine that in a moment of madness you binge on chocolates and other candy. What happens? Your insulin level rises, which reduces muscle protein degradation a little but mostly triggers an anabolic process in your adipose tissue. The result is that you get fatter with only minimal repercussions to your muscles.
What happens if people who have congenital lipodystrophy eat that much candy? They can’t add fat, as there’s no adipocyte to fill, and they don’t seem to develop new fat cells either, so the calories can’t make them fat. The elevation of insulin triggered by the sugar drives the calories into their muscles, since there’s nowhere else for them to go. Their protein synthesis rates increase while catabolism is slowed by the insulin. That’s unheard of in healthy people who have normal insulin levels. It’s proof of the validity of the anabolic competition hypothesis.
It’s also something you can experience temporarily after a very strict diet. When you resume eating (and overeating), your adipose tissue is not yet ready to receive the calories, and whatever you eat in the first few days will make your muscles grow. Once new fat cells have developed and the old ones are ready to be filled again, that’s the end of your postdlet honeymoon-another important argument for getting rid of as many fat cells as possible.
The Fat Cell Promoters
Insulin is one of the major contributors to fat gain. It supports the development of new fat cells and helps to hypertrophy the existing ones while preventing their shrinkage and their death. Insulinuike growth factor 1 (IGF-I) is endowed with roughly the same properties. Many growth factors produced locally in the adipose tissue will either mediate or duplicate the effects of insulin and IGF-1. When bodybuilders overeat, all those anabolic endocrine or paracrine factors participate in the development of their fat reserves. New fat cells are gained, old ones hypertrophy even more, and their death is postponed. As you can imagine, a severe low-carb diet can reverse most of that. Let me assure you that it’s easier to gain new fat cells than to get rid of them.
The Fat Cell Killers
The terms apoptosis, necrosis, dedifferentiation and reversion all refer to mechanisms by which adipocytes disappear. Th simplify things, I’ll refer mostly to apoptosis, which is a programmed cell death, in this discussion.
It takes a strict diet, rather than an increase in calorie expenditure, to get rid of extra adipocytes-which indicates that the adipocyte-preserving factors depend on nutrition. In one famous study Geloen deprived a group of rats of insulin. After four weeks the number of cells within the adipose tissue was reduced by up to 60 percent. It wouldn’t be healthy to deprive humans of that much insulin, but the study demonstrates that insulin protects the fat cells from dying. In scientific terms, we say that insulin is anti-apoptotic. All the genetic material for the programmed death can be found inside each of your fat cells. Insulin prevents it from being activated, but when you go on a low-carb diet for a long time, part of the protection is removed, and fat cell death is accelerated. Unfortunately, you lose muscle mass at the same time.
ThF: The Killer
Since anti-apoptotic factors exist (insulin and IGP are not the only ones), molecules that can trigger apoptosis exist as well. Tumor necrosis factor (TNF) is such a killer. At a proper dose it can destroy a fat cell neatly. TNF is released at an increasing rate during infections. That’s probably the reason doctors can detect apoptosis of the adipose tissue in sick patients.
TNF can also prevent the arrival of new adipocytes. The main problem is that it’s very hard to increase TNF levels. What’s more, the substance is catabolic for the muscles and can quickly cause a person to die if his or her levels are high enough. In short, even though it’s a very effective molecule, you cannot play with TNF. Your only chance is that research has shown that its effects are indirect. It stimulates phospholipase A2 activity in the adipose tissue. The interesting point here is that TNF’s killing action is stopped in the presence of a prostaglandin inhibitor.
TGF: The Eradicator
The administration of transforming growth factor (TGF not to be confused with TNF) is also a way of eradicating adipose cells and fat mass. Again, the problem is that high doses of TGF may be detrimental to muscle mass, although it has its place in the anabolic processes. It has been noted that TGF levels are lower than normal in obese patients. On top of that, their adipose tissue is less sensitive to the molecule’s dramatic effects. One mechanism is that TGF blocks the fattening effects of insulin. What you’d wish for, then, is a local elevation of TGF within your adipose tissue.
PGF2: The Terminator
While prostaglandin P2 can help build muscle, it’s also effective at reducing fat. Its first obvious mechanism is its ability to cause thermogenesis. 1y activating an uncoupling protein called UCP-2, PGF2 transforms the calories you take in into heat Instead of energy that can be used by the body. It causes calorie wasting. PGF2 is also a fat killer. It’s a likely mediator of some of the apoptotic effects of TNE Another remarkable effect is its ability to elevate TGF levels within the adipose tissue. That may be one of the ways PGF2 reduces appetite. TGF stimulates the adipocytes to release an appetite. suppressing hormone called leptin. PGFZ, at least indirectly, can raise leptin levels, and the extra local leptin may also promote fat destruction.
PGP2 is a very potent inhibitor of pre-adipocyte differentiation as well. As PGF2 and TGF act synergistically, it’s been suggested that they are physiological factors designed to keep the pre-adipocyte dormant. It’s clear that you want more PGP2 rather than less when you’re on a diet, which is why you should avoid aspirin. Aspirin prevents fat cell apoptosis, and I believe that it was added to some of the ephedrineand-caffeine stacks for that reason: so you would lose weight-but not too much weight-and become a repeat customer.
Modify Your Diet
Here is a summary of what goes into a diet designed to kill fat cells. Not everybody needs such a dramatic diet, but if you’re fat or want to be shredded, there aren’t many effective alternatives.
Diets are usually designed according to the last trends. Were told to eat only carbs or to strictly avoid them. Sometimes fats are said to be bad and are dropped from the diet. That may be good advice, but we are never told why.
Of course, my diet is designed for the purpose of losing bodyfat-but not in the classic way. The long-term destruction of your fat cells is the only way to stay lean permanently. With the following principles you can tailor the diet to your exact needs.
Insulin prevents apoptosis, so you should avoid carbohydrates. Train your body slowly to handle the carb shortage. Don’t drop your carbs quickly from one day to the next. There’s no hurry. Your body can handle it as long as you train it patiently. You don’t ask a beginner to bench-press 500 pounds on his very first day of training. You start with a light weight and go from there. Why not do the same with your diet? If you skip steps, your body pays for it.
For example, cut your carb intake by 20 percent each week. That doesn’t mean you should drop the whole 20 percent on Monday. Rather, you should cut your carb intake by 20 percent over the course of the week. If you feel tired, increase your carbs by 10 percent and wait until your body is used to it. Then resume your carb-reducing procedure. You also want to reduce your total calorie intake, but here, again, you should do It slowly and gently. As you’re dropping your carbs, add as much protein as needed to cover half the calorie loss that cut represents. For example, if you drop 50 grams of carbs, add 25 grams of proteins.
In addition to killing old fat cells, you also want to slow the development of new ones. In other words, you play on both ends of the adipocyte turnover. To accomplish that, you cut dietary fats next, as they act as local growth factors for the development of pre-adipocytes. By cutting your fat intake, you slow the development of new fat cells. I believe that most ketogenic, or low-carb, diets fail to eradicate fat cells sufficiently because the fat intake is conserved or Increased. On this diet you do keep taking omega-6 and GLA-in the form of five to 10 grams of evening primrose oil, for example. GLA will favor the local formation of PGF2 in the adipose tissue.
The big issue is your intake of omega-3. A small amount of that essential fatty acid is mandatory, but too much will reduce PGF2 formation, and you want as much PGF2 as you can get inside your adipose tissue. You can reduce omega-3 intake a little but not too much. One to three grams daily in the form of fish oils may be enough during the diet. In some people, however, omega-3 is strongly thermogenic, to the point where they start sweating. In that case, conserve the same omega-flto-omega-3 ratio.
Note that the lack of insulin will also tend to enhance adipose tissue PGF2 formation. As for proteins, I’d like you to be able to drop them, too, but that isn’t possible. The most effective way to kill fat cells is to starve completely for a long while, but your muscle mass would stiffer and its not healthy at all. So you keep and even increase your protein intake, although it doesn’t help your antiadipocyte crusade. Proteins are included in the diet by default.
An ephedrine-and-caffeine stack will also tend to slow the production of new fat cells, so it’s a big advantage to use one while you’re on a diet, as long as it doesn’t contain any aspirin-like substance (check the ingredients for salicin or white willow bark).
Of course, you cannot stay on the diet year-round if you want to keep increasing your musculature. After two months you can resume a normal but moderate diet. That will allow your adipose tissue to create new fat cells, so you do lose some ground. Once you feel ready again, resume the diet for one to two months. The goal is to get rid of fat cells over time. Within one or two years you’ll reach a new, lower threshold of adiposity, which will enable you to remain lean with no diet as long as you don’t overeat.
1 Futter, C. (1990). Increased growth and protein deposition in rats treated with antibodies to adipocytes. Am I Physiol. 258:E985.
2 Garg, A. (1991). Skeletal muscle morphology and exercise response in congenital lipodystrophy. Diabetes. 40(suppl):3 IA.
3 Copeland, K.C. (1993). Discordant metabolic actions of insulin in extreme lipodystrophy of childhood. I Clin Endocrin Metab, 77:1240.
4 Geloen, A. (1989). Regression of white adipose tissue in diabetic rats. Am I Physiol. 257:E547. 5 Cameron, UP (1995). Human adipocyte apoptosis occurs in malignancy. Biochern Biophys Res Corn. 205:625. IM