Science of Bodyfat

Most people think that fat cells are inert tiny blobs that do little more than make you look, well, fat. While it's true that the primary function of adipocytes, a.k.a. fat cells, is to store triglyceride, which consists of three fatty acids attached to a glycerol backbone, fat cells are far more than just dormant blobs. In fact, they produce various chemicals that influence health, metabolism and appetite. Fat cells even regulate their own metabolism through feedback messages sent to the brain.

Bodyfat falls under various classifications. The two primary categories found in fat cells are white adipose tissue (WAT) and brown adipose tissue (BAT), with white adipose tissue making up the majority of fat stored in the body. Brown adipose tissue is darker in color because it contains a relative preponderance of mitochondria, the parts of the cell where fat is oxidized. As such, BAT is the primary thermogenic tissue of the body, converting fat calories into heat. Scientific researchers debate its importance, but most agree that it has more significant effects in infants than adults.

Bodyfat is also characterized as storage, essential and sex-specific fat. Storage fat, such as the subcutaneous fat found under the skin, is largely expendable. Essential fat is located in areas such as bone marrow, heart, lungs, liver, kidneys and the surrounding nerve fibers. It makes up about 3 percent of total fat stores in men and 9 percent in women if you include sex-specific fat. That's the fat found in women in areas such as their breasts, hips and upper thighs. It's preserved to ensure that women have sufficient calories on hand to produce a baby. Nature is only interested in the perpetuation of the species, not in a woman's concerns about her figure.

In fact, men tend to store fat in the abdominal area, while women deposit more fat in the butt, thighs and hips. Such gender-related fat storage relates to hormones, with estrogen favoring the typical fat deposits in women. Estrogen is also responsible for the systemic fat pattern of subcutaneous fat and the additional subcutaneous fat that makes women's skin feel softer.

Testosterone in men has an inverse relationship to bodyfat, particularly in the abdominal area. Studies have repeatedly shown that low testosterone levels in men promote added fat storage in the midsection. Other studies have shown that anabolic steroids, which are synthetic versions of testosterone, promote less overall bodyfat, with a particular focus in the abdominal area. On the other hand, excess estrogen promotes fat deposition in men.

Excess fat in the abdominal area is associated with insulin resistance and an increased risk of cardiovascular disease and diabetes. That holds true for both men and women. Abdominal fat is labile, which means it's constantly being released from visceral fat cells in the abdominal area. The released fat travels to the liver, where it acts as a substrate for increased cholesterol formation. Excess fat also hinders the liver's use of glucose, which leads to insulin resistance.

Fat cell size and numbers are influenced by various factors, including heredity and how you were fed during the first four years of your life, when fat cells form rapidly. Obese people usually have both a greater number of fat cells and fat cells that are larger than those of other people. Previously held dogma stated that you could not lose or add fat cells, but more recent evidence dispels those notions. Once you get to a certain level of obesity, fat cells divide and form new fat cells, a process called hyperplasia. That's one reason not to engage in the old bodybuilding habit of bulking up, which is simply a euphemism for getting fat. If you let things get out of hand, you may wind up with more fat cells than you had previously, which makes it more difficult to get cut, especially as you age.

Savvy readers may be thinking at this point, 'Why worry about newly formed fat cells when I can get them sucked out through liposuction?' While it's true that the liposuction procedure can remove localized fat deposits, such as abdominal fat, it's also true that fat cells can return to the same area if you make a habit of eating too many calories and getting too little exercise. The notion that fat cells don't return once they're removed through liposuction is a myth.

Recent research shows that starvation-refeeding cycles in animals leads to an upgrading of lipogenic enzymes, which are enzymes that promote bodyfat synthesis.1 While researchers have so far only shown that to occur in rats, humans possess the same lipogenic enzymes, so the same scenario may also hold true for people. The message here is to avoid going on excessively low-calorie diets followed by eating binges, since the body may respond by upgrading your fat-producing enzymes.

Several years ago a national bodybuilding magazine featured a diet known as the ABCD diet. The diet worked by alternating high- and low-calorie periods, with the goal of maximizing anabolic hormone release'through dietary manipulation of insulin, testosterone and growth hormone levels'and fat loss. While the plan made perfect sense on paper, it failed miserably for most people who tried it. A recent study involving rats clearly showed why. Restricting the animals' food for a period followed immediately by a period in which they could eat whatever they wanted led to their accumulating bodyfat three times faster than the control rats, which ate normal diets.2 It seems the ABCD rats had resting metabolic rates that were 30 percent lower than the control rats' rates, which led to a significant drop in fatty acid oxidation, or fat burning. In effect, when the rats ate what they wanted after a period in which their food intake was limited, all excess calories went right into fat storage. A similar scenario occurred with the people who followed the much-vaunted but disastrous ABCD diet.

The simple cause of most cases of obesity is too much food in relation to physical activity. Eating too many calories, regardless of the source, will increase your bodyfat if you aren't expending those calories through exercise. While that's the generally accepted sequence of events that leads to obesity, advocates of various diets say it isn't as simple as it appears. They point to the effects of various hormones and enzymes on fat cell physiology. In effect, they're saying that it's not simply a matter of excess calories but a failure to dispose of those calories properly. Fat people have a disorder of lipid metabolism that favors fat storage over calorie disposal. Even when they exercise, they often fail to tap into fat stores as much as their leaner peers do. The big debate centers on exactly why that occurs.

ALLScientists thought they had the answer in 1994, when they discovered a protein produced in fat cells called leptin. In early studies done with mice and rats, rodents that had been genetically engineered to become fat'they had to be genetically engineered because wild rodents never have more than 10 percent bodyfat'appeared to be deficient in leptin. Researchers injected leptin into the fat rats, and the animals rapidly lost nearly all their bodyfat. When that information was released to the media, leptin was hailed as the cure for obesity.

Subsequent research involving humans, however, dampened the initial enthusiasm. The genetic defect that led to leptin deficiency in rodents rarely or ever occurs in humans. In fact, obese humans produce more leptin than thinner people. Leptin turned out to be a regulator of fat cells in the body, and in humans the defect doesn't involve a lack of leptin but rather a failure of the fat cells and the brain to communicate via leptin. Scientists are still trying to figure out why that occurs.

Another commonly offered reason for the existence of excessive bodyfat is low metabolism. According to that school of thought, fat people don't burn calories at an optimal rate. The thyroid gland often gets the blame, since hormones produced there control metabolism in the body. In fact, not only do fat people usually have normal thyroid hormone output, but they also have faster resting metabolisms than you might expect. Resting metabolism is related to lean mass, such as muscle, and it turns out that under all that fat, many fat people have enough muscle to maintain a normal or even elevated resting metabolic rate. On the other hand, recent studies show that in many cases thyroid hormone therapy may indeed help speed fat loss'although too much thyroid leads to excessive lean mass, or muscle, loss.

So it's not simply a matter of a lowered resting metabolism favoring bodyfat accretion. That's not to say, however, that obese people have no hormonal defects or defects in the way their fat cells function. The problem with the so-called low-metabolism issue is that the wrong hormones have been accused. Most scientists who've studied the causes of obesity in humans now point to defects in thermogenesis, or the way the body gets rid of excess calories, coupled with defects in insulin metabolism. In short, too much bodyfat leads to insulin insensitivity, which in turn results in excess insulin secretion.

The control of insulin is the basis for all low-carbohydrate diet plans. Critics of such plans say that insulin won't promote excessive bodyfat accretion unless accompanied by excessive calorie intake; however, that only holds true for people who have normal fat cell sizes and numbers. It doesn't account for the majority of people who have too much bodyfat. In addition, recent studies show that insulin self-regulates its own release in lean people, while the effect is lost in those who have high levels of bodyfat.3

Consider the recent discovery of a protein dubbed resistin. Resistin, like leptin, is produced directly in fat cells. It makes fat cells insensitive to insulin and is thought to be related to the onset of diabetes. Since enlarged fat cells don't act like normal-size fat cells, those ideas about calories and insulin simply don't apply.

While having larger numbers of and larger size fat cells does make it more difficult to lose bodyfat, the fact that countless people have done so proves that it's possible to control bodyfat. If you have the typical fat cell pattern associated with obesity, you need to deal with the defects in sympathetic hormonal response'that is, thermogenesis'and the excessive insulin activity. Simply reducing calorie intake across the board will lead to fat loss, but it's accompanied by a ravenous appetite that makes dieting difficult and weight regain likely.

You can deal with the thermogenic defect by following a judicious exercise pattern and using certain food supplements. Aerobic exercise favors the release of catecholamines, such as epinephrine and norepinephrine, that not only promote thermogenesis but also directly promote fat release from fat cells by activating the fat cell enzyme hormone-sensitive lipase.

People with higher bodyfat percentages should go easy with aerobic exercise at first, since they lack the oxidative enzymes needed to burn fat. As they progress, they can gradually increase exercise intensity and move on to using interval-style aerobics, characterized by alternating higher intensity periods, as determined by heart rate, with lower intensity periods during the same session. That produces the greatest fat-burning effect. As bodyfat levels decrease, hormones such as growth hormone will be more effectively released. Most obese people show blunted growth hormone release patterns, which also help to perpetuate obesity. Growth hormone's effects on fat cells are the reverse of insulin's effects; that is, growth hormone promotes fat mobilization rather than storage.

Weight training is also vital for bodyfat control, since it produces the greatest gains in lean mass, or muscle. As noted above, lean mass determines resting metabolic rate. In addition, regular weight training increases insulin sensitivity, leading to better insulin control and easier bodyfat management.

The supplements used to correct a defective thermogenic system in people who have high bodyfat levels usually include ephedra or ephedrine, caffeine and other ingredients, like green tea. Such natural substances simulate the effect of catecholamines, such as epinephrine and norepinephrine, in fostering thermogenic reactions that lead to increased fat mobilization and oxidation'if combined with aerobic exercise. Contrary to some reports, those thermogenic supplements are safe when users have no preexisting cardiovascular disease or thyroid abnormalities. Obese people are often admonished to eat a lowfat diet, which appears to be sound advice. At nine calories per gram, fat is the most concentrated source of calories, compared to four per gram for both protein and carbohydrate. In addition, while excess carbs and protein tend be oxidized by their own metabolism, that doesn't hold true for fat. Excess fat calories simply take an express route into the fat cells.

The problem with the lowfat-diet approach is that most lowfat eating regimens don't differentiate between the various forms of dietary fat and don't take into account the disordered carbohydrate metabolism that accompanies high bodyfat levels. Fat people simply don't oxidize carbs the way their leaner peers do, and they tend to store carbs as bodyfat due to their excess-insulin problem.4 In fact, a study presented at the 2001 Experimental Biology meeting found that when fat cells are exposed separately to glucose and insulin, nothing happens, but when glucose and insulin are combined, the fat cells enlarge rapidly.

Some types of dietary fat are beneficial for fat reduction in anyone, regardless of existing bodyfat level. They include monounsaturated fats, found in canola and olive oils, which maintains protective high-density-lipoprotein levels under dieting conditions. Another category of 'good' fat is the omega-3 fats, which are found naturally in flaxseed and fish oils. Omega-3 fats have actually helped to reduce fat cell size in animal studies, and they've also been shown to increase insulin sensitivity by altering the fluidity of cellular membranes, making it easier for insulin to interact with cellular hormone receptors. The types of fats to avoid are saturated fats and transfats'although both saturated and monounsaturated fats help maintain testosterone levels in men.

If you have too many enlarged fat cells, the only way to diet is with a low-carbohydrate plan. While such diets are frequently criticized because of their higher fat contents, many recent studies have shown typical low-carb diets to be both safe and effective for fat-loss purposes. They offer advantages over lowfat regimens because of greater satiety, or appetite control. That doesn't relate to the fat content, as you might expect, but to their higher protein contents. Protein offers potent satiety effects.5

The high-protein intake typical of low-carb diets also helps you maintain muscle mass while dieting. In a recent study involving 24 middle-aged women, a low-carb diet was compared to the standard USDA food-pyramid plan, which favors a high-carb, lowfat menu. Both diets contained 1,700 daily calories and led to an equal level of weight loss; however, the women eating the lower-carb, higher-protein diet lost far less muscle mass than the food-pyramid group, leading the researchers to conclude that the lower-carb/high-protein diet was twice as effective as the other diet. Those in the high-protein group also showed higher thyroid hormone levels and a lower level of blood triglycerides accompanied by increased high-density-lipoprotein levels, a scenario that protects against cardiovascular disease.

Based on the suggestions offered here, anyone can effectively control bodyfat levels, regardless of genetic proclivities. All it takes is consistency, desire and determination.

References
1 Karbowska, J., et al. (2001). Increase of lipogenic enzyme mRNA levels in rat white adipose tissue after multiple cycles of starvation/refeeding. Metabolism. 50:734-738.
2 Brooks, S., et al. (2001). Fatty acid oxidation and fatty acid synthesis in energy-restricted diets. J Nutr Biochem. 12:422-430.
3 Muscelli, E., et al. (2001). Lack of insulin inhibition on insulin secretion in nondiabetic morbidly obese patients. Int J Obesity. 25:798-804.
4 Marques-Lopez, I., et al. (2001). Postprandial de novo lipogenesis and metabolic changes induced by a high-carbohydrate, lowfat meal in lean and overweight men. Am J Clin Nutr. 73:253-61.
5 Long, S.J., et al. (2000). Effect of habitual dietary protein intake on appetite and satiety. Appetite. 35:79-88. IM