Read an Excerpt
The O Word: Obesity
For some of us are out of breath, and all of us are fat.
How much of a problem is obesity? According to the government, obesity is an enormous problem. The most recent figures, reported in 1995, place the segment of Americans who are "significantly overweight" at 33 percent--nearly a 30 percent jump in one decade while the population has cut fat consumption. Although the Centers for Disease Control had set goals for a reduction in obesity from the nation's lower-fat efforts, Americans went off in the opposite direction and got even fatter. If you believe your eyes, obesity is virtually epidemic--as anyone who's ever been to a shopping mall knows.
Despite the manifold health problems associated with obesity, people continue to gain weight; despite the many disadvantages obesity inflicts on its victims on the job, the cultural stigma against them, the plethora of weight-loss centers, books, and products available, more people than ever are overweight. Why?
How We Get Fat
Obesity is defined simply as the accumulation of excess fat on the body; obesity has nothing to do with excess weight. Based on the standard height-weight tables, Arnold Schwarzenegger would be considered overweight, but he obviously isn't overfat or obese.
Although it's almost always attributed to excess calories, obesity is more related to the multifaceted actions of insulin and glucagon on the storage of fat. As any juvenile-onset diabetic can readily attest, in the absence of insulin one can eat and eat and eat while continuing to lose weight; it's not just a matter of how much is consumed but the result of a complicated interplay among insulin, glucagon, and what and how much is consumed. These two hormones exert a profound influence on all the metabolic pathways, but especially on those involved in the burning and storing of fat and the development of obesity.
When you eat food, your body either breaks it down and burns it for energy or stores it away as body fat in the fat cells (or as glycogen, the storage form of glucose, in the muscles) for later use. Both functions occur simultaneously, and although both the storing and burning pathways are active to some degree all the time, one pathway usually predominates. What is important is the net direction of fat flow over time--i.e., are you mainly storing fat or mainly burning it for energy? Which pathway predominates most of the time? If you mainly store it, you develop obesity; if you mainly burn it, you lose weight.
The flow of fat is composed of the fat you eat, the fat released from storage in your fat cells, and the fat you make from excess protein and carbohydrate. Yes, the body can make fat from carbohydrate and plenty of it. That's why you can't eat fat-free cookies and ice cream and potato chips and expect to lose fat!
Obviously if the direction of fat flow is from our mouths to our fat cells for storage, we are going to gain fat; if this pathway predominates, in time we will become obese. Conversely, if the fat flows in the opposite direction, from the fat tissue to the muscle cells and other tissues to be burned for energy, we won't; in fact we will lose weight. If our goal is to remain--or become--slender and fit, obviously this second pathway is preferable. Is it possible to change the flow of fat and redirect it from the fat tissue to muscle cells? The exciting answer is yes, and here's how.
Directing the Flow of Fat Through Food Selection
Insulin and glucagon, the hormone twins, are the primary regulators of these metabolic pathways and actually direct the flow of fat down one pathway or the other. By altering the ratio of insulin to glucagon--which we can do through our selection of foods--we can determine which pathway predominates. Instead of allowing our biochemistry to control us, we can control it.
Taking as our starting point the fat in the blood, let's walk through the fat metabolism pathways and follow the flow of the fat molecules. Fat travels through the blood in a form called triglyceride, a molecule composed of three fatty acids. At the surface of the cells enzymes break down the triglyceride molecule, and the fatty acids can enter the cells.
Once inside the cells, fat reaches its first hormonal regulation point--the mitochondria. These tiny sausage-shaped power plants within the cells burn the fat--but only if the fatty acids can actually get into the power plant. To do that they need carnitine, which operates a little shuttle system to bring the fat in for oxidation. Insulin inhibits this fat-carnitine shuttle system, saying, in effect, "Hey, we're full; we don't need any more energy. Send that extra fat to the fat cells." Which is precisely what happens when there's too much insulin: the fatty acids turn back into triglycerides and move back into the blood. Glucagon in contrary fashion accelerates the shuttle, rapidly moving fat into the mitochondria. Glucagon's signal: "We need energy; let's start breaking that fat down and getting it in here to the furnace."
Muscle, liver, kidney, lung, heart, and other cells break down fat and burn it for energy, but it's a different story with the fat cells. Fat cells merely store the fat molecules. Residing on the surface of the fat cells are two enzymes--both regulated by insulin and glucagon--responsible for herding fat into or out of the fat cells. The first, lipoprotein lipase, transports fatty acids into the fat cell and keeps them there. (Lipoprotein lipase, as we shall see shortly, also plays a major role in the rapid regaining of lost weight that plagues so many dieters.) The other, hormone-sensitive lipase, does just the opposite--it releases the fat from fat cells into the blood. As you might imagine, insulin stimulates the activity of lipoprotein lipase, the fat-storage enzyme, and glucagon inhibits it; glucagon stimulates the fat-releasing enzyme, and insulin inhibits it.
The Built-In No-Win Situation
It turns out that the biological activity of this enzyme increases prodigiously immediately after weight loss. That's right, the very act of losing weight strengthens and makes more potent the enzyme that is in great measure responsible for the overweight state to begin with. Although it no doubt has an evolutionary purpose, this is a sorry state of biological affairs: while working hard to lose weight, you reinforce the biochemical underpinnings of your obesity. Add to this the fact that insulin by itself further activates the already hyperactive lipoprotein lipase and you begin to understand why 95 percent of people who manage to lose weight will not be able to keep it off.
What standard treatment is brought to bear against this combined force? The only weapon in the arsenal, the low-fat, high-complex-carbohydrate diet, a diet that stimulates the release of insulin. Expecting a formerly obese person with a history of hyperinsulinemia not to gain fat on a carbohydrate-rich diet is like throwing gasoline on a fire, then wondering why it flares. In fact, it's amazing that even 5 percent of successful dieters manage to keep it off. But that may correlate with the percentage of overweight people who don't have hyperinsulinemia and insulin resistance.
What about our goal, to divert the flow of fat away from the fat cells? Although we can't control lipoprotein lipase directly, we can control it indirectly by controlling the metabolic hormones--insulin and glucagon--that modulate it. By keeping insulin levels low, we can remove any stimulation this hormone provides; by keeping glucagon elevated, we can continue to inhibit lipoprotein lipase and thus counteract the stimulatory effect brought on by the weight loss. The nutritional plan in this book lowers insulin and raises glucagon levels, the ideal combination both to achieve and to maintain a lower fat mass. We've seen it happen in thousands of our patients, and in our experience it's the only approach that works.
Amazingly, obesity remains much less treatable than the vast majority of cancers, a grim statistic in and of itself. Are 95 percent of the overweight doomed to live out their lives swaddled in layers of fat?
Most physicians, dietitians, and nutritionists have been locked in the notorious clean and well-lit prison of a single idea for decades. These experts have been treating obesity with low-calorie, low-fat, high-complex-carbohydrate diets, then standing around wringing their hands, watching 95 percent of their patients regain their weight. Perhaps inevitably they blame the patient for the failure. In a brilliant and controversial essay on intelligence published in the winter 1969 issue of Harvard Educational Review, Arthur R. Jensen, a professor of psychology at the University of California at Berkeley, wrote: "In other fields, when bridges do not stand, when aircraft do not fly, when machines do not work, when treatments do not cure, despite all conscientious efforts on the part of many persons to make them do so, one begins to question the basic assumptions, principles, theories, and hypotheses that guide one's efforts."
The evidence seems clear that the low-fat, high-carbohydrate diet--the standard obesity therapeutic agent--is flawed in principle, out of sync with biochemical reality. So why not try something different?