How Science Found The Missing Article To The Weight-loss Puzzle

Two out of three Americans are overweight. And diet after diet, the pounds always return. Why hasn't dieting worked until now?

Scientist feverishly worked on the ultimate solution and in 1994 they discovered a communication system between fat cells and also the brain. Fat cells make a messaging hormone called leptin that signals inside your brain that you are full and may quit eating.

Another leptin message regulates weight by telling your body's cells to either burn up fat or store it. Scientists assumed that overweight people needed more leptin. They were wrong!

For much more effective weight regulation, it isn't the amount of leptin, but clarity of the message that counts. If we consistently overeat, the fat gained sends out excessive leptin which overwhelms the brain and body so they ignore the "stop eating start burning fat" message. This creates a vicious cycle: fat cells keep creating more and more leptin in an effort to be heard, resulting in the entire body storing much more fat. That fat creates more leptin. This cycle is usually called "leptin resistance" and it is a major factor in the fat gain cycle.

The revolution started in 1994 at New York's Rockefeller University, when Dr. Jeffrey Friedman and his research team discovered that the fat cells of genetically obese mice failed to produce a chemical called LEPTIN. Leptin was the first adipokine, the first hormone shown to be made exclusively by fat cells. Researchers soon discovered that administration of leptin curbed the appetite and stimulated the metabolism of laboratory animals. Injecting leptin into genetically obese mice restored them to normal bodyweight. Leptin appeared to function as part of what scientists refer to as a negative feedback loop. When an animal is overfed and begins to gain weight, the increase in body fat leads to an increase in production of leptin, which in turn suppresses appetite and stimulates weight reduction, restoring the animal to a normal lean weight. This process of internal self-correction is called "homeostasis" and it stabilizes the body's internal state.

Overweight humans are not leptin deficient: the more body fat, the higher the levels of leptin in blood. For people who are chronically overweight, the problem seems to be that leptin is not doing its job of reducing appetite and stimulating fat burning. The effect of leptin is blocked. Scientists call this state LEPTIN RESISTANCE. Leptin resistance makes losing weight difficult if not impossible. The goal of The Fat Resistance Diet is to help readers overcome leptin resistance through a diet and exercise plan based on health research.

Advice about eating less and exercising more has been a resounding failure. Diets, whether they're low calorie, low fat or low carbohydrate, all produce initial weight loss but do a lousy job of maintaining leanness. If there's a way that science can help us undo the damage technology has caused, then understanding and combating leptin resistance may well be the key.

Of all the theories that attempt to explain leptin resistance and suggest a way to reverse it, the one concept that best knits together everything we know about obesity and has the best chance of stopping this epidemic is the proven link between obesity, leptin and INFLAMMATION.

The plot gets even thicker. The inflammatory nature of fat is not only due to fat cells themselves. In addition to fat cells (adipocytes), fat also contains blood vessels and white blood cells. Fat specifically attracts a type of white blood cell called a macrophage. Macrophage literally means "large eater" and macrophages are large white blood cells that gobble up cellular debris. They are scavengers, sometimes called "garbage men of the immune system."

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