Since the discovery of leptin in 1994, many have hoped that the hormone would be a promising weight-loss treatment for humans. Leptin acts as a signal to help the body decide when it has eaten enough food to feel full. The amount of leptin in the blood has been directly linked to body fat.

After receiving leptin replacement therapy, research subjects with a recessive mutation in the obesity (ob) gene - a population both deficient in Leptin and morbidly obese - lost about half of their body weight while regulating their own food intake. (Medical news Today 4/5/2005).

If you take it at face value, it seems as if the research is saying that more leptin will help you lose weight. This research refers to subjects with a genetic basis for obesity who were deficient in leptin. But obese individuals tend to have more and larger leptin-producing fat cells than thinner people. They simply are not getting vital chemical signals to their brains that tell them to stop eating.

To illustrate my point:

Despite an assiduous search, scientists have found only a half-dozen people in the world who make no leptin. These people eat voraciously - one 3-year-old girl consumed 2,000 calories at a sitting. When several of these people were treated with leptin, they lost their appetites and their weight plummeted. (The New York Times 31/10/1999).

Don’t get me wrong, if it helps those who cannot make leptin, then this is a major breakthrough for them.

A study published in the Journal of the American Medical Association, goes a long way toward proving to me that more leptin does not equal less weight in very overweight people in the general population.

To make things worse, a hormone called leptin that was supposed to be the magic bullet for obesity, making people effortlessly lose fat while retaining muscle, looks like a bust. In a preliminary study reported last week, most people who took leptin lost little or no weight - one fat person who took the highest dose actually gained 20 pounds. (The New York Times 31/10/1999).

Researchers at Harvard School of Public Health in Boston say lean, physically active people have low levels of leptin, which is produced by the body’s fat cells and is believed to be a major culprit in causing obesity. The study finds that when couch potatoes start exercising regularly, their leptin levels decrease.

“As you get fatter, your body makes more leptin,” says Eric B. Rimm, Sc.D., associate professor of epidemiology and nutrition at Harvard School of Public Health, and a co-author of the study. “But when you exercise, the amount of leptin in the blood decreases. Most of the time, you also lose weight, which means your risk of heart disease decreases too.” (Science Daily 7/3/2000).

Normally, when leptin levels in blood go up, the brain signals us to stop eating. But since obesity isn’t the result of a lack of leptin, it is a lack of response to leptin, and obese individuals tend to have more and larger leptin-producing fat cells (leptin is a hormone secreted by fat cells) than thinner people, their leptin levels increase substantially with every pound of additional weight gain.

Correct me if I’m wrong, but there appears to be no logic in the idea of taking more leptin to reduce weight if you have an impaired response to leptin.

It is important to keep in mind that the study that showed that raising leptin levels in people who have already lost weight helps them to keep the weight off. It does not help people to lose weight in the first place. It prevents the yo-yoing that most dieters go through as their leptin levels drop and the brain tries to compensate by increasing hunger.

Weight loss lowers levels of leptin, which in turn can restore an impaired response to leptin signalling, thereby increasing your appetite. Therefore the first step, if considering using leptin, is to accomplish initial weight loss, thereby enabling supplemental leptin to signal you to stop eating.

For those first steps in accomplishing initial weight loss see my bio below for more information.