Using the hormone-like messenger protein leptin to shrink your fat cells is an intriguing, potentially key new concept in weight loss. Diminishing the body’s cravings that lead to overeating is another critical, new concept.

And with more and more of us dining out on, or taking out, industrialsized meal portions, it is clear that
shrinking our fat cells and reducing cravings that lead to overeating are potentially two very good things.

So what if we really could safely shrink our fat cells (without losing muscle)? What if we simply could
safely lose the cravings that cause us to overeat?

The science of slimming is now on the verge of such breakthroughs. We cannot assure everyone reading this report that the information we present will result in weight loss or conversion of fat to lean muscle, because the information is preliminary (and also individual biochemistry affects all outcomes).

But, many of us welcome all the help we can get when it comes to appetite control and weight loss. Our mission is to keep you informed of cutting edge breakthroughs in health. Anecdotal reports are coming
in now from individuals who are losing weight and/or becoming more trim with the use of a leptin-based
colostrum formula from TBR Labs. It is called Lepti-Trim. So we want to present this information. It may prove helpful to many of you.

Scientists Say Leptin Works

As a longtime consultant to the dairy industry, Dr. Al Fox has seen firsthand the beneficial impact of leptin on body mass composition. “I have been involved in studies with lean body mass and calves, and we have demonstrated that supplemental colostrum aids lean body mass. It seems likely that it is the combination of leptin and insulinlike growth factor-I (IGF-I) in colostrum that helps to create lean body mass,” says Fox, one of the world’s leading experts on colostrum, its formulation, utilization and applications. Dr. Fox is scientific consultant to TBR Labs.

“Leptin directs how you actually use fatty acids,” he continues. “Large fat cells indicate a leptin deficiency or
an inability to properly use leptin due to faulty cell receptors or other feedback mechanisms. It’s a vicious cycle. Once you get a lot of large fat cells you have inefficient uses of leptin and you end up with more fat cells and even more leptin because your body is no longer responding. But as people lose weight, their leptin levels decrease, making it difficult to reach ideal body weight. What we do know is that supplemental
leptin seems to work.”

Most telling is a 1999 study from the Journal of the American Medical Association that found that leptin not
only resulted in significant weigh loss, “more than 95% of weight loss was fat loss,” note researchers.

Meanwhile, researchers at the Howard Hughes Medical Institute have been using genechip technology—
a powerful tool for analyzing the expression patterns of thousands of genes at a time—and have identified a
number of genes that are specifically regulated by the hormone leptin.

Identifying genes regulated by leptin will improve knowledge of how leptin causes its effects on weight and appetite, and may also offer new targets for drugs designed to stimulate weight loss. Since the discovery of leptin in 1994, many have hoped that  the hormone would be a promising weight-loss treatment for humans.
Studies of the hormone’s weight-reducing effects in humans are underway, but researchers still have a way to go before they fully comprehend how the hormone affects the brain and other tissues.

In experiments described in the April 15, 2000, issue of the journal Genes & Development, Dr. Jeffrey M.
Friedman, an HHMI investigator at The Rockefeller University, and Rockefeller colleagues Alexander
Soukas, Paul Cohen and Nicholas D. Socci report that they are beginning to probe the genetic program orchestrated by leptin to induce weight loss.

FYI
Leptin Background
Leptin, a hormone-like messenger protein (known technically as a cytokine), is produced in relatively large
amounts by fat tissue and in smaller amounts by other peripheral organs, and then secreted into the bloodstream, where it travels to the brain and other tissues, causing fat loss and decreased appetite.

Once leptin has been secreted by your fat cells, it travels to the hypothalamus—the part of your brain that has an influence on eating behavior. In the medial hypothalamus, leptin activates “anorectic” nerve cells, which serve to suppress your appetite. At the same time, leptin prevents “orexigenic” cells from stimulating your appetite.

Leptin (from the Greek leptos, meaning thin) first came to national attention in 1994 when the obesity gene and its product leptin were discovered. It was shown then that obese mice dropped 40 percent of their body weight after only one month of treatment with leptin. Leptin also improved symptoms of diabetes.

Recently, the taste organ was found to be one of the peripheral targets for leptin. The hormone specifically inhibits sweet taste responses in lean mice. Thus, leptin appears to act as a modulator of sweet taste.

Leptin also suppresses a gene that produces an enzyme known as acetyl-CoA carboxylase, or ACC, which is essential for fat production. When researchers injected laboratory mice with leptin, previously obese mice became as thin as rodent track stars. Some researchers believe that leptin works, in part, by inhibiting the synthesis of fat in fat cells and increasing the burning of fat in muscle cells—that it works at an enzymatic, cellular level.