The FDA has approved a new over-the-counter weight loss drug called alli (orlistat) that is designed to absorb 25% of the fat from your meal. However, nutrition and fitness expert Dr. Len Lopez, author of "To Burn or Not to Burn, Fat is the Question" shares his reasons why the new approved weight loss drug may not be beneficial to your health.

New research is showing that medications don't make us healthier. Research is showing that losing weight with medications doesn't decrease the rate of heart attacks, strokes or diabetes. Add that to the fact that your body loses nutrients with these medications and you can easily see how these new weight loss drugs can hamper your health. Dr. Lopez discusses practical steps to losing weight which includes diet and exercise, but also covers how stress and adrenal fatigue can disrupt our hormones, such as cortisol and adrenaline. These hormonal imbalances can throw off our metabolism and take us out of our fat burning mode.

Both of Dr.Lopez's books cover a good deal of information to understand how we can correct our imbalances in piecing together the weight loss puzzle. His knowledge explores the roles of insulin and cortisol in weight gain, cravings, fatigue and more. He also explains how stress can take you out of your fat burning zone and helps you regain your blood sugar balance, as well as implementing the "Five and Two" dieting plan.

Say NO to the weight loss drugs and say YES to the empowering knowledge Dr. Lopez has to share.

Japanese scientists have discovered an imbalance that leads to the development of type 2 diabetes in mice. A gene called GCK is responsible for sensing changes in blood glucose levels. Researchers found a molecule known as insulin receptor substrate 2 (IRS2) was shown to influence the beta cell mass increase after GCK sensed an increased in blood glucose levels.

The Journal of Clinical Investigation focused on mice with little increase in beta cell mass regardless of a rise in GCK. Researchers found, in healthy mice, the insulin receptor substrate 2 (IRS2) was shown to influence the beta cell mass increase after GCK first sensed an increased in blood glucose levels.

Before a person becomes diabetic, his or her body tries to compensate for the increasing resistance to insulin by upping the amount of insulin secreted and the mass of insulin-secreting cells (beta cells) in the pancreas. Researchers will look for new ways of increasing beta cell mass to prevent the onset of type 2 diabetes. Here's where I get a little confused - another study conducted a few years ago found evidence that a sucrose-rich diet (SRD) produces an increase in the pancreatic beta-cell mass in the rat. I'm neither a rat, nor a scientist - but I think a meeting of the minds behind these two discoveries might result in some forward-thinking treatments for type 2 diabetes. What compels the IRS2 to defy the command center of GCK? Perhaps another piece is missing from the balance of this equation.

A study published in the online edition of the journal Nature, found a sensor in the liver (LXR) activated by glucose that controls the body's metabolism of cholesterol and fat.

Scientists fed synthetic LXR to mice eating a diet of mostly simple sugars. They discovered that the mice metabolized glucose more effectively and that activation suppressed new production of glucose in the liver. That prompted the scientists to study glucose levels as the LXR activating mechanism in the liver. By controlling glucose sensing and fat synthesis by LXR, scientists may explain and correct why low-fat, high-carbohydrate diets can lead to an elevated level of triglycerides in the blood. LXR can sense surplus glucose, induce fatty acid synthesis, and prompt the liver's export of triglycerides into the bloodstream rather than being stored as fat.

LXR could resolve the problem of hyperglycemia and atherosclerosis by binding to glucose and cholesterol buildup in the body. LXR induced regression of atherosclerosis, the clogging, narrowing, and hardening of the body's large arteries and blood vessels that can lead to stroke, heart attack, and eye and kidney problems. Contrary to conventional wisdom, this experiment led to the discovery that glucose binds directly to LXR, representing the first signaling pathway of this kind.