Dr. Faustman's lab is currently collecting blood samples from individuals with established Type 1 diabetes. These samples are being used to quantify the number of autoreactive T-cells and develop the adequate dosage for Phase 1 of human trials to cure Type 1 diabetes.

The research has been presented and the NIH confirmed it. By reeducating the confused T-cells and instructing them not to attack healthy islets, an apparent cure of established type 1 diabetes in non-obese diabetic mice is possible. Now, Dr. Faustman is collecting human samples to bestow the same cure for diabetes in humans.

If you wish to be a part of this revolutionary event for curing Type 1 diabetes, please contact the Clinical Coordinator or call Dr. Faustman's lab at (617) 726-4084. Each participant is asked to bring a control person along with them - an unrelated person without Type 1 diabetes or another autoimmune disease. Diabetic or not - you can be a part of history in curing Type 1 diabetes!

Allow me to explain my choice of photographs. I choose to spot the picturesque sunset over the Ventura Beach horizon, where I will NOT be attending the upcoming Gordon Research Conference on Oxidative Stress and Disease. For those who will be there, do me a favor and drop me a line on Section 3: Oxidative Stress and Diabetes. Here's what I've got so far...

Alpha-lipoic acid is approved in Germany as a drug for the treatment of diabetic polyneuropathies. Alpha lipoic acid shows evidence of being effective in the treatment of diabetic neuropathy and may be useful in treating some other aspects of diabetes. It may help prevent the oxidation of LDL cholesterol and may be protective against oxidative stress. As much as I wish I could jump forward in time, I'll make a forward-looking statement about an upcoming event and come back to update it, after March 11th. Here's my forecast: the Gordon Research Conferences is holding a conference on Oxidative Stress and Disease and it just so happens that section 3 of the Monday night speakers will address topics such as: A radical explanation for diabetic complications, A role for ROS in the etiopathogenesis of insulin resistance, and Mitochondrial dysfunction and type 2 Diabetes. If you need me to drop names to lift your scientific credence in this convention - the speakers come from Harvard Medical Scool, Yale University School of Medicine and Albert Einstein College of Medicine.

These people don't mess around! I close with a big thank you to the creator of Miracle Muffins, for taking an interest in his mother and sharing it with the rest of us battling frustrating complications of diabetes. I'll be actively checking to see how the experts diagnostically address the role of oxidative stress and what they perceive as the best resolution. Until we hear better in days to come, let's keep betting on the benefits of a little ALA in our day.

Novartis SA reports the U.S. FDA has demanded additional data, including a clinical study in patients with kidney impairment, before giving Galvus its approval. Why the holdup?

The FDA wants more data studying Galvus in patients with impaired kidneys. It had been thought that Galvus might have an advantage because it is not processed by the kidneys, while Januvia is. But another molecule created when the body metabolizes Galvus does build up in the kidney.

In the Feb. 1 issue of The New England Journal of Medicine, David M. Nathan, a Harvard Medical School endocrinologist, noted that it was surprising that the FDA decided to clear Januvia at all, given the "paucity of published data from long-term clinical trials on its safety and efficacy." Nathan is a consultant for Novartis and other drug makers but not Merck.

There are several potential concerns about DPP-4 drugs, clear evidence has not turned up in clinical trials so far. The medicines could affect the immune system, because a receptor on immune cells is very similar to DPP-4. Merck says that Januvia was designed to bind only to the DPP-4 enzyme, reducing the chances of these side effects. Patients with impaired kidneys have more of the drug in their bloodstream and would be more likely to experience side effects.

A Harvard Medical School scientist's experiments with fish discarded along the coast near Boston have led to a new class of diabetes drugs. The latest, from Novartis, may get U.S. approval this week.

In the late 1970s, Habener, a doctor specializing in diabetes care, began buying discarded fish to learn about the ways animals controlled blood sugar. By 1987 Habener discovered a protein in the pancreas of anglerfish that tells the pancreas to produce insulin. He called it glucagon-like peptide-1, or GLP-1. In 1995, researchers uncovered another use for Habener's discovery to treat diabetes. The scientists found an enzyme that digests GLP. By blocking the enzyme, they could increase the body's reserves of GLP, thereby raising insulin levels. Twenty years later, we will soon have the pleasure of meeting Novartis' concept for this chronology of discoveries in the form of liraglutide.

In clinical trials, patients taking liraglutide attained normal blood sugars without the common side effect of weight gain. In fact, liraglutide was more likely to make the patients slightly leaner. Depending on dosage and length of treatment, it may help patients to lose weight. The drug does not cause a change in appetite. Furthermore, none of the liraglutide patients experienced episodes of low blood sugar levels throughout the trials.

I'm no fisherman, but if all the seagulls of Big Pharma are swarming overhead - there's bound to be a school of fish below. However, this school is quite competitive. At last count, the five largest diabetic drug makers are using Habener's findings to create new medicines.

Genetics affects diabetes risk...but lifestyle is still the most important factor at play. That's the conclusion of a new study, which showed that a certain gene variant gives people a substantially increased risk for developing Type 2 - an eighty percent higher risk, in fact.

But before you throw up your hands and say "I can't fight Mother Nature," bear this in mind: the researcher also said that a healthy lifestyle is enough to pretty much cancel out that genetic risk. In essence, lifestyle trumps genetics, says study author Dr. Jose C. Florez, from Massachusetts General Hospital and Harvard Medical School. And the lifestyle changes required are nothing too major: just losing a little weight and exgaging in moderate daily exercise is enough to do the trick. "Environment can overcome the genetics you have received," says Florez.

The gene in question is known as TCF7L2 and had been identified with Type 2 diabetes by a previous study. This latest study aimed to see if variants in the gene could be usued to predict who would have Type 2 diabetes. Health information was gathered for nearly 3,500 people and, for those people, the researchers gathered genetic information along with a check on insulin secretion and sensitivity. This was repeated one year later. This data was used to calculate risk in each participant.