In the Houston Chronicle, People's Pharmacy columnists Joe Graedon and Teresa Graedon remember a drug scandal from 1970 that mirrors today's Avandia troubles almost exactly. Orinase, a popular diabetes drug was found to be increasing the very heart trouble it was designed (and marketed) to prevent.

Orinase's active ingredient is tolbutamide, a substance that stimulates the pancreas to produce insulin. According to the Graedons, the heart damage being caused by Orinase-takers was first revealed by the University Group Diabetes Program in 1970 following an extensive analysis of diabetes care in the US. Like the Avandia controversy, experts also debated the results of the University Group's conclusions on Orinase, yet it was more or less eventually accepted as fact that drugs belonging to the class sulfonylureas, including tolbutamide, do indeed increase the likelihood of heart problems. I say "more or less" because many authorities still hedge their bets. Example? The health site Drugs.com copies info on Orinase provided by Thomson Healthcare/Micromedix. According to that source, sulfonylureas, have been "reported, but not proven in all studies, to increase the risk of death from heart and blood vessel disease." [My emphasis.] This, thirty-seven years after the release of the study demonstrating such risk!

Orinase is still prescribed in certain situations. Is Avandia destined to end up sidelined, yet still on the market, like Orinase? Seems to be headed that way. In the meantime, the unfortunate reality is that new drugs will continue to be rushed to market and serious side effects discovered (or made public) only after they have been prescribed to thousands of people. The fact is, today's high-tech (and high-priced!) wonder drugs all come with a dose of risk.

Did you know type 1 diabetes can take months or even years to develop? It makes perfect sense considering my entire family developed type 1 diabetes at varying points in the life cycle -- teen, young adult and middle-age.

Research has shown the pancreas is stubborn and strong, requiring the loss of over half of the beta cells before symptoms of type 1 kick in. Researchers are taking the next logical step and enrolling relatives of type 1 diabetics in various studies to try and delay or even prevent the onset of the disease.

The University of Florida Health Science Center and Shands at UF are one of 14 centers nationwide dedicated to Type 1 Diabetes TrialNet, a research group dedicated to a host of prevention and early treatment studies.

Now here is a study I feel like enrolling in. TrialNet is testing whether a one-a-day oral insulin capsule can prevent or delay onset of type 1 in high-risk individuals. An earlier trial suggested oral insulin might delay type 1 diabetes up to 4 years in a portion of participants with islet cell autoantibodies in their blood. Makes me wonder if I have any autoantibodies swirling around in my blood.

It is well known that people with type 2 diabetes are at increased risk of pancreatic cancer, and now it seems that the risk extends to those with type 1 diabetes.

The risk was assed as small, but nonetheless - increased compared to those without diabetes. The research found that the likelihood of developing pancreatic cancer was twice as high in subjects with type 1 or young-onset diabetes as in people without diabetes. This increased risk is similar in magnitude to that seen with type 2 diabetes. There are many theories about the link between diabetes and pancreatic cancer. A cancer-inducing role of the insulin-producing beta-cells in the pancreas, is ruled-out because in type 1 diabetes these cells have largely or entirely been destroyed. The researchers want to stress that people with type 1 diabetes should not be overly concerned. The leading scientist issued a statement, "pancreatic cancer is an extremely rare disease, and twice a tiny risk is still a tiny risk."

In light of the study results, the researchers encourage diabetics to stay the course and focus on preventing the common complications of diabetes such as heart disease, eye disease and kidney disease. Good plan, good doctor. Thank you for the reassuring news – phew!

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.

Like a dog chasing its own tail (but nowhere near as funny), type 1 diabetes is caused by a self-imposed attack on insulin producing cells. Here's your chance to chat live and learn about the latest discoveries to interfere with the automimmune confusion. Chat live with the head of the Immunogenetics Program at the Diabetes Research Institute, Alberto Pugliese, M.D.

The DRI program is specifically focused on understanding how genetic and immunological factors play a role in the development of type 1 diabetes and how certain genetic and immunological factors may actually afford protection from diabetes. The program is uncovering ways to interfere with the immune cells that attack the insulin producing cells in the pancreas resulting in diabetes.

In plain English, join Dr. Pugliese to enlighten yourself and ask any questions you may have regarding this impressive research. The chat begins at 9pm EST and those who miss it can catch the excitement in the transcript, to be posted shortly thereafter. I hope to see fellow IDDMs on the chat roster.

Chromium picolinate is one of the most widely debated supplements in diabetes health. A study has shown that it improves glycemic control in patients with type 2 diabetes not adequately controlled while taking sulfonylurea, a drug that increases insulin release from the beta cells in the pancreas.

A 40-week study was designed to examine the effect of adding daily chromium picolinate supplementation to an antidiabetic medication, sulfonylurea. A commonly prescribed treatment for type 2 diabetes was given to 29 subjects for 24 weeks, in conjunction with either chromium picolinate or a placebo. Blood sugar levels of study participants taking chromium picolinate dropped significantly compared to the placebo group. In addition, insulin sensitivity for participants taking the chromium picolinate was increased when compared to those in the placebo group. Study participants taking chromium picolinate also experienced significantly lower abdominal body fat accumulation than the placebo group, and experienced less overall weight gain.

This study demonstrates that chromium picolinate supplementation for type 2 diabetes who are taking sulfonylurea agents significantly improves insulin sensitivity and glucose control. In addition, chromium picolinate was shown to reduce weight gain and fat accumulation compared with the placebo group. The results of this study were first published in August 2006 - but knowing about chromium picolinate today leaves you with ample time to adjust for greater insulin sensitivity and less fattening days to come!

Scientists have found that mice lacking a protein known as SH2B1 throughout their body are obese and ultimately develop diabetes. Researchers replaced SH2B1 in the brain of obese mice and it seemed to deter the onset of obesity. The study reveals that targeting SH2B1 in the brain might be a new avenue of treatments for obesity and type 2 diabetes.

SH2B1 is expressed in tissues related to obesity, including the brain, liver, pancreas, and fat tissue. Replacing SH2B1 in the brain of mice lacking SH2B1 prevented the mice from becoming obese. It also prevented the mice from developing obesity after being fed a high-fat diet, indicating that SH2B1 in the brain is required to regulate body weight and fat content.

This study implies that SH2B1 in the brain is a practical target for the development of new drugs to treat obesity and type 2 diabetes.

New research is revealing that cells passed from mother to child during pregnancy could be used to treat diabetes. Scientists found these cells can develop into functioning islet beta cells which produce insulin in the pancreas.

Scientists studied 172 individuals and took pancreatic tissue from four deceased males. They found small numbers of female islet beta cells able to produce insulin. There was no evidence the mother's cells were causing damage or becoming the target of an immune response. However, the team found more maternal DNA in the blood of children and young adults with type 1 diabetes than in healthy individuals. Researchers believe the maternal cells may be helping to regenerate tissue in the pancreas.

I heard about this study last year. It sounded quite promising and led me to wonder if I had a child - could the stem cells from the umbilical cord become healthy beta cells for me? Sure. However, the big question still remains - how can I stop the killer Ts from spanking my islets in the first place?

Okay, so it's not just an immune blunder anymore. Canadian-led research suggests immune cells aren't the only culprits in developing type 1 diabetes - the nervous system also plays a pivotal role.

With Type 1 diabetes, the destruction of the islet cells in the pancreas leaves the body without insulin to regulate the metabolism of blood glucose, or sugar. In studies of laboratory mice specially bred to make them susceptible to Type 1 diabetes, researchers discovered that a control circuit exists between insulin-producing cells and their associated sensory, or pain-related, nerves. It turns out that this control circuit is necessary to retain the health and normal function of islet cells. Researchers have found that the immune system is under much closer control by the nervous system than previously thought.

In other words, a dysfunctional immune response is not the only thing needed to get diabetes - the nerve cells are also critical. The researchers also found that injecting a substance into mice whose islet cells were inflamed and on the way to being destroyed not only eliminated the inflammation but actually reversed it. "The blood glucose normalizes overnight and it stays low for weeks to months - this is with a single shot," enthused one researcher. "We now have four-month-old mice that are non-diabetic that used to be diabetic" - a period equivalent to six to eight years in humans. Heck, I'll take a 6 to 8 year vacation from 10 finger sticks a day, 3 SYMLIIN injections a day, and a bi-weekly pump change. O Canada!

Chemical engineers at the University of Houston's Cullen College of Engineering have made what's being described as a major breakthrough in the field of diabetes research. You probably understand that Type 1 diabetes is associated with insufficient insulin production, something that takes place in the pancreas. Well, these researchers say they have discovered a new mechanism for forming insulin crystals -- the form taken by insulin in the pancreas before it is released into the blood. (Pictured here are a bunch of insulin crystals. Pretty, aren't they?) The scientists theorize that insulin deficiency may be caused when the crystals don't form properly. As a result, they have been engaged in the study of crystal formation. Without getting too technical, they used a very high-tech-sounding method called atomic-force microscopy to find a new way to get the essential insulin crystals to form. Read more in this article at Medical News Today.

Wow, so much pancreas-related news this week. In addition to the fab discovery (mentioned in my previous blog) that it is possible to apply PET imaging techniques to the pancreas, scientists have also discovered a non-invasive way to deliver insulin-producing genes to the pancreas. The method in question is actually a rather cunning form of gene therapy. It involves "smuggling" insulin-producing genes into the body concealed inside gas-filled micro-bubbles. Such bubbles have been successfully injected into the pancreas of mice, then burst with sound waves, thereby freeing the good genes to do their work protecting the pancreas. The technique is still very much in the experimental phase, but it is nonetheless of great potential importance for diabetics.