A type 1 diabetic mystery is why do some Type 1s get complications and others seem to never get them? A massive Japanese study of Type 1 diabetics found that those with fulminant diabetes developed complications much faster and more severely than those with non-fulminant diabetes.

The difference between fulminant and non-fulminant is the speed and intensity at which the disease develops. Fulminant Type 1 diabetes typically develops suddenly with near total loss of beta cell function. This type of diabetes is confirmed with testing c-peptide levels. Non-fulminant type 1 diabetes has residual c-peptide levels that eventually taper to undetectable. Sometimes this is seen through many years of the Honeymoon Period.

This study may be the antithesis of conventional wisdom for preventing complications. Staking all hopes on blood sugar control is heavily optimistic. Yes controlling blood sugar does lessen the workload for existing beta cells, and thus extends the lifespan of each beta cell. Research suggests that c-peptide offers protection to beta cells, both from apoptosis (cell death) and encourages new cell growth. This new cell growth applies to beta cells and other cells of the body that endure long-term Type 1 diabetes complications.

Diabetics are instructed that maintaining normal blood sugars is the Holy Grail of preventing long-term complications. Yes and no. The truth is controlling your blood sugar will not allow complications of Type 1 diabetes to develop as quickly, presuming you still had some level of beta cell function upon diagnosis (i.e., c-peptide). That doesn't sound like a reward as much as it does a delayed punishment. I'd like c-peptide with my insulin, please. It's off the à la carte menu? That's fine - serve it up! I want to thank Klausen for bringing this study to my attention.

In two weeks, Bernard Farrell will be riding in the Bike the Miles annual fundraiser to support Dr. Faustman's research to cure Type 1 diabetes. His participation is especially intrinsic because it is one day away from his 35th anniversary of becoming a Type 1 diabetic.

Bernard plans to raise $10,000 for Dr. Faustman's research. Last year he raised $7,500. The entire event raised a whopping $301,000! All of this funding is going toward the human trials to cure Type 1 diabetes. After discovering that the insulin-producing islet cells of the pancreas are capable of regeneration, Dr. Faustman now needs to test her treatment, already known to be safe in humans, to see if the effects are as positive as they were in the animal model.

It goes without say that this is terribly important for Bernard as much as it is for every man, woman and child touched by Type 1 diabetes. Bike the Miles is an annual event that was started by Susan Root and Jacqueline Fusco in 2004. Both, Susan and Jacqueline, have children who are Type 1 diabetics. Please visit Bernard's site to support his ride and the drive to cure Type 1 diabetes!

Read all about it. Professor Vincent Marks, a world expert on insulin who has assisted in some high profile cases of insulin murder, has written a book - the 'Insulin Murders - True Life Crimes'.

The first recorded incident of insulin used for murder was in 1957, and since then there have been about 50 cases globally of insulin being used for murder. Although insulin can be used to kill, Professor Marks said it was actually a very poor murder weapon. Detecting its use was difficult, but not as many assumed...impossible.

It is not a very good weapon especially nowadays. More tests are available to prove the misuse of insulin. If a non-diabetic is dead on arrival without a usual suspect - I suggest the coroner check the patient's blood sugar. If that's hovering around absolute zero I'd put a request in for the insulin antibody kit!

When Dr. Denise Faustman revealed her ground-breaking discovery 5 years ago, most of the biomedical world turned their noses up. Dr. Faustman said she had cured diabetic mice by getting them to regrow their insulin-producing cells. Today Faustman dismisses the initial pessimism by looking at the bright-side "a lot of groups are working on this now," she says. "If imitation is the best form of flattery, then I'm flattered."

To correct the autoimmune attack, Faustman injected mice with a cocktail that made their bodies churn out a signaling chemical called TNF-alpha. This compound destroyed the defective T-cells that mistakenly targeted islets. When a surgeon implanted islets on the kidneys of each mouse, the transplants could take root, make insulin and restore normal blood sugar control. To eliminate the problem of the bad T-cells returning, Faustman borrowed an idea from the transplant specialists, who have found that liver or spleen cells can "reeducate" a recipient's immune system to treat the new cells as welcomed guests.

Patience is a virtue and Dr. Faustman deserves the crown. Until recently, it was taken for granted that once the beta cells are lost, they can never grow back. This past March, three separate scientific studies confirmed that they had repeated Faustman's protocols and reproduced her most important result: it is possible to stop the mistaken T-cell attack and when you do, the animals recover normal function. "The results are fantastic, coming from these groups, which were each paid $1 million to spend three years showing that I was wrong," she remarks. "I mean, they were all funded by the JDRF." Dr. Faustman, when you're right - you're right. And for the salvation of every person living with an autoimmune disease: you're right!

If you've ever wondered why diabetics are particularly susceptible to persistent infections and health complications following relatively mild infections, the answer may be at hand. Researchers working at Schulich School of Medicine and Dentistry, Canada, have just published a study on the topic in Clinical Immunology. They found that diabetics have compromised immune systems resulting from problems with their dendritic cells. Dendritic cells (see image) regulate the body's T-cells, which fight infection. The study, which looked at both people with Type 1 and Type 2 diabetes, showed that the dendritic cells of diabetics are poor producers of an anti-viral agent that is important in activating T-cells. Without enough of that agent, T-cells can't do their job fighting infection.

The immediate lesson to be learned, says Dr. Bhagirath Singh, lead author of the study, is that strategies to control or avoid infection in diabetics (such as vaccinations) are of critical importance.