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!

Howard Hughs Medical Experts have discovered the key to a longer life is lower insulin levels. Less insulin helps cells fend off diseases that lead to early death like heart disease, cancer and diabetes. So how does one lower their insulin levels? Caloric restriction by way of eating less carbohydrates.

Caloric restriction postpones the onset of life-threatening conditions like cancer, diabetes, and heart disease. It may still happen, but at a later age. Scientists manipulated genes in mice to produce 50% less insulin and saw the mice live 18% longer. While lowering insulin throughout the body can lead to a diabetic state, scientists found that allowing insulin levels to be high throughout most of the body, and lowering the insulin signaling only in the brain through genetic manipulation, extended the life of mice.

Although the mice were overweight, they lived longer and seemed active and youthful. Scientists believe that this research explains why some people who live past 100 may have a natural genetic tendency for lower insulin signaling in the brain. They eat a normal amount of calories and may even be a bit overweight, but still enjoy the benefit of life extension. This begs the question: if all diabetes oral meds multiply the effect of insulin -- doesn't this increase the chances of heart disease and cancer? New Rule: Black box warning on ALL prescription diabetes drugs!!

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!

Circumstances of confusion invalidated a Diamyd clinical trial to protect insulin-producing cells in diabetes patients. This confusion amounts to a speed bump, but Diamyd intends to press on.

The company admitted that the Phase II clinical trial of its gene therapy had been botched following a mix up over which patients received the drug and which got placebo. Diamyd is a vaccine based on GAD65, a major factor for diabetes due to an autoimmune reaction. The company designed the vaccine to reduce the need of insulin injections and prevent the destruction of beta cells that produce insulin in the pancreas. Also, by protecting these cells, it may allow them to regenerate in a non-autoimmune environment, and possibly set the stage for a cure of the disease.

Anders Essen-Möller, CEO of Diamyd, said: "Was the drug mixed up? We do not know. Could there be a mix-up at some other times in the study? Yes it is possible, but that is not certain." Essen-Möller is determined not to let the mistake ruin the vaccine's progress towards approval. Essen-Möller also said he believes that the invalidation of the trial will not adversely affect any ongoing meetings with potential partners.

Chat live with Dr. Pugliese, an expert on the immunology and genetics of diabetes at The Diabetes Research Institute. His work has been focused on preventing the autoimmune attack that leads to diabetes. This research is very important for future prevention strategies, as well as stopping autoimmune destruction of transplanted islets.

Dr. Pugliese's has studied the role of the thymus gland in the immune system and he describes it as the "school for the immune system". All immune cells are forced to pass through the thymus gland where they are exposed to the antigens present throughout the body. Immune cells that bind to these normal antigens are destroyed, thereby preventing the later destruction of healthy cells. If no binding occurs, then the cell is deemed to be friendly to host tissue and is released to become part of the immune system. The insulin producing cells of the body - islets -- are not the only body cells that release insulin. Dr. Pugliese's research has shown that there are other cells that release tiny amounts of insulin, but not in response to blood glucose. These cells present insulin to the visiting immune cells in the thymus, and any immune cell that binds is killed. It is believed that a low insulin output in these decoy cells in people who develop diabetes may be the reason that immune cells are allowed to live that will later track insulin back to its source and destroy healthy islets. In people who have the genetic markers that protect against diabetes, these cells secrete more insulin than they do in people with genes that pre-dispose them to diabetes. The more insulin in the thymus, the more likely that insulin-specific autoreactive lymphocytes will be killed, with fewer chances of developing diabetes.

Confused yet? Yeah, me too - but my confusion feeds my insatiable curiosity. That is precisely why I will be joining the rescheduled chat with Dr. Pugliese. Please, be there on March 15th at 9pm Eastern Standard Time on Diabetes Talkfest. Make it a date: you, me, Dr. P and the most informed people in the diabetes community. Once again, thanks to Gina and Jon for Linking Diabetics Coast to Coast!