Not exactly romantic like a honeymoon, but definitely a significant event preceding a life long commitment -- the Honeymoon Period is a period of time when a patient is first diagnosed with type 1 diabetes.

During this time, patients sometimes seem as though their diabetes appears to go away. The patient's insulin needs are minimal and some patients may actually find they can maintain normal or near normal blood glucose taking little or no insulin. This can last between a few months to as long as a year.

Dr. Richard Bernstein, the best-selling author of "The Diabetes Solution" answered the following question from a mother regarding her child's diabetes and the influence of diet. He said:

If every newly diagnosed child with diabetes were put on our program at the time of diagnosis, we would rarely encounter the horror stories that we hear from nearly every parent. These include the roller coaster blood sugars with frequent and severe hypos, the need for snacks, the fear of delayed meals, personality changes and growth retardation. Furthermore, we find that the "honeymoon period" can be prolonged indefinitely if blood sugars remain within the normal range (about 90 mg/dl). Prolongation of the honeymoon period not only makes diabetes control much easier, but also preserves the pancreatic beta cells.

If Dr. Bernstein's idea about controlling the length of the Honeymoon Period through diet is possible - is it possible to ward off the onset of autoimmune diabetes (type 1 diabetes) through diet. The belief may be heavily supported by contrarians, who traditionally contest conventional medical wisdom. I'll admit - I could be one of them. I own Dr. Bernstein's Diabetes Solution and I have to hand it to him - at first glance I thought I voluntarily entered a diabetic Twilight Zone. Then I reminded myself why I bought the book in the first place.

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!

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.

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?

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.

New research reveals that faulty nerves in the pancreas may be one of the causes of type I diabetes, a condition where the immune system mistakenly attacks islets. Substance P was found to be responsible for healthy function and protection of islets.

Toronto researchers injected substance P into diabetic mice to reverse new onset diabetes. Sernova Corp is leading research into reversing insulin dependent diabetes by implanting a small device containing insulin producing islets to reverse diabetes, and Sertoli cells to naturally protect the islets from the body's immune system.

There is no point in scaring you like a virgin on prom night by telling you where the Sertoli cells derive. Where they're taking us along the path to cure type 1 diabetes is of greatest importance.