Sleep disorders have been linked to exacerbating or even precipitating diabetes as well as depression. Poor sleep robs people of their health in general. But, for diabetics it can cause a worsening of their condition. A hypnotist can assist a person with diabetes by helping them to positively alter their behavior.

A study explained how people who do not get enough sleep on a regular basis tend to become less sensitive to insulin over time. The study found that healthy adults who averaged 5.2 hours of sleep a night secreted 50% more insulin than their more rested counterparts, who averaged 8 hours of sleep a night. As a result, "short sleepers" were 40% less sensitive to insulin.

Devin Hastings is a certified hypnotist who has been helping people change their lives for over 24 years. Devin has created a series of informative articles that will help diabetics transform their debilitating habits into healthier habits. See Devin's site for more details.

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.

Today I compose an ode in remembrance for our islets of Langerhan. Their job is far more complex than balancing blood sugar. They balance everything in our metabolism, starting with the hormones that tell us to eat or stop eating. The islets of Langerhan house 4 critical cell groups: beta cells, alpha cells, delta cells, and gamma cells - also referred to as the PP cells and D1 cells.

Beta cells are activated by a rise in glucose which results in secreting insulin. As this insulin lowers the blood glucose, amylin is also released. Amylin supports the stability of blood glucose levels by slowing the rate that digested glucose enters the bloodstream. The alpha cells are the opposite - they are responsible for preventing hypoglycemia by secreting glucagon. Glucagon helps maintain the level of glucose by causing the liver to release stored glucose. Delta cells secrete somatostatin, which is like the hold button of the alpha-beta cell connection, restraining the release of insulin and glucagon. The last of our Langerhan lineup, and seemingly the least understood, is the gamma cells, PP and D1. These cells affect appetite through the secretion of ghrelin or leptin. Ghrelin is a stimulant for appetite and feeding. Leptin is a hormone that suppresses appetite and speeds up metabolism.

To recap Team Langerhan: beta cells respond to rising blood glucose with insulin, alpha cells respond to falling blood glucose with glucagon. Delta cells respond to perfect balance in blood glucose by suppressing insulin and glucagon, and the gamma cells keep an appetite on an even keel with ghrelin and leptin. If the initial blood glucose lowering medicine prescribed affects any one of these hormones (as you can see it does) - it is definitely causing an imbalance in metabolism. As we memorialize the islets of Langerhan- let us consider all they have done for us. Pay tribute to your islets of Langerhan by doing all that is naturally possible to restore metabolic balance in the future. I have a few ideas - but your job today is complete. You are enlightened. Please have a happy and safe Memorial Day!

The scientists at University of Pennsylvania School of Medicine discovered that it is possible to regenerate damaged cells of the pancreas. Although the cells that revealed this discovery are not the beta cells of the pancreas, researchers believe that this research could find new ways to replenish the organs ability to produce insulin in diabetics.

The pancreas is made up of two compartments with different functions: the islet compartment of insulin-producing beta cells and the much larger exocrine compartment composed of duct cells and acinar cells that make and deliver enzymes to the intestine for digestion. Diabetes is caused by the failure of the beta cells to make insulin, whereas pancreatic cancer usually originates from the exocrine compartment. Under certain conditions in tissue culture, acinar cells can synthesize insulin as well as amylase, a digestion enzyme.

Evidence from this research is pointing to the beta cell itself as the most promising source for generating new beta cells. The focus of research is now shifting toward the direct stimulation of islet cell growth in live animals. In contrast, once acinar cells are removed from the organism and placed into culture, they may have greater potential to change into other cell types, including beta cells. As a result, Stoffers' animal model and technical approach is currently being used by other groups in the United States, Europe, and China to determine conditions under which acinar cells can take on the features of duct cells and beta cells.

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.

A study suggests problems with cholesterol regulation in the insulin-producing cells of the pancreas may be responsible for the development of Type 2 diabetes.

A thesis paper written by a graduate student, Dr. Liam Brunham, addressed the fact that a dysfunction in cholesterol regulation is found in beta cells in the pancreas. A thought-provoking connection to this thesis was the fact that beta cells are the cells responsible for producing insulin. A beta cell expert decided to see what would happen if researchers genetically engineered mice without the ABCA1 gene. The ABCA1 gene is the gene responsible for cholesterol regulation in beta cells. Dr. Brunham appears to be the first to identify the role of cholesterol dysfunction resulting in the beta cells inability to properly secrete insulin.

This new research is promising and obviously raises questions in other researcher's minds. One is - what happens when amylin, a hormone produced by the beta cells, builds up to excess amounts? Does this, in fact, impair the beta cells' ability to function properly? Could this be another thesis that trumps Dr. Brunham's hunch for the cause of type 2 diabetes? Some researchers believe that the over-production of amylin and cholesterol may be due to a yet unidentified problem. Of course that is always an option. Science labs across the world could come to a screeching halt if doctor's stopped hypothesizing. As research continues, we will anxiously await the next best thesis paper, courtesy of our promising Graduate Students. Be cool - stay in school!

Neuropeptide regulating appetite may help in developing new diabetes treatments. The neuropeptide called melanin concentrating hormone (MCH) plays a role in the growth of insulin-producing beta cells and the secretion of insulin. MCH is found in the brain and regulates energy balance and appetite.

A previous study conducted at Joslin found an association between high levels of MCH and an increase in the number of beta cells in mice. When we eat food, our body needs more insulin. When MCH induces appetite, it simultaneously increased insulin secretion. This calls upon the beta cells and enhances their growth. If the proteins that mediate the growth mechanism can be identified, it could lead to the development of new drugs that would enhance beta cell growth to treat type 1 and type 2 diabetes.

Sounds great! However, this sounds similar to the function of SYMLIN, which is the synthetic form of amylin. Amylin is a hormone secreted by beta cells at the same time as insulin. If you've heard of Byetta - you've heard of Amylin Pharmaceuticals, the makers of SYMLIN. The researchers at Joslin and the guys at Amylin should get together and do lunch. They might have a lot to discuss between this research and the development of yet another biotechnological blockbuster drug.

In the summer iof 2004, research funded by JDRF revealed that a mutation of the SUMO-4 gene is a strong factor in the development of type 1 diabetes and the potential associated complications, such as kidney failure.

The gene called SUMO-4 is responsible for signaling the proteins that regulate the intensity and duration of the immune response. When the gene is mutated, it has an increased response to the stimulants of the immune system, that cause it to overreact. This overreaction results in a person's inability to distinguish between self and foreign cells, thus causing type 1 diabetes. The mutated SUMO-4 gene may exacerbate the inflammatory process, influencing the complications of diabetes.

The most influential genes in the development of type 1 diabetes are found in the HLA or human leukocyte antigen region. These genes help regulate the immune system by guiding it to differentiate between self and non-self. Variants of the DR and DQ genes in the HLA region are found in 95% of type 1 diabetics. Another gene that increases the chances of developing type 1 diabetes has been found in the region immediately preceding the insulin gene. This region contains a VNTR or variable number of tandem repeats. This refers to specific chemical bases that make up DNA. Inheritance of certain VNTR's increases the risk of developing type 1 diabetes.

Again I reiterate this research was unveiled in 2004. SUMO-4 was identified as a prime target to control the inflammatory process leading to the destruction of islets. As I search Google for, "sumo4, drugs, JDRF" I am terribly disappointed to see that my yearning for answers remains unrequited. Did SUMO-4 fall too hard too fast?

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!

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?

The Juvenile Diabetes Research Foundation announced that they have formed a partnership with MacroGenics. JDRF is providing up to $2 million to fund a clinical trial of a compound called anti-CD3 that has shown promise in slowing the progression of type 1 diabetes.

Anti-CD3 is capable of reducing the autoimmune attack that destroys insulin-producing beta cells. The treatment preserves beta cell function in newly diagnosed patients, and has the potential to decrease insulin requirements, leading to better glucose regulation, and decrease the complications of diabetes. Anti-CD3 blocks the function of CD3 cells - the T cells that destroy islets. The antibodies prevent "activation" of the T cells after they have identified their target, disarming them launching the attack on islets.

Let's hope the peace talks between JDRF, MacroGenics, anti-CD3 and killer Ts result in progressive measures to make the type 1 diabetic body a peaceful place, once and for all.

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.

Diamyd Medical's flagship drug, Diamyd, is showing promising results in reducing the need of insulin injections and preventing the destruction of beta cells.

Diamyd has demonstrated significant efficacy in preserving insulin production in 70 children and adolescents with type 1 diabetes. No serious adverse events associated with the therapy were observed. The results from the Diamyd study demonstrate that the group of 35 recently diagnosed type 1 diabetes patients that received Diamyd produced approximately twice as much meal stimulated insulin (as measured by C-peptide) 15 months after the first treatment as compared to the placebo group. Preserving insulin-production is crucial for delaying the complications associated with long-term diabetes which cost billions of dollars to treat. Furthermore, it may allow for regeneration of beta cells in a non-autoimmune environment, thus setting the stage for a cure of the disease.

"We look forward to opening the dialog with the FDA regarding the potential initiation of our clinical program for Diamyd in the US" says Anders Essen-Möller, CEO of Diamyd Medical. "We obviously cannot predict the outcome of any meeting with the regulatory authorities, but we hope we will gain some valuable guidance towards structuring a suitable US clinical program for the continued development of Diamyd as a therapy for type 1 diabetes." Anders-you let me know if the regulatory authorities give you any funny business. I'll see what the diabetic community has to say about it. The buck stops here!

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!