We've long known about Type 1 diabetes. Most people know about Type 2 diabetes, too. But would you believe it's possible that a discovery may warrant a Type 3 diabetes? Researchers have discovered that the suppression of insulin signaling in the brain raises the possibility of a Type 3 diabetes.

Researchers have known for some time that insulin is not just produced in the pancreas, but also in the thymus. It is also known that insulin resistance, a characteristic of Type 2 diabetes, is tied to neurodegeneration. While scientists have suspected a link between diabetes and Alzheimer's disease, this is the first study to provide evidence of that connection. The study identified a gene abnormality that blocks insulin signaling in the brain. A drop in insulin production in the thymus contributes to the degeneration of specific regions of the brain. These abnormalities do not correspond to Type 1 or Type 2 diabetes, but reflect a different and more complex disease process that originates in the CNS (central nervous system). This raises the possibility of a Type 3 diabetes.

Those who suffered from Alzheimer's disease had a deficiency of growth factor in the hippocampus. The hippocampus is the part of the brain responsible for memory. The absence of these growth factors causes cells in other parts of the brain to die. Reserachers found that insulin was significantly reduced in the areas of the brain responsible for reasoning, planning, speech, movement, emotions, and problem solving. Researchers conclude that there is a genuine need for comprehensive study of the neuropathological changes associated with diabetes treatment and the affects of specific medications on insulin signaling. I agree with the researchers!

Ever wonder what would happen to a non-diabetic's blood sugar if they loaded up on a pile of concentrated sugar, preservatives and weird science fats? Doctors and the ADA call it prediabetes. This clip takes it to the extreme by sandwiching the center of 16 double stuff Oreos! Sometimes you have to be insanely blunt to make your point.

This is a brilliant example of the diabetes epidemic in action. In today's world -- many people are eating for convenience without realizing the consequences. More convenient equates to less nutritious - more preservatives, more sugar and even more fattening (the wrong fats, too!) The combination increases the amount of time our digestive enzymes need to work on these lab-derived ingredients. This sustains an elevated blood sugar following the time of consumption. Add the ADA definition of pre-diabetes (a blood sugar between 140 to 199 mg/dl 2 hours after a meal) and there you have it -- a potential player on Team Diabetes!

Think what would happen if this guy was in his doctor's office 2 hours after this stunt. I'd like to thank his employer for keeping him busy (whatever he's paid to do) well after the lunch hour - and protecting him from becoming another statistic. Big ups to HR for hiring this guy!! If he's not in marketing already -- you might consider a transfer and give this guy a raise. He's my Oreo hero.

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!!

I was excited to see my friend, Lissa Coffey, appearing on The Today Show this morning. Lissa is a PhD, a relationship expert and sociologist. Lissa shares her ancient wisdom and modern style through her site, Coffey Talk, and her newsletters. A recent newsletter addressed homeopathic medicine and I share with you how this applies to the treatment of diabetes.

Homeopathic medicine is a natural pharmaceutical science developed in the early 1800s. It uses small doses of natural substances (animal, vegetable, and mineral) to stimulate the body's own defenses. Homeopathy is a word derived from the Greek words for similar and disease. It is medicine based on the law of similars that says a substance will help to heal symptoms similar to those that it is known to cause. This is the same principle behind immunization.

When I received Lissa's newsletter on homeopathic medicine immediately I thought of how this applies to diabetes - a disease of insulin antibodies attacking the naturally produced insulin in the body. Why would you treat a disease with the exact hormone that caused it? Novo, Lilly, Aventis - you are all making a grave mistake in forcing American's to use GM human insulin, both Type 1 and Type 2. The extinction of porcine and bovine insulin has consequently proven to be detrimental to diabetics over the last 25 years. Studies show tighter control - yet complications on the rise. How do you explain this? I'm not excited for what the future holds, unless we see a return of these similar but not exact insulin forms.

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.

Just like a referee to normalize play throughout the game - DiaKine Therapeutics is developing ways to normalize the body's immune system.

The new drugs modulate cytokines, part of the body's immune system, which mistakenly attack normal organs and tissue and cause diseases such as: diabetes, multiple sclerosis and inflammatory bowel disease. Research by Dr. Nadler and his collaborators published in 2006 showed that controlling certain cytokines can arrest the progression of, or reverse, type 1 diabetes in an animal model.

The company's first product, IsletLifeLSF Media 1 is designed to improve the viability and insulin producing capabilities of harvested islet cells prior to transplant. This would potentially improve the success rate of the procedure. Additional therapeutics under development by DiaKine include: adjunct therapy to islet cell transplants, halting the progression of type 1 diabetes in newly diagnosed adults, treatment and prevention of Latent Autoimmune Diabetes of Adults (LADA), treatment and prevention of insulin requiring type 2 diabetic, treatment and prevention of diabetes complications.

It all sounds like good stuff in the works. Keep an eye on the progress and press releases of DiaKine, as well as their research partner - the Diabetes Research Institute. A lot is happening these days. What else have you seen or heard about in the autoimmune arena?

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!

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.

Metabolex is a company dedicated to the discovery and development of novel therapeutics for diabetes and related metabolic disorders. They recently announced the launch of a double-blind, placebo-controlled Phase 2a, proof-of-concept study for MBX-2044, an oral insulin sensitizer for the treatment of type 2 diabetes.

Metaglidasen and MBX-2044 address insulin resistance, the underlying cause of type 2 diabetes, by enhancing insulin sensitization. The currently marketed insulin sensitizers, Actos® and Avandia®, carry warnings of increased risk of congestive heart failure due to edema and cause significant weight gain, which compromises patient compliance.

Metaglidasen and MBX-2044 have been specifically designed to address the shortcomings of the currently marketed insulin sensitizer drugs. Clinical testing of metaglidasen suggests it has comparable efficacy with an improved safety profile. Now we're getting somewhere with this medical advancement stuff! A new drug that does the trick sans the undesirable side effects - attaboy, Metabolex!

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!