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.

The Chicago-Sun Times just ran a piece about area dentists who are doing their bit for type 2 diabetes prevention. These docs are screening all patients with gum disease for high blood sugar. They hope this will help with early detection, since gum disease is a risk factor for diabetes. (In fact, gum disease is a risk factor for tons of health issues, running the gamut from minor to life-threatening.)

The paper profiles, among others, dentist Dr. Ronald Schefdore. Whenever Schefdore gets patients coming in with gum disease, he automatically gives them blood tests that measure cholesterol and blood sugar levels, as well as inflammation. Schefdore describes a success story involving one patient who, thanks to the tests, got an early diagnosis of pre-diabetic symptoms and now, with the help of his PCP, has his blood sugar back under control.

Schfdore has also trained about five hundred other dentists (wow) how to collect blood samples using the finger-prick method. "If every dentist practiced this way," he comments, "we could improve the health of the world overnight."

This is preventive care in action. People like this are raising the bar for everyone. Cheers!

A glucosamine-like dietary supplement has been found to suppress the damaging autoimmune response seen in type 1 diabetes, according to University of California, Irvine health sciences researchers.

In studies on mice, researchers found that N-acetylglucosamine (GlcNAc), which is similar but more effective than the widely available glucosamine, inhibited the growth and function of hyperactive T-cells that cause diabetes. GlcNAc increased sugar modifications to the T-cell proteins, preventing the hyperactive immune response. This therapy normalized T-cell functions and prevented development of high blood glucose levels in type 1 diabetes.

GlcNAc decreases pain and inflammation, which likens the results of the Irvine study to a study that was conducted in Toronto last December. Researchers found they were able to cure diabetic mice overnight by injecting them with something called Substance P. Substance P is involved in the transmission of pain impulses from peripheral receptors to the central nervous system. Diabetes is like a rat without the ability to feel pain. The naked mole rat lacks Substance P and cannot feel pain when painful stimuli are administered to the skin. Snapple fact, folks!

Benfotiamine can help diabetics protect delicate microvessels. Much of the damage of diabetes is caused when glucose-derived compounds, called triosephosphates, accumulate in small vessels. Transketolase, turns these toxic compounds into harmless chemicals that can be removed from the body. benfotiamine increases transketolase activity, thus reducing or eliminating the complications associated with diabetes.

Administration of benfotiamine helped to prevent retinopathy in test subjects with diabetes. Study subjects who received benfotiamine for 36 weeks demonstrated completely normalized levels of damaging toxins in the retina, preventing or delaying the onset of diabetic retinopathy.

In a 24-week study, benfotiamine was shown to improve kidney function. This was shown by a 50% reduction of toxin levels in the kidneys, and a reduction in oxidative stress associated with diabetes. Subjects exhibited a 70-80% inhibition in the development of microalbuminuria, protein in the urine that serves as an early sign of kidney dysfunction.

Benfotiamine mitigates oxidative stress in the eyes, the kidneys, the heart, and even the brain that typically occur with diabetes. Researchers conclude that benfotiamine may offer critical protection for the delicate nerves of the eyes, the kidneys, the peripheral limbs, the heart and the brain by shielding them from damage caused by diabetes.

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?

Remember that movie with Billy Crystal and Robert De Niro, Analyze This? Well we all don't have super-risky mobster lifestyles to induce depression like Paul Vitti's, but according to a new study of depressed type 2 diabetics -- depression has a negative impact on blood sugar control.

Researchers treated 93 patients with type 2 diabetes and depression with the antidepressant bupropion (Wellbutrin). They chose the drug because it is capable of reducing depression and weight simultaneously. The hypothesis behind the treatment was mood enhancement and weight reduction would, in fact, improve blood sugar control. (Always a gold star day in my book!) The results were documented in the March issue of Diabetes Care, and showed that antidepressant treatment produced benefits beyond just mood improvement. Patients also lost weight, improved self-management of their diabetes, and improved their A1c levels.

In the 6 months following the conclusion of the study, depression improvement predicted maintenance of improved blood sugar control. This confirms the research hypothesis that depression improvement can produce better blood sugar control, independent of weight loss and overall diabetes management. The importance of weight-independent physiological factors like insulin sensitivity and inflammation improve during depression relief and contribute to better long-term control of diabetes.

The moral of this story? You tell me. I spotlight the research - I like it when you guys give me answers.

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?

It never ceases to amaze me how many new benefits related to strength training are discovered. Once considered to be the workout for the guy who no longer wanted to get sand kicked in his face at the beach, weight lifting has grown to become a doctor recommended way to maintain health. Serving as a testament to this is the recent discovery that strength training improves insulin sensitivity.

In the September 2006 Journal of Endocrinology Metabolism, French researchers published data suggesting that resistance training may fight against inflammation in internal tissues and organs. Specifically, they found that it improves insulin sensitivity and blood sugar metabolism without any effect on C-reactive protein, a marker of inflammation. What's more, not only does this help to prevent diabetes, it appears as though weight training's effect ability to fight inflammation can also aid in the fight against cancer and coronary artery disease.

In a related study, researchers from the University of Southern California studied weight training's effect on insulin Resistance and body fat in Latino boys aged 14-17. They found that 16 weeks of strength training improved insulin resistance, reduced body fat and increased lean body mass by 91 percent.

A study has identified the ingredients in cinnamon, the yummy spice found in everything from muffins to air fresheners, that appear to benefit diabetics. It was already known that cinnamon seems to help diabetics by reducing inflammation and by helping control blood sugar levels. Until now, however, it was not know why this might be the case, hence the purpose of a recent Maryland study, in which the fragrant spice was examined for the active ingredient responsible for these beneficial effects. The researchers concluded that, in the case of reducing inflammation, it all comes down to antioxidants called polyphenols found in cinnamon, which boost levels of three beneficial proteins. As for controlling blood sugar, it appears cinnamon contains a natural compound that has insulin-like properties. The study was carried out at the Department of Agriculture's Beltsville Human Nutrition Research Center in Maryland. Results were presented at the Experimental Biology conference held in San Francisco, April 1-5 of this year.