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.

Thousands of pre-school age children are being diagnosed with Type 1 diabetes as new figures show a dramatic rise over the past 20 years.

Between 1985 and 2004, the study conducted by Bristol University, has seen an increase in cases of type 1 diabetes in children under the age of 5 five times the previous average. Type 1 diabetes is an auto-immune disease in which the body fails to produce insulin or makes only a little. One of the theories leading to the rise in type 1 diabetes is due to infants being exposed to exorbitantly clean households. The researchers found that incidence in all children under 15 had doubled. But the incidence of type 1 diabetes in children under the age of five went from .2 cases per 1,000 to 1 case per thousand.

The hypothesis offered by Prof Bingley leads to a very good argument. He said, "the increase is too steep to be put down to genetic factors, so it must be due to changes in our environment. This could mean that we are being exposed to something new or that we have reduced exposure to something that was previously controlling our immune responses". Much like the denouement in a game of CLUE: perhaps it was Mr. Clean, with the mop, in the kitchen!

The results of this study do not surprise me at all. Researchers have found that psychosocial factors like cynical distrust, chronic stress and depression, may be associated with higher levels of inflammatory markers. These inflammatory markers are related to an increased risk for cardiovascular disease, the leading cause of premature death among people with diabetes.

The study included 6,814 men and women between the ages of 45 to 84. Participants were assessed for their levels of depression, chronic stress and cynical distrust. Blood samples obtained at the start of the study were analyzed for markers for inflammation. The researchers found associations between all three psychosocial factors and inflammatory markers.

A high stress lifestyle may increase the chance that an individual engages in social behaviors that increase inflammatory markers. The same high stress lifestyle may contribute to obesity and related metabolic problems. Furthermore, socioeconomic position is likely to be a precursor to psychosocial characteristics. True. But let's not wager our lives on a dollar-denominated scale. Consider the Chinese proverb, those who know when they have enough are rich. Now ask yourself where you stand in the socioeconomic parade. If you put it that way - I'm on easy street! Too bad it's in the wrong neighborhood.

The immune system is sort of like your offensive linemen in football. It protects the body from invading disease and infection, just as the offensive line protects the quarterback from being sacked by members of the opposing team. When using this analogy, a specific group of white blood cells called T cells can be considered your All-Pro linemen, your best protection against against invading pathogens. These T cells are controlled by a second group of cells called regulatory T cells. In keeping with our football analogy, let's think of these regulatory T cells as our offensive coordinator, calling the shots from the sideline. What these regulatory T cells do is prevent the T cells from attacking the body's own tissue. Think of it as an offensive coordinator who tells his lineman not to sack their own quarterback or block their own players. But, when the regulatory T cells (offensive coordinator) fail to control the T cells (offensive linemen) from attacking a body's own tissue, this is what causes autoimmune disease.

I apologize for the "...and that's how a bill becomes a law," type explanation, but I thought it was important to get that information out before mentioning a related study that appeared in the January 21 online edition of Nature. In the study, scientists from the Whitehead and Institute and the Dana-Farber Cancer Institute identified a key set of genes that lie at the core of autoimmune disease. A previous discovery that regulatory T cells are controlled by a master gene regulator called Foxp3 (okay, back to the football analogy. Consider Foxp3 the head coach). Foxp3 is so vital that when it stops functioning, the body can no longer produce working regulatory T cells. As a result, the T cells (linemen) damage organs and tissue, causing symptoms of type 1 diabetes and Chrohn's disease. But, until this study, there had never been a full understanding of how Fox3p controls regulatory T cells because they did not know exactly which genes fell under Foxp3's command.

Using DNA microarray technology to scan the entire genome of T cells and locate the genes under Foxp3's purview, approximately 30 genes were uncovered. One in particular, called Ptpn22, showed an especially strong connection. This was quite a discovery for the scientists, as it had been known that Ptpnn22 is strongly related to type 1 diabetes, lupus, rheumatoid arthritis and Graves' disease. What wasn't known, however, is that Ptpnn22 could be linked to regulatory T cell function.

This discovery is a solid step forward in the effort to understand how Foxp3 enables regulatory T cells to prevent autoimmunity.

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.

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!

Upon losing his wife to type I diabetic complications, Mr. Iacocca and his family began a journey to support innovative diabetes research nationwide. Recognizing that medical research is costly, Mr. Iacocca devoted his efforts to providing the funding necessary to keep the most promising diabetes-research projects moving forward. Twenty-two years and over $23 million later, The Iacocca Foundation has supported amazing scientists and helped advance exciting research.

Without evoking the same deer in headlights reaction I flaunted, I'll provide a brief description of a few projects (due, in part, to the fact I am too simple to understand them all in detail). I welcome you to continue reading the full details of all the research projects from the Iacocca Foundation website. Without further adieu, here are a few details on some projects underway:

The Nathan/Faustman Project is preparing for a Human Clinical Trial to stop the autoimmune attack in type 1 diabetes.

Dr. Jerry Nadler is researching the effects of Lisofylline (LSF), a novel small molecule immunomodulator that has been shown to be effective in halting autoimmune damage to pancreatic insulin producing beta cells.

Dr. Chan's project proposes the use of gene therapy to produce new islet cells.

Without question, the Iacocca Foundation has made it possible for these innovative, promising, and undeniably remarkable projects to see their way to fully-funded fruition. Mr. Iacocca, if you have not heard it before, I will say it now: Thank You. On behalf of the diabetic community, I would like to express our appreciation for your tremendous efforts and the priceless gift of hope.

Today's Scary Statistic: a Denmark study indicates that Type 1 diabetics are more than - get ready - three (!) times more likely than non-diabetics to develop multiple sclerosis.

According to the researchers, there are indications that MS and Type 1 diabetes may be somehow linked within what one might call 'disease families.' Why? Because Type 1 diabetes and MS are both autoimmune diseases, which cause the body to attack its own tissues. In the case of Type 1 diabetes, the body reacts against insulin-producing cells, whereas in the case of MS it attacks the myelin shealth that surrounds neurons in the brain.

Previous studies have indicated a link between Type 1 diabetes and MS, however, this is the first large-scale study to investigate the connection.

See the following Reuters report to learn more. The full results of the study have been published in the latest Archives of Neurology (July 2006).

The Weizmann Institute of Science has posted a description of a new breakthrough discovery by a team of its researchers. The description can be viewed on a page of the Institute's website creatively titled the Weizmann Wonder Wander -- love it!

Basically, the big news is this: researchers have known for a while that a certain protein (HSP60) can fight Type 1 diabetes, and they have been working towards developing a vaccine for Type 1 that incorporates that protein. The Weizmann team had discovered that a peptide (p277) constituting a fragment of the HSP60 protein could shut down the autoimmune response that causes Type 1 diabetes. However, until now no one knew exactly why the protein was effective. Now we know it works like this: the p277 peptide helps regulate potentially harmful T cells. The T cells then secrete anti-inflammatory substances instead of the inflammatory ones they would normally make -- ones related to autoimmune disease. What a fantastic discovery!