Nutrigenetics is the study of the interaction of genes and diet. The Diet Channel has published an article explaining what nutrigenetics is and how it will revolutionize the world of diabetes.

Researchers believe elevated blood sugar can be mapped back to a genetic reaction. Drugs are only overriding the cause of elevated blood sugar and forcing the sugar into the cells, causing damage over time. Nutrigenetics is addressing the cause of the elevated blood sugar and may suggest a better diet to control your diabetes. Genes control how you metabolize certain vitamins, minerals, and nutrients. These genes can vary from one individual to the next. See what happens to Buddy the Elf when he consumes way too much coffee? Yes, I know - that's Hollywood. Nevertheless - a comical example of what nutrigenetics explores.

Consumer-friendly tests are available for these gene and diet interactions. The tests are done with a cheek swab. You send your swab off to a specialized lab, which analyzes DNA from the cheek cells. You receive a report identifying your gene variations. A qualified health professional can explain the test results, and make specific diet and supplement recommendations to optimize your health. If this is a test you're interested in taking, Sciona's Mycellf Program will be happy to prepare your profile. Open up and say Ahhhh.

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!

Off-label use is the practice of prescribing drugs for a purpose outside the scope of the drug's approved label. The FDA requires numerous clinical trials to prove a drug's safety and efficacy in treating a specific symptom. Once deemed safe and effective, physicians exercise discretion for the use of the drug. It is entirely legal in the United States and in many other countries to use drugs off-label.

More physicians are discovering that many drugs are effective for off-label uses and apply to the needs of their patients. Off-label prescription drugs have become so popular that, today, 1 out of every 4 prescriptions written is off-label. The antiseizure drug gabapentin (Neurontin) is used off-label to treat people with diabetic neuropathy. Another drug used off-label is Lucentis, manufactured by Genentech. It was originally approved for age related macular degeneration, but is now in FDA trials for the treatment of diabetic macular edema. If Lucentis is approved, it would be the first drug to treat this debilitating complication of diabetes.

There are advantages and disadvantages to off-label uses. First (and foremost) is the risk versus reward. You could be the first to experience a breakthrough treatment or you could suffer irreparable consequences from the off-label use. Another consideration is feasibility - often times an off-label treatment may cost you substantially more than the other treatments approved for use. For example, without enrolling in an FDA trial to receive intravitreal injections of Lucentis - it would cost me $2,000 a pop. My peepers are precious, but my pockets aren't that deep! What off-label drug would you consider for use?(With your doctor's blessing, of course).

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?

Scientists have mapped the genes responsible for causing type 2 diabetes. This new research is giving hope to new tests that can predict an individuals risk for developing the disease and future treatments.

The study compared the genetic make-up of 700 people with type 2 diabetes and a family history of the condition, with 700 diabetes-free people. Four points on the gene map linked to a person's diabetes risk and were confirmed with another group of 5,000 type 2 diabetics. The findings of this research could explain up to 70% of the genetics related to developing diabetes. A particular zinc transporter, known as SLC30A8, which regulates insulin secretion, was shown to have a mutation. Researchers feel they may be able to treat some cases of diabetes by correcting this mutation.

These findings will allow for the creation of a genetic test to predict people's risk of developing type 2 diabetes, as well as better treatments for the presiding cause of their diabetes. Nary a day passes that I am not motivated for the future of all diabetics. This is the type of research that strengthens my faith in the coming of a cure. Identify the nature of the problem and nip it in the bud.

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.

Genetics affects diabetes risk...but lifestyle is still the most important factor at play. That's the conclusion of a new study, which showed that a certain gene variant gives people a substantially increased risk for developing Type 2 - an eighty percent higher risk, in fact.

But before you throw up your hands and say "I can't fight Mother Nature," bear this in mind: the researcher also said that a healthy lifestyle is enough to pretty much cancel out that genetic risk. In essence, lifestyle trumps genetics, says study author Dr. Jose C. Florez, from Massachusetts General Hospital and Harvard Medical School. And the lifestyle changes required are nothing too major: just losing a little weight and exgaging in moderate daily exercise is enough to do the trick. "Environment can overcome the genetics you have received," says Florez.

The gene in question is known as TCF7L2 and had been identified with Type 2 diabetes by a previous study. This latest study aimed to see if variants in the gene could be usued to predict who would have Type 2 diabetes. Health information was gathered for nearly 3,500 people and, for those people, the researchers gathered genetic information along with a check on insulin secretion and sensitivity. This was repeated one year later. This data was used to calculate risk in each participant.