Thomas Smith began reviewing scientific literature after conventional medicine failed him in controlling diabetes. Smith found research that shows dietary toxins impair cell membrane function. These toxins include trans fatty acids and refined sugars. Cells begin to have trouble absorbing nutrients, and the blood sugar rises. Over time, this results in chronic elevated blood and urine sugar levels. Sounds like a growing epidemic, doesn't it?

This damage to cell membranes, caused by a poor diet, can be repaired. The diabetic syndrome can be cured by eliminating all processed fats and oils. The protocol calls for supplementing high-dose Omega-3 fatty acids. This protocol normalizes blood sugars because the body is continuously repairing cell membranes by using the fats and oils available in the diet. One caution: the speed of recovery is related to the length of the illness. Some Type 2 diabetics may require up to one year for dramatic reductions in blood sugar.

A gaping hole exists between conventional medicine and diet. Conventional medicine claims that the cause of Type 2 diabetes is unknown. Medical doctors, as practitioners of conventional medicine, are not trained to explain how it happened. They treat symptoms with medicine. The business of medicine is medicine. The business of diabetes would be devasted if the cure was as simple as diet. The explanation Thomas Smith provides in his empirical studies is fascinating and I encourage anybody with competing or supporting evidence to open the debate.

It's free, it covers 70% of the Earth's surface, and it's a remedy for all living things. So why do physicians rarely promote the curative properties of water?

Every plant needs it to survive. Every living thing on Earth requires water - even the cacti of the Sahara Desert. We are no different. Mike Adams, of News Target, was one of the last people to interview the late Dr. Batmanghelidj. The things he learned about "The Healing Power of Water" left him in awe. The conversation revealed which ailments and "diseases" are actually caused by dehydration, why the general population is chronically dehydrated and henceforth labeled diseased, what ingredients deplete the body's water reserves, why thirst is not a reliable indicator of dehydration, the dynamics of cholesterol and how water keeps it in balance, how dehydration impairs mental functioning and potentially causes depression, in addition to recognizing signs that your body is starting to dehydrate.

It's a world of answers to an often overlooked question. The premise of the interview is this one thing: the human body manifests dehydration by producing pain, and pain is a sign of water shortage in the body, and water shortage is actually the background to most of the health problems in our society. If the aforementioned interests you in the least - I strongly encourage you to follow the river of curiosity to its source. Who knows? Maybe we're all dying of thirst.

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!

Did anybody catch the first ever YouTube democratic debate last week? It was cosponsored by CNN and the cool thing about it was this: all the questions came in from Americans like you and me. Turns out two of the candidates spoke out on behalf of diabetes. Here's what they had to say...

Governor Richardson mentioned the fact that 33% of Medicare is wrapped up in diabetes costs. He suggests, "Let's have major prevention programs, and also ways that we can ensure that we find a cure." He still has not announced a plan to ensure a cure. But if he does - I'm willing to bet all of his campaign funding from Big Pharma might mysteriously disappear.

The other candidate addressing diabetes was Senator Chris Dodd of Connecticut. Dodd's promise came after from a woman's question about stem cell research. Somehow the senator was able to plug an endeavor to "deal with diabetes". However, much like Governor Richardson - he has yet to announce a plan to cure. Politics as usual. Stay tuned for the LIVE Republican Debate on September 17th.

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.

Diabetes is making a name for itself and it's spreading like wildfire. Politicians are uniting to build a $120 million campaign to educate diabetics to prevent the spread of the disease and its complications.

Senator Clinton criticizes the reaction to the problem, rather than taking measures to prevent it from occurring. She questions why current money is unquestionably $pent on treating complications from diabetes -- such as amputations and dialysis. Good point, Senator. Ask Bush if he's got any friends up at Eli Lilly. A good answer can always be found in a temporary restraining order. She and fellow politicians propose more money be spent on programs for weight-loss, nutrition education and other preventive efforts to best curtail the growing number of diabetics in the United States.

The legislation proposed would provide $90 million to the Centers for Disease Control and Prevention's Division of Diabetes Translation for diabetes surveillance, research and educational activities. It would also allot $30 million for three four-year projects that would examine how best to translate diet and exercise interventions into effective clinical practice.

If you read a warning label on your insulin that said - may decrease the amount of insulin you produce - would you think twice about injecting?

Any foreign matter that enters the body can stimulate antibody production. Foreign insulin, especially genetically modified human insulin (GM insulin), is no exception to the rule. More importantly, in relation to its increasingly exclusive dominance in the USA [since 1983], are the types of antibodies created by GM insulin. They could be similar to the types of antibodies that cause type 1 diabetes - also known as insulin-dependent diabetes.

Insulin auto-antibodies (IA-A) and c-peptide measurements can help you tell if your injected GM insulin is stimulating 'anti-your-own-body' cells. This response is often referred to as an auto-immune or inflammatory disease. This is because IA-A can trigger inflammation and an attack by specific immune system cells. For example IA-A can attract a targeted attack on your beta bells (the cells naturally producing your own insulin and c-peptide) by exciting your seek and destroy cells (aka the the IA-A militia).

Research has found that GM insulin can stimulate approximately 60% more IA-A than porcine (pig) insulin. Also because GM insulin is more identical to human insulin, than porcine insulin, GM IA-A are probably more efficient than porcine IA-A, at duplicating the effects of natural human I-IA. Type 1 or type 2 diabetes can be considered an inflammatory disease when the beta cells become an inflamed 'war zone' resulting from IA-A helping to target natural insulin at its production site.

If you are a type 2 diabetic injecting GM insulin - please strongly encourage your doctor to continue measuring your c-peptide level regularly (and make sure you find out what your c-peptide is before you start injecting!). Once your c-peptide level begins dropping to normal or low - suggest pumping the brakes on your GM insulin regimen. Research suggests that prevalence of IA-A is related to duration of insulin therapy, so BEWARE, you could be headed toward GM insulin-dependent (type 1) diabetes

Diamyd showed promising results in slowing the attack on remaining islets in recently diagnosed type 1 diabetics. Diamyd is a therapy specifically designed to preserve residual beta cells in recently diagnosed type 1-diabetes.

The results from the Diamyd study demonstrated 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 levels. These results were present 15 months after the first treatment. Insulin and C-peptide are produced in equal amounts. As C-peptide is easier to measure, meal stimulated C-peptide levels is the most important parameter to follow in a type 1-diabetes study where the aim is to preserve beta cell function. C-peptide levels in both groups experienced a decline but the decline was significantly reduced in the Diamyd group. There were no significant differences in fasting C-peptide levels between the two groups.

There was no difference in HbA1c levels between the Diamyd group and the placebo group. This is consistent with type 1-diabetes patients striving to reach normal blood glucose levels through their standard insulin treatments. There was a tendency of increased GAD antibody levels in the Diamyd group, indicating that the drug candidate has an immunomodulating effect. Diamyd treated patients with disease duration of less than 3 months showed improved C-peptide levels at 15 months, whereas placebo treated patients showed a decline.

These results provide strong support that the administration of Diamyd is effective in preserving islet cell function in type 1-diabetes patients. Additionally, maintenance of endogenous insulin production is important as it helps patients to better control their disease and reduce long-term complications. There were no serious adverse events reported that were related to the Diamyd treatment.

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.

Islet transplantation has become an enticing answer for a better Band-Aid in treating diabetes, both type 1 and 2. In type 1 diabetes the problem is the destruction of islets. About 15% of those with type 2 diabetes have the same problem of islet destruction, just as in type 1 diabetes. The age old problem with all transplanted cells is the recipient's immunity rejecting them as foreign bodies. Look no further than the ocean blue for a promising resolution.

Cerco Medical is developing a better Band-Aid to treat diabetes with a seaweed encapsulation technology. Their method uses a thin-sheet of encapsulated islets that is surgically attached to the liver. The sheet of islets is thinly coated with kelp to prevent immune rejection, and allow the islets to release insulin without allowing T-cells to enter and destroy the islets. This is a promising technique to potentially restore normal blood sugar control in diabetes.

Of course, the biomedical industry is quickly becoming the next dot-com. So the islet shortage is not a concern. With the advent of remarkable technologies, we can conceivably generate our own islets without having to sacrifice fetuses, wait for islet donors to die, or slaughter Billy Bob's best porker. The future of the better Band-Aid is closer than we think!