Meet the Face of Change is a photo exhibit owned by Novo Nordisk featuring YOU -- the face of change. Change for what, I asked? Well, it seems Novo would like to change your opinion of the barriers to insulin treatment for Type 2 diabetics. The common belief of insulin treatment for Type 2 diabetes is that it is the point of no return. Why? First instincts are usually correct.

Studies have shown that Type 2 diabetics injecting insulin create insulin antibodies (IAA). Type 1 diabetics have these antibodies upon diagnosis. Type 1 diabetes was also formerly referred to as insulin-dependent diabetes. Insulin antibodies (IAA) develop and attack the natural insulin produced, resulting in insulin dependence. Type 2 diabetics do not have the same level of IAA. Once they begin injecting insulin that looks like human insulin (the kind Novo makes) - you run the risk of developing IAA. The use of animal-insulins did not cause the development of IAA to the same extent. If you plan to start injecting insulin - ask your doctor if he will check you for IAA. As a Type 2 diabetic, you DO NOT have to become an insulin-dependent diabetic.

I asked Novo to explain what Meet the Face of Change is about. What are they trying to change? The response I received from Nov explains their wishes to strengthen the drive of their business, among other core values. Now I ask you - how do you drive a business that sells insulin? Sell more insulin. For the 16 million Type 2s not yet in this lineup- please consider if insulin-dependent diabetes is the face you want to meet. Don't add insulin to injury. It may not be the path of least resistance, but cut back on simple sugars, increase fiber consumption, and take a walk after dinner. Meet the face of change by putting your best foot forward, not your face on a campaign for vulture capitalism.

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

The Juvenile Diabetes Research Foundation announced that they have formed a partnership with MacroGenics. JDRF is providing up to $2 million to fund a clinical trial of a compound called anti-CD3 that has shown promise in slowing the progression of type 1 diabetes.

Anti-CD3 is capable of reducing the autoimmune attack that destroys insulin-producing beta cells. The treatment preserves beta cell function in newly diagnosed patients, and has the potential to decrease insulin requirements, leading to better glucose regulation, and decrease the complications of diabetes. Anti-CD3 blocks the function of CD3 cells - the T cells that destroy islets. The antibodies prevent "activation" of the T cells after they have identified their target, disarming them launching the attack on islets.

Let's hope the peace talks between JDRF, MacroGenics, anti-CD3 and killer Ts result in progressive measures to make the type 1 diabetic body a peaceful place, once and for all.