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.

I'm outraged at the coverage CNN provided on diabulemia. They accuse diabetics who suffer with the condition of doing the wrong thing. CNN neglected to address the cause of diabulemia. The drug all insulin dependent diabetics must use is a synthetic hormone that has been genetically modified. It is nothing like human insulin or any natural vertebrate insulin, for that matter.

The fact that 1 in 3 diabetics choose to take less insulin is not because they wish to eat more food. It is a reaction provoked by an inadequate and dangerous genetically modified drug. The reason a diabetic would take less insulin is to avoid experiencing the unnatural side effects the insulin is causing. CNN sensationalized diabulemia and put a damaging veneer on the victims without fully researching the facts. Genetically modified insulin does not penetrate the blood-brain barrier like natural human insulin. Genetically modified insulin distorts hormone responses to hunger. Genetically modified insulin does not protect diabetics from entering ketoacidosis when their blood sugar becomes too high. An inadequate drug causes diabulemia. Accuse the drug manufacturers of making the wrong choice. Or is that biting the hand that feeds you?

Make it right, CNN. Mass media should be the defenders of righteousness, not the accomplices to Big Pharma. Do a study comparing human insulin (natural vertebrate insulin) and genetically modified insulin. The comparison should include: penetration zones of the body, hormonal reactions stimulating and suppressing hunger, amino acids, c-peptide, lipophilic and hydrophilic nature, and pH values. The difference in natural human insulin and Lantus pH is remarkable: 7.5 to 4.0. How similar is that? CNN you've slipped on the peel and missed the facts. Now perform your due diligence to help make it right. I ask every insulin dependent diabetic to email CNN and ask them to put the facts on the line. Link to this blog so they have an idea of where to start. Thank you!

I contacted Novo Nordisk back in March to tell them about the remarkable effects C-peptide had on reversing complications of Type 1 diabetes. I asked if they would bring the drug to market. A mass of excitement overwhelmed me when I learned about C-peptide missing from insulin all these years. The response from Novo? No thanks, it's not one of our targets. Targets, eh?

C-peptide is a byproduct of the production of insulin. In Type 1 diabetics, the level of C-peptide eventually becomes undetectable due to the body not making any insulin of its own. Long-term complications of diabetes frequently develop despite insulin therapy and optimal blood glucose control. C-peptide could quite possibly be the missing link in perfect diabetes control. I sent the following document to Novo Nordisk and asked them to make C-peptide available to reverse and ameliorate renal and nerve dysfunction for Type 1 diabetics. Read the document and see for yourself the eye-popping beneficial results C-peptide offers Type 1 diabetics. I received it directly from Dr. Wahren, lead researcher for C-peptide.

After 5 months consideration, Novo called me back. They said C-peptide is not a target for their company. I understand and now Levemir is not a target in my diabetes control, either. For all the Type 1 diabetics out there controlling your sugars with insulin not really made with you in mind -- do you understand why Novo does not wish to develop this critically important treatment? I guess insulin is good enough, right? Wrong. It's a tough job but somebody's got to do it. Just not Novo. When you are in the business of diabusiness -- no thank you says so much about what could potentially hurt your business.

Hear ye! Hear ye! I have an announcement to make. About 3 months ago, a committee formed to explore the possibility of creating a new conference series for adults with type 1 diabetes. Most conferences are currently geared towards all types of diabetes, but a group of us felt there should be more for the unique challenges that are posed to adults living with type 1.

With that in mind, we are conducting an interest study for the conference. Who would you like to see at the conference? Tell us what is missing from Type 1 diabetes (besides the obvious **cure**). This will help us with programming, as well as securing sponsorships for the event. Besides giving you all you want from the latest and greatest in type 1 diabetes - you have a chance to leave your mark on this revolutionary event. At the end of the survey, there is a question about creating a name for the conference. The committee will choose the winning name. The winner will receive an autographed copy of Know Your Numbers, by Amy Tenderich and Dr. Richard Jackson. The second and third places prizes are a Six Until Me mug and a Diabetes Mine mug, donated by Kerri Morrone and Amy Tenderich.

The survey closes on Friday, September 7, 2007 so don't miss your opportunity to voice your opinion. Take the survey today!!

The scientific community has been in a heated debate about xenotransplants (transplanting pig islets into humans). Although the procedures are showing to be effective - is the insulin secretion entirely pig? Some experts surmise that after the transplants, diabetic patients are actually able to produce some insulin on their own, after all.

The latest press release from Tissera, Inc (an Israeli-based company) made a statement that raises my hopes. It was, "By the fourth month after transplantation, the insulin dose needed to maintain near-normal blood sugar levels decreased by more than 90% in comparison with the insulin dose needed before transplantation, meaning that endogenous insulin production was predominantly responsible for blood sugar control."

The question of the origin of endogenous insulin was addressed by measurement of blood C-peptide. C-peptide splits from insulin and indicates the level of insulin secretion from the patient. C-peptide levels were measured both at baseline and in response to a sugar load, which brings about a rise in blood C-peptide. The measured C-peptide was shown to be predominantly of pig origin. So herein lies my question: is predominantly more than 50%? A type 1 diabetic has undetectable levels of C-peptide. Period. After the xenotransplant the C-peptide level is all of a sudden detectable? Could these islet transplants assist in regenerating the diabetics' own islets?

Imagine taking insulin was as easy as applying skin cream. Guess what - it's not so far fetched an idea, thanks to Phosphagenics and it may be coming soon!

Phosphagenics' has patented a transdermal carrier technology (TPM) that rapidly transports insulin across the skin without disrupting or damaging its surface. The company has recently announced successful results from clinical trials in Australia. This confirmes the TPM technology is safe and effective at delivering insulin into the bloodstream, without adverse events. The trial showed that the insulin safely penetrated through the human skin and delivered insulin into the bloodstream over a sustained period of time. Could this be the next generation of basal insulin? Adios Lantus. Arrivederci Levemir! Almost -- TPM/Insulin, applied topically, delivered insulin through the skin and into the bloodstream for up to 8 hours. So like sunblock -- you'll probably have to reapply.

Weep not, fellow Americans. Although Phosphagenics is based in Australia, they are in the process of applying for Phase 2 clinical trials in the U.S. Big ups to the Muffin Man for keeping me abreast of his leading-edge news from the diabetes-friendly forefront!

A little over 2 weeks ago I posted something about diabulemia on site where diabetics exchange their feelings, frustrations, and experiences with the disease. Two Type 1 diabetic women took the time to write me a very thoughtful hate mail. Hate is a strong word but these are some strong accusations. For starters, they said, "There ain't no such word as diabulemia. It's called diabetic stupidity." That is cut directly from the email, and as you can see - it was written with an arrogant disregard for the 450,000 people suffering from this serious condition.

I understand strong words come from passion. An email with the subject title "There's type 1, and then there are fools with type 1" could only have been composed with hateful passion. Within the passionate lines of this email were statements like "Insulin shock therapy was used in mental institutions (where you belong)." Not exactly nice words to come from a teacher - but again, the words were incensed with passion. Good, bad or ugly - feedback is terribly important to me because it conveys what matters to you. Knowing is half the battle.

By logging my experiences with diabetes on the web, these hate mailers refer to me as "You fool" for exercising my Freedom of Speech (First Amendment). To this I add -- thank goodness for the Freedom of Information Act. If I'm a Fool for sharing my experience with overcoming diabulemia and trying to lend consoling advice to others struggling with it - I'm a damn proud Fool! Hate on, haters!

What is the purpose of body fat? We all have it, some of us a little more than others. As we grow older, some of our diets fall out of balance with our energy needs causing our white fat cells to become swollen.

White fat cells secrete leptin, adiponectin and resistin. Leptin and adiponectin work together in suppressing appetite. Resistin is the newest discovered - and has been found to participate in the inflammatory response and resistence to insulin. It also triggers an immune response to irritation, so it may be the fat cells attempt to shut your piehole because we're not gonna take it. As the white fat cells take on excessive calories they begin swelling, resulting in an inflammatory response.

Inflammation, by definition, is a protective attempt to remove the injurious stimuli (excess calories) and initiate the healing process. As the fat cells dispatch hormones signaling inflammation - one could hypothesize that Type 2 diabetes is a response to an imbalanced diet - calories in versus calories out. So what do our white fat cells do for us? They are designed to store energy for use in times of need. When your body is sending out DEFCON signals of inflammation - I'd say that is a time of need, indeed. Would inducing ketosis till the swelling goes down help?

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.

Today I compose an ode in remembrance for our islets of Langerhan. Their job is far more complex than balancing blood sugar. They balance everything in our metabolism, starting with the hormones that tell us to eat or stop eating. The islets of Langerhan house 4 critical cell groups: beta cells, alpha cells, delta cells, and gamma cells - also referred to as the PP cells and D1 cells.

Beta cells are activated by a rise in glucose which results in secreting insulin. As this insulin lowers the blood glucose, amylin is also released. Amylin supports the stability of blood glucose levels by slowing the rate that digested glucose enters the bloodstream. The alpha cells are the opposite - they are responsible for preventing hypoglycemia by secreting glucagon. Glucagon helps maintain the level of glucose by causing the liver to release stored glucose. Delta cells secrete somatostatin, which is like the hold button of the alpha-beta cell connection, restraining the release of insulin and glucagon. The last of our Langerhan lineup, and seemingly the least understood, is the gamma cells, PP and D1. These cells affect appetite through the secretion of ghrelin or leptin. Ghrelin is a stimulant for appetite and feeding. Leptin is a hormone that suppresses appetite and speeds up metabolism.

To recap Team Langerhan: beta cells respond to rising blood glucose with insulin, alpha cells respond to falling blood glucose with glucagon. Delta cells respond to perfect balance in blood glucose by suppressing insulin and glucagon, and the gamma cells keep an appetite on an even keel with ghrelin and leptin. If the initial blood glucose lowering medicine prescribed affects any one of these hormones (as you can see it does) - it is definitely causing an imbalance in metabolism. As we memorialize the islets of Langerhan- let us consider all they have done for us. Pay tribute to your islets of Langerhan by doing all that is naturally possible to restore metabolic balance in the future. I have a few ideas - but your job today is complete. You are enlightened. Please have a happy and safe Memorial Day!

For more the more than 300,000 users that once relied on animal-derived insulin, the final chapter of animal insulin is finally ending for the US market. In December 2007, Novo Nordisk has officially decided to discontinue making animal-insulin. Their explanation doesn't go into great detail why they chose to discontinue it. But the supporting evidence they use to warrant the decision is a little weak.

Novo says, animal insulin is derived from the pancreas of slaughtered animals. This statement is as true as the statement "human insulin is derived from the pancreas of slaughtered humans". Novo continues, since that time there has been significant improvement of insulin quality and formulation. Absolutely true! In fact, a Novo pork product was shown to be greater than 99% pure, while an Eli Lilly human insulin only exceeded the 97 percentile. As a consequence, demand for these old animal insulins has declined by as much 20% in the last year to a point where approximately 2% of all insulin users are currently using these products. Largely due to the fact doctor's were advising their patients they must prepare to switch to GM insulin because animal-derived insulin would be nearly impossible to obtain. True. The research that introduced GM insulin (back in the 80s) was preemptive, at best. The claims supporting it was better than the existing insulin choices was clearly debatable .A telling similarity to the discovery about Avandia.

The long-term results of GM insulin and its analogs would prove to be a nightmare if the right questions were asked, and the data properly collected. Is it fair for any of the companies to ask us to change from an insulin product we have grown to love? No, but much like the off-Broadway play suggests: We love you (as a customer). Your diabetes is perfect (for our bottom line). Now change your insulin (we don't feel like making that kind anymore). Too bad type 1 diabetics forced to change to GM insulin didn't have the outspoken advocates like those taking Avandia.

The discovery of insulin, in 1922, was a breakthrough in the treatment of diabetes and it produced a remarkable increase in the life expectancy of diabetic patients. Animal-derived insulins have been used to treat people with diabetes since insulin was first discovered and continuously subjected to various purification technologies. In 1973, Novo produced a purer type of insulin, called monocomponent insulin. This set a new standard in purity. In 1982, Human Monocomponent was the world's first insulin preparation identical to human insulin. It was actually pig insulin, modified by enzymes, to appear identical to human insulin.

When Novo tried to introduce monocomponent insulin into the USA, Lilly fought back with 'human' Humulin insulin. Before Humulin insulin became available, insulin had been produced from animal sources, pigs and cows. It is believed by some that the animal insulin provided the diabetic with better awareness of hypos, and it is certainly true that the long-acting animal insulin such as Ultralente are longer-acting than their 'human' equivalents. The fact that both pig and cow differ from human insulin by certain amino acids (1 in pig and 3 in cow) has lead the majority of physicians to recommend 'human' insulin. 'Animal' insulin became increasingly hard to find, particularly in the USA (see This Little Piggy Left the Market).

In the late 1990s Eli Lilly developed Lispro, brand name Humalog. This was approved for prescription use in the UK and the US by 1996. This insulin has a shorter activity curve than Regular. This means it can be injected closer to the meal time, even after it. Studies have shown that it does not improve control as measured by long-term indicators (Hba1c), but that it does decrease the number of hypos. Glargine, brand name Lantus, was approved for use in the US in 2004. It has become widely touted as better than other long-acting insulins because it has a plateau effect on glucose control that lasts for approximately 24 hours. Some people find it acts a little shorter (and some doctors don't believe that's possible!) So there you have it - the short and sweet version of the history of insulin. I strongly suggest anyone who wishes to fill the spaces between the discovery in 1922 and present day to pickup The Discovery of Insulin (Michael Bliss). I welcome all comments to fill-in the pivotal details I've failed to include.

Mad Money is a stock show on CNBC hosted by Jim Cramer - a well-known iron fist on Wall Street. He has a following of stock enthusiasts who regard his recommendations (buy or sell) as gospel. Why is he so good at what he does? He just wants to help you make money.

And to this end -- the reason I bring Cramer's passionate drive to The Diabetes Blog is simple: last week he called Novo Nordisk as a SELL. Cramer said he's beginning to worry about a backlash on drug stocks. He advised that viewers should not be greedy and should take gains in Novo Nordisk (NVO).

Perhaps the NY Times article raised some eyebrows at Big Pharma. It appears doctors are receiving handsome gifts and stipends for handing out samples of drugs that were not all that safe for most patients. The payments give physicians an incentive to prescribe the medicines at levels that might increase patients' risks of heart attacks or strokes. In light of this blood curdling synopsis Novo got a dishonorable mention. Novo Nordisk professes to operate their company in two parts: biopharmaceuticals and Diabetes Care. The Diabetes Care segment provides insulin analogues, human insulin and insulin-related products, and oral antidiabetic drugs.

The cross examination of the C-peptide disappearing act and mysterious insulin auto-antibodies appearing where they shouldn't is just getting started. Thanks for making them sweat, Cramer!

Like a student driver -- the function of proinsulin (c-peptide) is as critically important as driver's education. The research was done, but because the information highway was just picking up speed (at the time back in '88) dissemination of such research was difficult, at best. Never fear - I found a good study to start things rolling.

Proinsulin (c-peptide) is made along with insulin in a 1 to 1 ratio from the beta cells. After a dose of proinsulin was administered - it took 5 to 10 minutes longer to lower a patient's blood sugar in comparison to insulin, alone. The rise of blood sugar following the lowest point was much slower, as well. In lay terms this means that insulin, coupled with proinsulin (c-peptide), results in a more controlled reaction. Kind of like the teenager with his permit to drive and Dad riding shotgun. The permit gives the kid the right to drive the car, but Dad is telling the kid when to accelerate and when to slow down. Insulin and proinsulin are quite similar in nature except we're talking about a life threatening hormone without the parental guidance.

The antilipolytic effect of proinsulin (tapping fat cells for energy and ANTI means this is stopped) was significantly stronger in comparison to insulin alone. Human proinsulin has a stronger effect on prevention of fat burning for energy in the absence of insulin (ketoacidosis). This seems logical because if you metabolize the glucose in your blood for energy - you will have little (if any) residual glucose to store as fat. Type 2 diabetics have a plethora of c-peptide in their body upon diagnosis but their blood sugar is also high. Looks like insulin and proinsulin reduces the risk of ketoacidosis and regulates fat metabolism.

Why did they decide to manufacture human synthetic insulin without it again? A personal experience pumping piggy proinsulin for 2 days now and I've seen definite control in my blood sugar fluctuations - less than 20 mg/dL in any testing window. It feels like the newly introduced highly purified porcine proinsulin came with a built-in continuous glucose monitor (i.e., C-peptide). More to come...

As a diabetic with the esteemed honor of pouring my heart and soul out for an audience as well-informed as you - I feel it is OUR job to inform our doctor's of the important discoveries being made in diabetes. The discovery I am most concerned with these days is raising awareness of C-peptide.

When I learned that all forms of synthetic human insulin these days DO NOT have C-peptide (like natural human insulin does) I asked my doctor what C-peptide does. My doctor explained, "C-peptide is nothing more than a biomarker to tell us [doctors] how much insulin your body is naturally producing."

When Chrissie in Belgium asked her doctor he told her that [C-peptide] has absolutely no importance. Uh oh...

Doctor's are convinced that C-peptide is useless for type 1 diabetics. Give the next paragraph consideration and you and your doctor might have a new perspective on the importance of C-peptide.

In a healthy, nondiabetic individual -- islets produce insulin. Insulin is made of 51 amino acids in 2 chains, with a tail of something called C-peptide (connecting peptide). Insulin grabs sugar from the blood and transports it into the cells where it becomes energy. It gets into and out of the cells through cellular pathways that are monitored by a delicate balance of sodium (Na) and potassium (K). This balance is regulated by C-peptide. The movement of insulin and glucose through these cellular membranes without C-peptide is dangerous and causes diabetic complications that develop in small vessesls of the eyes, kidneys and nerves.

Tight control of diabetes results in complications over time. If you find 500 mg of protein in a 24 hour urine collection - it's a complication (nephropathy). If your nerve conduction velocity reaction time is measured at 5.0 seconds - it's a complication (neuropathy). You take your insulin -- these complications should not occur, right? The reason for diabetic complications may not be your insulin at all. It may be the thing that your insulin is lacking.

So here's a little community service we ALL can do to enlighten our doctor's. Ask your doctor about C-peptide. Chances are you will get the same answer Chrissie in Belgium and I did. When this happens - smile, and politely hand your doctor a printout of this blog.

After all, if the Creator put receptors in our cellular membranes - He must've done it for a reason. The path to enlightenment is paved with gold.