Far from being inert and unchanging, a mere scaffolding to which the body's muscles and organs attach themselves, bones change constantly. Old bone cells die. New ones are born. But that's not all. According to an exciting new discovery, bones play a role in regulating blood sugar levels and fat deposits.

How is this possible? Bones act like a kind of endocrine organ, releasing osteocalcin, a hormone that influences bone formation. This hormone also increases both insulin production and the body's insulin sensitivity. It also reduces fat stores. Basically, osteocalcin levels in the bones are linked to blood sugar and body fat levels, and there is some sort of interaction back and forth.

It's a surprising finding for the uninitiated. However, some scientists are saying it makes sense when you think about it. Says Ronald Kahn, director of Harvard's Joslin Diabetes Center, "Obviously there does need to be some coordination between skeletal growth and body mass. If you carry around extra weight, your bones need to hold up under the extra pressure, so it's not surprising that your bones have a sense of body fat."

I was excited to see my friend, Lissa Coffey, appearing on The Today Show this morning. Lissa is a PhD, a relationship expert and sociologist. Lissa shares her ancient wisdom and modern style through her site, Coffey Talk, and her newsletters. A recent newsletter addressed homeopathic medicine and I share with you how this applies to the treatment of diabetes.

Homeopathic medicine is a natural pharmaceutical science developed in the early 1800s. It uses small doses of natural substances (animal, vegetable, and mineral) to stimulate the body's own defenses. Homeopathy is a word derived from the Greek words for similar and disease. It is medicine based on the law of similars that says a substance will help to heal symptoms similar to those that it is known to cause. This is the same principle behind immunization.

When I received Lissa's newsletter on homeopathic medicine immediately I thought of how this applies to diabetes - a disease of insulin antibodies attacking the naturally produced insulin in the body. Why would you treat a disease with the exact hormone that caused it? Novo, Lilly, Aventis - you are all making a grave mistake in forcing American's to use GM human insulin, both Type 1 and Type 2. The extinction of porcine and bovine insulin has consequently proven to be detrimental to diabetics over the last 25 years. Studies show tighter control - yet complications on the rise. How do you explain this? I'm not excited for what the future holds, unless we see a return of these similar but not exact insulin forms.

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!

A report published in Diabetes Care says C-peptide improves sensory nerve function in type 1 diabetic patients with early-stage diabetic neuropathy. Thanks to Scott Strumello's comment, earlier today, I couldn't help but query the world wide web for more information on this C-peptide revelation. If I forget to mention it - thanks a million, Scott!

C-peptide was shown to be a significant factor in the maintenance of microvascular function. In a 6 month study of type 1 diabetes patients receiving replacement C-peptide, their nerve functions improved remarkably. A randomized study of 139 patients received one of 3 daily treatments: 1.5 mg of C-peptide, 4.5 mg of C-peptide, or placebo. At the beginning of the study, the sensory and motor nerve conduction velocities were significantly reduced compared with normal. After 6 months of treatment, peak sensory nerve conduction velocities improved in the groups treated with low-dose or high-dose C-peptide, but not significantly compared with the control group. The study showed a significant advantage in nerve functions for those treated with C-peptide (37%) verses those in the control group (19%). Overall, there were no adverse drug reactions reported from treatment of C-peptide.

At this time, there is strong evidence supporting the belief that C-peptide may be beneficial not only for nerve function, but also for the treatment and prevention of other long-term complications caused by type 1 diabetes such as nephropathy and perhaps retinopathy. Phase II clinical studies are ongoing at this time to demonstrate the safety and efficacy of C-peptide replacement therapy for the treatment of diabetic peripheral neuropathy. I can hear the trumpets playing already. I'll be right there with pen-in-hand ready to sign the dotted line for such a study. Thank you, Scott and thank you, Creative Peptides.

According to scientists at Washington University School of Medicine in St. Louis, interrupting nerve signals to the liver can prevent diabetes and hypertension in mice.

Mice were treated to become diabetic with glucocorticoids, a class of steroid hormones characterized by an ability to bind with the cortisol receptor. Once diabetes was established, the researchers surgically removed the vagus nerve. The vagus nerve is the only nerve that starts in the brainstem and extends all the way down to the abdomen. More impressive is the fact that once the nerve was removed from the diabetic mice, insulin resistance and high blood pressure was prevented or reversed. This is an interesting discovery because people with asthma, arthritis, and organ transplants often rely on steroid treatments. It just so happens that many of them go on to develop insulin resistance.

Don't go ripping your vagus nerve out just yet. A fun fact about the vagus nerve is that it's name is taken from the Latin word meaning "wanderer". The vagal nerve pathway can influence seizures, depression and other disorders. Although the research is thoroughly enlightening, it is still very green. Hang on to your vagus nerve while the research continues.

Cancer researchers are exploring possible links between diabetes and breast cancer. In an article just published in Breast Cancer Research and Treatment, researchers describe how they identified such a link: diabetic women are more likely than non-diabetics to have had breast cancer. That is, at least according to the results of their study, which found that of 82,000 diabetic women and 400,000 non-diabetic women, the diabetics were thirteen percent more likely to have had breast cancer.

The mystery is why this might be. Possible factors that need to be examined include diet and lifestyle, body weight, and reproductive factors. The role of hormones is also considered important. In particular, it has been thought that estrogen levels may play a role. With the identification of diabetes as a factor, however, attention is now shifting to the possible role that insulin plays in all this.