February 18, 2009
The link between Alzheimer's and diabetes — and how to stop both
You may have heard of type-1 and type-2 diabetes. But did you know that there may be a type-3 diabetes? Researchers recently confirmed that this new form of diabetes does, in fact, exist. And, more amazingly, this new diabetes may have a direct connection with Alzheimer's disease.
Juvenile (type-1) diabetes is where the pancreas simply doesn't produce any insulin. It's by far the most severe. In adult or type-2 diabetes, your pancreas does make insulin, sometimes even too much. But due to diet, weight, and other factors, your body loses its sensitivity to it. And your blood sugar goes up, damaging your organs. This new type-3 diabetes is similar to type-2, except that the damage is concentrated in your brain.
In Alzheimer's, toxic proteins build up and damage the neurons in your brain. In this study, the researchers took neurons from the brain's memory-learning center, the hippocampus. They treated the cells with insulin. The insulin protected the toxic proteins from attaching to and damaging the cells. Furthermore, they found that they could enhance the effect of low level insulin with the drug rosiglitazone. This drug enhances cellular sensitivity to insulin.
The toxic proteins were really the beta amyloid I've told you about in the past. It builds up in Alzheimer's brains and directly damages neurons. Insulin seems to reduce the places where this toxic protein can bind to and disrupt synapses, the connections between neurons.
Announcing a Pain-Relieving Formula Designed Especially for Aching Knees
Studies show it reduces pain and swelling, increases mobility, and even increases synovial fluid!
Click Here To Learn More
When your cells become insensitive to insulin (type-2 diabetes), the insulin can't protect your cells from these toxins. In the past, I've referred to insulin as the hormone of aging and death. You need it to live. But if your body becomes resistant, your body will make more and more. That's not necessarily good, since too much results in faster aging, heart disease, and possibly cancer. If your body maintains sensitivity to the hormone, you can thrive with less insulin. It's more effective and can do much more.
The authors confirmed this in their conclusion. But, of course, their solution is to use drugs to make your cells more sensitive to insulin. Lead author William L. Klein, a researcher in Northwestern's Cognitive Neurology and Alzheimer's Disease Center said, "Therapeutics designed to increase insulin sensitivity in the brain could provide new avenues for treating Alzheimer's disease."
Currently, there is no cure for Alzheimer's. So if you already have the disease, this type of drug therapy might make sense. The researchers showed this type of therapy might work: "Our results demonstrate that bolstering insulin signaling can protect neurons from harm."
But Big Pharma won't stop there. You can be sure that the drug companies will look for a drug that you can use as prevention. But you don't need a drug to do that. I've told you how to do it with 100% safety. It's completely effective. And, best of all, it's free.
The first step is to eliminate all refined foods. Next, eat a low-fat diet. Fat binds to insulin receptors making them less sensitive. A 10% fat calorie diet, which includes plenty of uncooked living foods, is ideal.
I again recommend the 80-10-10 Diet book. I've seen many cases of stubborn type-2 diabetes. And, I have yet to see even one case not respond to rigid adherence to this diet. Not one single case! Even if you can't do it completely, any movement toward this type of diet will undoubtedly have a positive effect on your insulin sensitivity. And a small improvement in insulin sensitivity is better than none at all. You can order a copy of this book from my publisher at 800-728-2288 or by following this link.
With this advice, you can effectively avoid any type of diabetes. And, just as importantly, you also can avoid Alzheimer's disease.
Yours for better health and medical freedom,
Ref: www.chinaview.cn 2009-02-03.