The Next Global Epidemic
Type 3 Diabetes is when the brain stops or reduces the acceptance of the brain’s secreted insulin within the brain’s cell receptors. Diabetes type 1 and type 2 derive from the decline of insulin produced within the pancreas to the point where there is no insulin produced. Yet, in recent years, scientists have found that insulin is also produced within the brain. This has led to the recognition of diabetes type 3 in 2005.
Emerging research on the widespread degenerative brain disease known as Alzheimer’s suggests that this prevalent form of dementia is actually a type of diabetes. Published in the Journal of Alzheimer’s Disease, a recent study out of Rhode Island Hospital (RIH) confirms that Alzheimer’s is marked by brain insulin resistance and corresponding inflammation, a condition that some researchers are now referring to as type-3 diabetes.
Type 3 diabetes symptoms includes memory loss, confusion and dementia are the only known symptoms at this point and those symptoms were derived from the newly discovered link to Alzheimers. The diagnosis of type 3 diabetes is done by a functional MRI scan of the brain and often times in older people type 3 diabetes is missed because of the aging process. Our biofeedback devices can detect the early stages of type 3 diabetes before the advanced symptoms becomes debilitating.
During a study done by the Rhode Island Hospital and Brown Medical School, the researchers discovered that the hormone insulin was not only released from the pancreas but from the brain as well. This discovery is how diabetes and Alzheimer became linked. When the brain does not produce enough insulin, the cells begin to die. Alzheimer disease involves hypometabolism and Type 3 diabetes.
Alzheimer disease is probably the most serious disorder facing an aging population and a disease for which mainstream medicine offers no cure, no treatment to halt progression, and almost insignificant symptom control. When things get bad, the answer is to use drugs from the arsenal of powerful antidepressants and antipsychotics to address behavioral and control problems.
Type 3 diabetes is known as a hybrid or binary form of diabetes. A person must first have type 1 or type 2 diabetes to develop type 3 diabetes. Many researchers believe the key to avoid the double dose of diabetes is to maintain a healthy weight. Obesity seems to plan a large role in the double diagnoses and women seem to be hit the hardest by this double diabetes phenomenon.
Our own research show the resemblance of Diabesity and Type 3 Diabetes. Obesity play an important link in Diabetes, Insulin resistance and dementia as well as Alzheimer.
Symptoms of type 3 diabetes includes: Memory loss, confusion and dementia are the only known symptoms at this point and those symptoms were derived from the newly discovered link to Alzheimers. The diagnosis of type 3 diabetes is done by a functional MRI scan of the brain and often times in older people type 3 diabetes is missed because of the aging process. We have utilized Biofeedback devices as a non invasive and accurate screening tools for Type 3 diabetes with reproducible and useful findings.
Just as insulin produced by the pancreas helps regulate blood sugar levels in the body, scientists discovered that the brain also produces insulin of its own, critical in the formation of new memories.
Couple two growing, national epidemics obesity and diabetes with an aging population, and this double threat becomes poised to become a public health concern, experts say. This new global epidemic is reversible and preventable through proper life style modifications. Please review our blog on Diabesity for details.
The role of insulin in the brain and the link between Type 2 diabetes and Alzheimer’s is a multi-faceted one. Studies have shown that diabetics have a 30 to 65 per cent higher risk of developing Alzheimer’s disease. Either the brain is not producing enough insulin, which is crucial for memory formation, like Type 1 or juvenile diabetes, or the brain has become insulin-resistant, like Type 2 diabetes.
In the brain, insulin and insulin receptors are vital to learning and memory, he said. Insulin is a hormone which binds to receptors at synapses, points of communication between the nerve cells in the brain. It is in this tiny gap where cells communicate with one another one nerve cell releases a signal, which is received by another. And insulin, Klein discovered, plays a huge role in brain signalling. Researchers at the medical school discovered that many type 2 diabetics have deposits of a protein in their pancreas which is similar to the protein deposits found in the brain tissue of Alzheimer’s sufferers.
Types of diabetes
Type 1 Diabetes: Juvenile diabetes, a form of diabetes mellitus that is most common in children or at any age.
Type 2 diabetes: Once called adult-onset diabetes (and also known as non-insulin-dependent diabetes mellitus – NIDDM), type 2 diabetes is now also found in young adults and children.
Type 3 Diabetes: Diabesity and Memory loss
Gestational diabetes: that type comes with being pregnant.
Diabetes Mody: MODY is not linked to obesity, and typical MODY patients are young and not necessarily overweight.
Diabetes Lada:Patients with LADA may lack some of the type 2 diabetes symptoms.
Diabetes Insipidus: leads to frequent urination, and this is the most common and clear symptom. Frequent urination, unusual thirst, and dehydration are all symptoms of Diabetes.
Extensive disturbances in brain insulin and insulin-like growth factor (IGF) signaling mechanisms represent early and progressive abnormalities and could account for the majority of molecular, biochemical, and histopathological lesions in Alzheimer.
Treatments & Prevention:
Mainstream medicine treats early to moderate stages of AD with cholinesterase inhibitors (Aricept, Exelon, Razadyne and rarely Cognex). For moderate to severe stages, memantine, a drug that regulates the activity of glutamate, a chemical involved in learning and memory, is frequently employed. According to Herrmann et al in a recent journal article, Currently available treatments for AD are symptomatic and do not decelerate or prevent the progression of the disease.
There is considerable support for this view. Statins, which seem to have been tried for almost every sickness of mankind, are described in a recent Cochrane review as having insufficient evidence to recommend their use in the treatment of dementia.
One recent pharmaceutical approach involves monoclonal antibodies which target beta-amyloid in the brain, in keeping with the long-held but frequently debated view concerning the role of this peptide in the pathophysiology of AD. The drug companies Pfizer and Janssen announced in early August that they were halting the development of the anti-amyloid drug bapineuzumab after a series of negative clinical trial results. Other anti-amyloid strategies have also yielded disappointing results in patients with AD . One example is semagacestat, a drug expected to decrease beta-amyloid build-up. Compared to a placebo, it actually appeared to worsen the disease and increase the risk of skin cancer. The clinical study of this drug was halted in the fall of 2010. In fact, the beta-amyloid hypothesis has dominated AD research for over 3 decades but success of this theory in informing therapy has been disappointing.
Another new approach, which recognizes that insulin problems may play a role, involves intranasal introduction of insulin into the brain. This new approach has shown short term benefits in cognition.
What is interesting is the focus in this research on the connection between insulin and signalling pathways and also beta amyloid insulin competition rather than hypometabolism, mitochondrial dysfunction and the need for an alternative
fuel on a daily basis.
In a recent review in the journal Nutrition, Cunnane et al present a three phase view of the concept. Phase 1 involves the development of brain glucose hypometabolism which leads to Phase 2 where it is postulated with supporting evidence that pathological changes occur in the microvascular system, reactions involving tau protein, brain shrinkage, beta amyloid deposition, mitochondrial dysfunction and regional brain starvation. The end result is Phase 3 where clinical manifestations of AD finally appear. The Phase 2 neuropathology can also aggravate brain hypometabolism, creating a vicious cycle. The authors suggest that this cycle can be effectively broken by sustained improvement in brain metabolism, which can be achieved with ketones which act as replacement fuel for glucose.
Perspective regarding the role of ketones in brain metabolism can be gained by considering that during starvation or very low carbohydrate intake, the liver turns to making ketones which then support cerebral metabolism. This defense mechanism evolved eons ago and was likely necessary for human survival.
Preventing Obesity trough proper life style modification is the first step in dealing with Type 3 diabetes. See www.academyofwellness.com/wellnessIQ for details.
Integrative Medicine approach is the most sensible approach to prevent the spread of type 3 diabetes global epidemic. Reversing diabesity as early as possible is the least cost effective and most logical approach to prevent and treat this growing problem.
Dr. George Grant, I.M.D., Ph.D.
Article Source: GreenMedInfo