How to Cure Diabetes (AODM-2)

How to cure AODM. (Type 2 adult onset diabetes)

By Herb Wiggins, M.D.; Clinical Neurosciences; Discoverer/Creator of the Comparison Process/COMP Theory/Model; 14 Mar. 2014

This is the first of several articles which will show how to potentially “Win a Nobel Prize”. & will be written about 2-3 per month to show creativity at work.

Within a few years AODM will become a far more serious problem because the incidence of it is markedly increasing every generation, possibly due to more person being overweight and lack of exercise, also.

From the American Diabetes Association:

“The diabetes epidemic is taking a devastating physical, emotional and financial toll on millions of people across the nation. Currently, in the U.S. there are nearly 26 million people living with diabetes and another 79 million with prediabetes. The national annual cost of diagnosed diabetes is an estimated $245 billion, representing a 41 percent increase over a five year period.””

See more at: http://www.diabetes.org/newsroom/press-releases/2013/2014-legislative-priorities.html#sthash.EZjvpxuX.dpuf
But there is a very real, potential cure for diabetes coming. It’s very simple, actually, and holds the key to a cure for AODM for most if not all who have it. What has been seen any times and is well documented and scientifically reported, is that when the distal 2/3 of the stomach is removed surgically, or otherwise bypassed or compromised, that within 2-3 months most of those with AODM no longer need medications. Blood sugars in almost all cases return to near normal. This is unexpected to say the least. Even those who get gastric sleeves, which decrease the digestion in the stomach also find their diabetes gone in several weeks. This does not mean the potential for diabetes is gone, but the damaging high blood sugar goes away.

How and why does this occur? No one completely knows, but it’s where the potential for a Nobel Prize in medicine and Physiology must very likely come.

But why does diabetes have such a high incidence in the first place? and the answer might be had from looking at the condition in native Americans in Arizona. Among the Pima Indians on the American side of the border, the incidence is about 85%, one of the highest in the world. It’s known that in most cases the AODM gene is a dominantly inherited gene, which means a person only needs a single gene change to get diabetes, although there may be other factors which influence the expression of the gene, both environmental and genetic.

But why should a gene which can be potentially lethal exist at a high incidence? It’s well known that in thalassemia and sickle cell disease, the diseases exist in an environment with epidemic malaria. And both those conditions provide a modest but significant resistance to malaria in those persons with one, recessive gene. This is an example of genetics which contributes to reducing mortality because it has beneficial effects, too, although it can be very bad to carry both recessive genes.

The same is probably true of AODM. Why it exists is very simple. The brain and rest of the nervous system can only survive if there is blood sugar, glucose, present in high enough quantities to keep the nervous system working and undamaged during famine. In cases of famine, which is also wide spread and endemic, if a person is moderately diabetic, this will spare the person’s nervous system from serious damage, esp. in cases of short term famine.

On the Arizona border area, this is exactly the case. On the American side there are more than adequate food supplies in most case, the person can grow obese with the rich American diet and get diabetes. On the south side, food is much less available and more traditional diets low in sugars and starches, and most importantly calories are found. Thus those south of the border are not as likely to get diabetes. But since they are essentially the same genetics, the food rich north side gets diabetes and the food poor south side does not so much, and they survive better in famines to have children and pass the diabetic gene on to their children, who also are more likely to survive. The border acts as a kind of controlled study comparing diet and obesity to incidence of diabetes type 2.

In the diverse American population, for example there is a typical Caucasian gene for diabetes, tho there are also central Asian, Suomi as well as Magyar forms of the disease exist which are not the same gene as in most of Western Europe in those of not Asian ancestries.

But everyone in all societies in the past 10,000 years has experienced famine and thus the widespread development of the gene in societies, about 30% in most, although it’s not always expressed. Thus the high prevalence of the gene in Eurasian peoples, because the diabetes is, during child-bearing years, rarely expressed. It is expressed at later ages, and thus individuals survive through the child bearing years to have children and pass it to the next generation.

The characteristics of AODM are that there is an insulin resistance in the disease, which is associated with higher insulin levels and occasionally hypoglycemia, which is often an early sign of AODM. In addition, this form of diabetes comes on with aging, usually above 45, with obesity, that is large fat deposits, and in many cases with high starch/sugar intake. In order to explain these findings, then the following hypothesis is likely to be correct.

Clearly, in the case of blood sugar control, the body has many, many mechanisms to raise blood sugar. The liver can create glucose from Muscle use glycogen stores to raise blood sugar. Release of adrenaline and cortisol during stress raises blood sugar also, as well as the obvious, taking glucose/sugar containing foods in liquid form which can raise blood sugar levels within minutes.

But where is the control on insulin levels? When blood sugar goes up too high, insulin levels rise to control that. But where is the control for too high blood insulin? Simply cutting back insulin release by the beta cells in the pancreas does little to cut back the too high insulin levels in the blood. No one knows how insulin levels and activity is controlled. As is so often the case, the absence of something is often an important clue as to what’s going on.

The stomach is a very active hormonal and biosynthetic organ. It makes gastrin, secretin, VIP’s & GIP’s of many types, and intrinsic factor, among others. These are all polypeptides. Because removing the stomach and even the distal 2/3 of it effectively eliminates high blood sugars in those with AODM type 2 within several weeks, that means a substance is being taken away which the stomach creates. Something which can compete with diabetes on insulin receptor(s). And it takes a number of weeks for those receptors to be turned over, recycled and resynthesized, thus eliminating the insulin-like binding polypeptide/protein which is blocking the insulin for control.

Interestingly, AODM is insulin resistance. In other words there is a lot more insulin in the blood than expected and it’s not as effective in acting to reduce blood sugars. This is consistent with an agent produced by the stomach which is blocking insulin on the insulin receptor(s). All too often in AODM one sees hypoglycemia, as a manifestation of this. We also know of ILGF, insulin-like growth factor, which also binds to insulin receptors, so this model has solid support from existing mechanisms.

Thus, we must look for a polypeptide/protein which is insulin-like, which acts as part of a mechanism to control too high insulin levels. Thus completing, at least in part, the other side of the equation in blood sugar control. The insulin receptors must be specifically investigated to find what else besides insulin is binding to them. This will in time show the polypeptide/protein with insulin-like activity/binding which is being synthesized by the stomach.
Simply blocking this factor will abolish the insulin resistance, which will act effectively to cure the AODM.

The surgical approach to curing diabetes is a brute force method full of problems and even can be lethal. Blocking the specific polypeptide cause of AODM is a technical finesse which is far, far safer, simpler and to the point. & by this new knowledge of what it is in the stomach which causes AODM-2, we will gain a great deal more understanding about how insulin works and is regulated, too.

Curing most all AODM with this new knowledge very likely will result in another Nobel Prize in Medicine and Physiology for the person/team who finds the insulin-like agent which causes AODM. And that person(s) will have the distinction of curing/highly controlling a new epidemic in mankind which will undoubtedly become much, much worse over the next generation. For which tens of millions of people will owe a huge debt of gratitude, and a Nobel Prize.

One caveat is that it’s unknown why AODM waits until middle to older age person to present itself. Finding the right polypeptide/protein which becomes more active/binding in those age groups, will be confirming evidence that’s what is going on and what, specifically, the agent or agent family is.

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