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Thursday, 15 December 2016

ADA Sweet Money. Would They Stop Diabetes? December 14, 2016

Research Programs Grant Portfolio

Since the American Diabetes Association started its Research Programs in 1952, it has invested more than $735 million in more than 4,500 diabetes research projects. In 2015 alone, the Association made more than $31 million available to support 354 new and continuing research projects at 145 leading research institutions.
As it was said in very famous movie with great money come great responsibility.  What ADA studied and in what projects they invested? Interesting question. Let us take a look at inside what is claim as its aim and on what we do have hope.
Pathway to Stop Diabetes is a bold, innovative initiative designed to radically transform diabetes research. Our Vision is simple yet revolutionary: find a new generation of brilliant scientists at the peak of their creativity, and provide them with freedom, autonomy, and the financial and professional resources to set them on the road to breakthrough discoveries.
WOW! I did think that they are looking to the Pathway how prevent us, diabetics type 2 from suffering and timeless death. I was wrong. They are looking in other direction. Who is top of FDA? Third generation of medical care, doctors. Right according to the

The Hippocratic Oath

To hold him who taught me this art equally dear to me as my parents, to be a partner in life with him, and to fulfill his needs when required; to look upon his offspring as equals to my own siblings, and to teach them this art, if they shall wish to learn it, without fee or contract; and that by the set rules, lectures, and every other mode of instruction, I will impart a knowledge of the art to my own sons, and those of my teachers, and to students bound by this contract and having sworn this Oath to the law of medicine, but to no others.
Now it is all on its place. As I said before, and many times, do not donate to ADA. They do not look at how to treat and how to cure diabetes. They are looking for financial resources, and Diabetes type 2 just is perfect opportunity to find one.
     Now, in 2015, 31 millions in grants. Who was the Recipients? What did they studied? How studies help to stop diabetes, if really they did?

Phillip James White, PhD

Duke Molecular Physiology Institute, Duke University, Durham, NC
A New Homeostatic Mechanism for Metabolic Control
Grant #1-16-INI-17
Very frequently, fatty liver and insulin resistance precede the onset of type 2 diabetes. Compounds called "branched chain amino acids" (BCAAs), which come from certain proteins in our diets, are linked to insulin resistance and risk for developing type 2 diabetes. However, precisely how circulating BCAAs are connected to abnormal glucose and lipid metabolism is unclear. Dr. White has discovered that some of the components of the molecular network that go awry in protein metabolism and prevent BCAAs from breaking down also interact with both glucose and lipid metabolism pathways in the liver. Dr. White's project will examine this network and how it is controlled. He hopes to further define how the molecules interact to control fat and glucose metabolism – and then to identify where new drug development efforts may be focused to treat prediabetes, fatty liver disease and type 2 diabetes.
If Grants are granted then it does not matter what to study, grants will drop in to account, and it is final.  Just present to the committee from what generation of Medical Organization doctor come and Grants are guaranteed. Pay attention, how long this recipient can be in business?   "which come from certain proteins in our diets" is endless possibility. Phillip James White, PhD never will run off business, of cause as long as grants are grantee

Daniel J. Ceradini, MD, FACS

Wyss Department of Plastic Surgery, New York University Langone Medical Center, New York, NY
Therapeutically Targeting Keap1/Nrf2 Dysfunciton in Diabetes
Grant #1-16-ACE-08
Diabetes is the leading cause of non-healing wounds and lower extremity amputation in the U.S. Despite efforts to tightly control blood glucose in people with diabetes, poor wound healing persists as a common complication. Dr. Ceradini has discovered that high blood glucose levels associated with diabetes disrupt antioxidant networks important for tissue regeneration. His project seeks to determine whether restoring this critical antioxidant pathway to normal will reverse the impaired tissue regeneration caused by diabetes. Using innovative approaches and technologies, Dr. Ceradini will develop and test a novel therapy to restore the antioxidant protection program and determine whether it can overcome poor wound healing in diabetes.
Sorry, MD, it is not the fact. If blood sugar is under tight control, then wounds are healing.  The question is, what is "the tight blood sugar control"? How do you identify it? Well, one day I will publish very tight investigation how diabetes diagnosed, and how it is possible to have tight blood sugar control, MD so easy take for granted. There are 95% of Diabetics type 2 in America, insulin independent, insulin resistant, non-sugary diabetics who die because of sugar in blood is so high, it simple does not move in blood vessels. In diabetes type 2 tight blood sugar control never possible, because of diabetes is not the high level of sugar in blood but low level of insulin, insufficient insulin secretion. Big difference I would say.

Zachary A. Knight, PhD 

University of California, San Francisco
Reinvestigation of the Arcuate Feeding Circuit
Grant #1-16-ACE-29
Because the brain controls food intake, it is likely to be an important target for new therapeutics to reduce obesity. However, little is known about the specific site in the brain where environmental or dietary signals override the system that normally regulates feeding and weight maintenance. Dr. Knight's project will use new technologies to investigate the key neurons in the brain that control food intake. If successful, this project will identify the signals that are responsible for activating the sensation of hunger, determine how the neurons motivate food consumption, and clarify how obesity leads to dysregulation of these neurons. Understanding of these networks in the brain may lead to development of new therapies to treat or prevent obesity by stimulating or inhibiting the neurons responsible for hunger and feeding behavior.
Very interesting, what generation of Medical Care this PhD come from? Very sophisticated project. In this project there is not only never stopped possibility to study, but also there is no one possibility to understand studies studee study what?  Typical Charlatanism to Dress The King.

Praveen Sethupathy, PhD

University of North Carolina at Chapel Hill
Systems Approach to Defining Genetic Regulation of Intestinal Physiology and Gut Microbiota in Diet-Induced Obesity
Grant #1-16-ACE-47
In the human body, microorganisms outnumber human cells ten to one. These microorganisms, mostly bacteria, are influenced by both diet and genetic factors and are linked to metabolic disease. The gastrointestinal tract is home to a significant population of microorganisms and is the primary organ system responsible for absorbing nutrients from food. Obesity and diabetes are associated with changes in the microbial communities of the gut and with impaired intestinal function. Dr. Sethupathy's project seeks to identify the genetic factors that contribute the most to shaping the way our intestines respond to gut microorganisms under normal conditions and in diet-induced obesity and diabetes. These studies could lead to the identification of new therapeutic targets that may be leveraged to prevent or effectively treat obesity and diabetes.
"Dr. Sethupathy's project seeks to identify the genetic factors that contribute the most to shaping the way our intestines respond to gut microorganisms under normal conditions and in diet-induced obesity and diabetes" but where idea that diabetes induced by diet come from? So, at first it was induced that diabetes induced by diet, and then Dr. study how diet indused diabetes  and lead to obesity, right? Well, it is easy to understand that level of sugar in blood high because of our diet. Why level of insulin is low? How diet effect level of insulin in blood, and how insulin secretion effected by diet? Right, it is very different story. There is no one investigator, no one studier to study. And why they need it? To stop diabetes? You must be kidding! Who need this type of studies? Diabetes must be run forever because of new and new generations of MD and Phd come to business, and they all need financial support.

Andrew Scharenberg, MD

Seattle Children's Hospital and Seattle Children's Research Institute, Seattle, WA
Regulatory T-Cell Stabilization via Gene Editing as Novel Therapy for Type 1 Diabetes
Grant #1-16-VSN-26
Development of type 1 diabetes is known to involve the immune system inappropriately attacking the body's own insulin-producing beta cells. Several lines of evidence suggest that dysfunction of a type of immune cell, known as a thymic regulatory T-cell (tTreg), leads to a breakdown of normal protection from the immune system in insulin-producing beta cells. When the tTreg cells fail, the immune system begins to attack and destroy the body's own beta cells, leading to type 1 diabetes. Dr. Scharenberg is applying an innovative approach that he developed for "editing" genes to try to tackle type 1 diabetes. Using this technology, his Pathway to Stop Diabetes project aims to edit genes in tTreg cells to preserve their function and protect the beta cells from autoimmune attack, potentially preventing or reversing type 1 diabetes.
Love this studies! Let them reverse Diabetes type 1! They can do it! Really, why we can reverse diabetes type 2 with right diet and they cannot reverse diabetes type 1 with right genes selection? They must chose right genes, so they will not have diabetes type 1. Just BRILLIANT!

Mayland Chang, PhD

University of Notre Dame, South Bend, IN
A Strategy to Accelerate Diabetic Wound RepairGrant #1-15-ACN-06
A serious complication of diabetes is the inability of wounds to heal, which contributed to 73,000 lower-limb amputations in the United States in 2010. Currently, no therapeutic agents for the treatment of diabetic wounds are approved and there is a paucity of research to understand why diabetic wounds are difficult to heal. Preliminary work has identified enzymes called "matrix metalloproteinases" (MMPs) that seem to influence wound healing in diabetic mice. In addition, a drug has been identified that selectively blocks the detrimental MMP, is not toxic to mice, and is poised for development as a topical therapy for diabetic wound healing. This project proposes to validate the beneficial and detrimental roles of MMPs in human samples and to understand how MMP inhibitor drugs may improve diabetic wound healing. The combination of studies applying selective MMP inhibitors and using samples from people with diabetes is expected to lead to a new treatment for this serious complication of diabetes.
Great way to collect sweet money. Our wounds never heal. They come from inside. Then close diabetic to the final breath then more wounds open every day. Our bodies slow rotten, painfully ding. 73,000 amputations, just in one year 2010! Great input on bloody business. It is wound care, and so much other types of  care.... . Would Medical Organization be happy to lost this business just providing insulin injection? Do not even hope for that. They already do have  what they need, so they are ready to study how to put and what on our wounds. Most important, wound never heal. They do take great care for that.

Stephen Parker, PhD

University of Michigan, Ann Arbor, MI
Deconstructing type 2 diabetes using genome-wide high-density multi-tissue 'omics' profiling
Grant #1-14-INI-07
Susceptibility to type 2 diabetes is partly encoded in the genetic code, or DNA. Exactly how changes in DNA lead to diabetes susceptibility and progression, however, currently remains unclear. Recent studies suggest that most disease-associated genetic variations reside not within the coding regions of genes, but instead outside the genes—in regions generally referred to as regulatory elements. These elements control when, where, and how much a gene is turned on. This project is geared to identify these hidden regulatory elements and link them to the genes they control. Such information can lead to quantitative disease surveillance over time, and will help identify the next generation of type 2 diabetes drug targets. Integration of these results with a personal DNA code can help guide "custom" treatment strategies based on the specific combination of risk changes an individual may have.
Do you see, one generation after another, they study what treatmnt they can develop. Is there are any  hope we will ever  have insulin level tested before any treatment started? Not at all. If so, then all those studies have no grants. So, they take as fact, diabetes type 2 is the diet induced misconduct, and then eat up millions in grants to develop a new generation of medicine how to change our behavior. Still, blood sugar is high and we die because of low insulin secretion by our very ill pancreas.

Joshua Thaler, MD, PhD

University of Washington, Seattle, WA
Modulating glial-neuronal interactions to treat obesity and diabetes
Grant #1-14-ACE-51
Therapies for diabetes have largely involved insulin: providing insulin, making the body produce more of its own insulin, or making the body more sensitive to the effects of insulin. All of these approaches work directly on the insulin target tissues (liver, muscle, fat) and are critical parts of diabetes treatment. However, because the brain also helps control blood sugar, medications that target brain systems as opposed to insulin target tissues could be a useful new approach to managing diabetes. We have found that the brain becomes impaired in obesity in a way that may affect body weight and blood sugar balance. This project explores the possibility that glial cells (the brain's damage response cells) in the hypothalamus area of the brain play an important part in the process of becoming obese and developing diabetes. We are using a wide variety of techniques to study and manipulate glial cells in order to determine the extent of their contribution to weight and blood sugar regulation and whether they can be engineered to help reverse obesity and diabetes.
"Therapies for diabetes have largely involved insulin: providing insulin, making the body produce more of its own insulin, or making the body more sensitive to the effects of insulin." These are the all types of medicine. But say me, how these medicine can work for type 2 diabetics? At first we do have medicine to force our already very ill pancreas to work harder to secret our own insulin. Say me, how it is possible to keep pancreas 'healthy'? It is already ill, so the treatment leads to deeper reduction in insulin secretion, right? 
Sensitivity to insulin, what does this mean? If my body system lack in insulin secretion, my ill pancreas does not secret insulin in sufficient amount, how medicine which force my muscle to demand more insulin will lead to healing of my ill pancreas? Never. So, diabetes type 2 is progressive. With treatment for diabetics type 2 progression to the fatal end is faster then without treatment. 
So, only one type of treatment still valuable, providing insulin in injections. It works perfectly. Diabetics type 1, who diagnosed in early childhood not only survive for the next 60 ears and more, but with time the dose of insulin they inject drops. Why? Diabetes type 1 is regressive. It can be reversed with right insulin therapy regime.
     In contrary, diabetics type 2 do have two other types of treatment and when insulin finally come into diabetics type 2 medical box it is limited in dose, usually about 20 units daily dose, and it is way too late.

Wolfgang Peti, PhD 

Brown University, Providence, RI
Novel, innovative insights into insulin signaling and regulation using NMR spectroscopy
Grant #1-14-ACN-31
The prevalence of diabetes in the US is now at epidemic levels. In order to develop new drugs that not only improve treatment, but eventually provide a cure, requires a full understanding of the signaling pathways in the body that drive this disease. The aim of this project is to apply state-of-the-art molecular approaches to study the protein enzymes that regulate insulin signaling and glycogen metabolism. This project uses nuclear magnetic resonance (NMR) spectroscopy, the high-resolution cousin of magnetic resonance imaging (MRI), to study these proteins. This cutting edge technique will provide insight into how these enzymes function—down to the atomic level. More importantly, it will enable the investigation of how the intrinsic functions of these enzymes can
be used to design novel, more potent drugs to fight diabetes.
Great! Why do not start from simple understanding, before start to study signaling system, let us test, if insulin is in blood stream, and it is in sufficient healthy amount?
     BTW, how insulin was found in first place? It was discovered that diabetics pancreas looks different then those non-diabetics. It was discovered with  autopsy, study of Death body. In all the studies where grants were granted there is no one study or test, how healthy or not pancreas of diabetic type 2? If my pancreas is ill, then what is the point to study what  to eat? It must be treatment provided, medicine developed how to heal ill pancreas.
Did some one see any studies of diabetic pancreas? How pancreas health ever tested? What test run to diagnose diabetes? Level of sugar in blood. What test never run? The condition of pancreas, if it is healthy or not for insulin secretion in sufficient amount. Why? With these studies diabetes type 2 myth would be broken. How many sweet pies our highly sophisticated medical Care Industry will lost? It is much better to say that diabetes type 2 can ce reversed with Starvation Diet. It is even not diabetes, but misconduct. So easy and so simple.


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