New Test for Diabetic Nephropathy Could Be Giant Leap

One of the big problems with kidney disease is you don't know you have it until a lot of damage has been done. It is rare for a patient or physician to identify diabetic kidney disease, or nephropathy, early on. The urine test just does not pick up the proteins that indicate damage until a lot of damage is done.

So, it is exciting news when scientists publish an article in the journal Diabetes Care outlining a new test that can predict a fair amount of diabetic nephropathy before it even begins.

It appears that they still have some fine-tuning to do, but if they can pull this off they could extend the lives of countless people by allowing doctors to treat diabetic kidney disease early on.

100 Bottles Of Red Wine May Keep You Happy Like Some Lab Mice

There are so many people that would love to find out that wine was more healthful than harmful. As time goes on science will help us separate the facts and understand the truth. In the mean time, a compound derived from red wine, reversitrol, increased the life span and health of obese mice.

“After six months, resveratrol essentially prevented most of the negative effects of the high calorie diet in mice,” said Rafael de Cabo, Ph.D., the study’s other co-senior investigator from the National Institute on Aging’s Laboratory of Experimental Gerontology, Aging, Metabolism, and Nutrition Unit. “There is a lot of work ahead that will help us better understand resveratrol’s roles and the best applications for it.”

So, now scientists and non-scientists are speculating that reversitrol may be a miraculous substance that can enhance the health of portly people as well as people who maintain a healthy weight.

You can read more about the research on reversitrol by following this link. We encourage you to pay special attention to the cautious words of Dr. Eisenson. He reminds us that results that we see in lab animals often do not occur in humans. So, lets see what happens.

We would be thrilled if reversitrol had miraculous effects on people. We would be hard-pressed to chug down the 100 bottles of wine we would need to consume to get the equivalent reversitrol that the mice in the study got. However, we are sure that scientists can figure out how to put it in a pill – without the hangover.

So, while scientists subject the preliminary data on wine extracts to more scrutiny, we can point you to another strategy for health that is well-founded. According to this New York Story the current Arkansas Governor, Mike Huckabee, is going to run in the New York City Marathon this weekend. In response to diabetes, he willed his way through dramatic weight loss. He went from significantly overweight, to marathon runner.

Scientists Find One More Type 1 Diabetes Gene

During ongoing research to pinpoint genes that may contribute to the risk of developing diabetes, researchers at The Children's Hospital of Philadelphia and McGill University in Montreal have identified a gene variant that raises a child's risk for type 1 diabetes. The research team uncovered new type 1 diabetes instigators on chromosome 16, occupied by a gene called KIAA0350As. Investigators have their eyes on providing a scientific basis for designing better treatments and preventive measures for the disease.

The research adds a new gene and new knowledge to the four genes previously discovered for type 1 diabetes. As the project continues, the study team expects to identify additional genes—perhaps as many as 15 or 20—thought to interact with each other in the disease.

The study appeared July 15 in an advance online letter in the journal Nature. In the discovery phase of the study, the investigators examined the genomes of 1,046 children with type 1 diabetes. These DNA samples came from patients and families followed in pediatric diabetes clinics in Philadelphia and four Canadian cities. Specifically, the researchers compared the genomes of 563 patients with type 1 diabetes with those of 1,146 matched control subjects. Those results were combined with data obtained from an independent analysis of 483 family trios, in which the genomes of a child with the disease and both parents were examined.

This project confirmed the four previously identified locations for genes contributing to type 1 diabetes, as well as pinpointing the KIAA0350 gene.

Constantin Polychronakos, M.D., director of Pediatric Endocrinology at McGill University and senior author of the study, said that better knowledge of genes that predispose to type 1 diabetes may later enable physicians to screen newborns at high risk for the disease.

The gene implicated in the current research, KIAA0350, is known to be active almost exclusively in immune cells. Although scientists do not currently know the exact function of the protein the gene encodes, other research has predicted that it produces a protein called C-type lectin that is located on the surface of immune cells and binds to groups of sugars in the body.

"The role of KIAA0350 needs to be investigated," said Hakon Hakonarson, M.D., Ph.D., the director of the Center for Applied Genomics at The Children's Hospital of Philadelphia. "However, a special cell type called a natural killer (NK) cell expresses this gene abundantly, although at different levels based on these gene variants. Our hypothesis is that a special mutation in KIAA0350 may influence the sugar binding of the protein, and trigger an autoimmune response that activates these NK cells in such a way that they attack and destroy the islet cells in the pancreas, resulting in type 1 diabetes. A particular version of the gene protects against this inappropriate autoimmune response, while a different version of the gene makes it more likely to happen."

Although much research remains to be done, better understanding of the disease process may guide doctors to new and improved therapies. "If we know the gene pathways that give rise to type 1 diabetes, we hope to intervene early in life with targeted drugs or cell therapies to prevent the disease from developing," Polychronakos said.

The current research used a technique called genome-wide association, in which highly automated analytic equipment rapidly scans each patient's DNA for more than half a million genetic markers. It was performed at the Center for Applied Genomics at Children's Hospital. The Center's tools spell out a patient's genotype—the specific pattern of variations among an individual's 30,000 genes. Established in the summer of 2006, the center is taking on one of the largest genotyping projects in the world, and is the largest one dedicated to genetic analysis of childhood diseases.

"This study is the first one that our center has published on a gene associated with a complex childhood disease, but we have many projects under way and several other papers in press," said Hakonarson. "Our goal at the Center is to discover the major disease-causing variants and genes that influence complex pediatric diseases, thus providing a scientific foundation that is based in biology for translating those discoveries into successful treatments."

Source: Children's Hospital of Philadelphia news release

Insulin Problems May Signal Alzheimer's

Older men who with type 2 diabetes are at more risk of developing Alzheimer's disease as they age. Glucose may deposit in the brain damaging the large and small vessels there. That damage can lead to Alzheimer's.

Fifty-year-old men with impaired insulin secretion and glucose tolerance demonstrated an increased risk of Alzheimer’s disease later in life, according to a new study.

This study, published in Neurology comes on the heels of a similar project that identified that diabetics with the gene protein APO 4 are more likely to experience dementia or Alzheimer’s as they age than non-type 2 diabetics with the trait. That study, published in the Archives of Neurology proposes too much glucose to the brain may cause deposits to form and damage both large and small vessels of the organ. Diabetes has long been suspect in cerebral vascular disease and dementia. Narrowing vessels impair the passage of proteins vital to the brain’s functional cognitive abilities.

In the most recent study, researchers concluded there is a link between poor insulin secretion in mid-life and Alzheimer’s. While Alzheimer’s is a form of dementia, not all dementia is Alzheimer’s. Dementia is defined as having two or more problems with brain functions like cognitive ability and memory, or speech, etc. It is actually a group of disorders. Alzheimer’s is a progressive disorder that eventually robs individuals of memory and ability to function, ultimately leading to death. It generally begins after age 60. Not all memory loss is dementia either.

Finally, these studies only analyzed male type 2 diabetics, and only those who developed diabetes around the age of 50. The implications may not apply to all diabetics. There are differences between type 1 and type 2. Surely the proposal about hyperglycemic conditions having the potential of impairing brain function may apply to both. The rest remains to be seen with more studies and time.

Gene Variation, Poor Glycemic Control Increase Heart Risk

Certain genetic variations can increase the risk of developing coronary artery disease in the general population. For people with type 2 diabetes with that same genetic variation, their risk increases significantly with poor glycemic control.

Patients with type 2 diabetes who have poor glycemic control and a certain genetic variation have an increased risk of coronary artery disease, according to a study in the November 26 issue of JAMA.

Among the known risk factors for cardiovascular disease, diabetes mellitus ranks as one of the most potent. It increases the lifetime risk of a major cardiac event by 2 to 4 times, relative to individuals without diabetes, according to background information in the article. A substantial proportion of cardiovascular risk is under the control of genetic factors.

Genetic variation on chromosome 9p21 has been associated with increased risk of coronary artery disease (CAD) in the general population. Alessandro Doria, M.D., Ph.D., M.P.H., of the Joslin Diabetes Center, Harvard Medical School, Boston, and colleagues examined the association of this genetic variant with coronary artery disease in individuals with type 2 diabetes and whether the association is affected by poor glycemic control.

The researchers conducted two studies, with one including 734 type 2 diabetes patients (322 with angiographically diagnosed CAD and 412 with no evidence of CAD), who were recruited between 2001 and 2006; the other study included 475 type 2 diabetes patients whose survival status was monitored from their recruitment between 1993 and 1996 until December 31, 2004.

Participants for both studies were tested for a gene variation of chromosome 9p21 as well as their glycemic control by averaging measurements of hemoglobin A1c (HbA1c) taken in the years before study entry.

Researchers found that patients with the gene variation, but good glycemic control had double the risk of CAD. Patients with both the gene variation and poor glycemic control had four times the risk of developing coronary artery disease.

A similar interaction between the 9p21 variant and poor glycemic control was observed with respect to the rate of death after 10 years.

"In conclusion, 9p21 [variant] and poor glycemic control interact in determining the odds of CAD in type 2 diabetes,” the authors write. “This finding may have implications for our understanding of atherogenesis [the process of plaque forming in arteries] in diabetes and for the design of more effective prevention strategies."