Why does basketball make Arden's BG rise?

Arden brings the ball down the court, passes and looks for a rebound.

Last week during Arden's quarterly Endo appointment I brought up an issue that I had identified but couldn't figure out. I explained to our nurse practitioner that when Arden exercises her BG falls. Riding a bike, running around, recess at school, really all of the her physical activities decrease her BG... except sports.

I, of course, am aware that activity can cause a decline in BG but our issue didn't seem to be following that "rule". It took me a while to be able to see past the expectation that physical exertion would decrease Arden's blood glucose level. Inexplicably, I was having trouble with her BGs actually going up during basketball games and practices this winter. When I finally thought back, I realized that I saw similar BG trends last summer during softball.

Our NP asked about Arden's level of competitiveness, as she spoke I began to understand what she was getting at...

Arden is a very competitive little girl, when it counts. That is to say that if she goes out back with her brother to shoot baskets her BG falls from the activity as you may expect but when she is in a game, when there is a score being kept and winners and losers are recorded - Arden's BGs go up.

I explained to our NP that Arden entered her last basketball game with a BG of 125 and that by the end of the game, just one hour later with no food or carbs in her system, her BG was 220 and climbing. I was bolusing during the game, which was nerve wracking when you consider that the expectation is that there will be a fall from the activity.

The NP described to me that this is a phenomenon that they generally see with boys, then she turned to Arden and said, "so, you like to win huh?". Apparently it's common for very competitive people to access their flight or flight response (also known as 'the stress response') during a sporting competition. Their desire to win is so strong that they feel the game on a different level. Adrenaline is released and their body prepare to battle as if they are fighting for their lives.

Next week when we arrived at the gym. I am going bolus as if Arden was about to consume a 15 carb juice box (the ones we use for low BGs). I'm confident that the insulin begins to act it will find a rising BG to tussle with, if I'm wrong... we'll just drink the juice. I'll report back and let you know what happens... Never a dull moment with type I diabetes.

Pathway to Stop Diabetes

Image courtesy of Pathways to Stop Diabetes

The American Diabetes Association has just announced an initiative called Pathways to Stop Diabetes. Here is a brief snippet from their website about the program's intentions.

We realize that it takes more than natural talent for young researchers to realize their full potential. It takes comprehensive support every step of the way. To make the career commitment to diabetes research attractive, fulfilling and rewarding, Pathway to Stop Diabetes will provide that support in every way.

I think that it's very exciting to see such a large organization thinking about research in a different way. It's also encouraging to see that program financially backed so significantly by pharma companies. I hope you can take a few minutes to learn more about Pathway.

If you are a brilliant young scientist, are raising one or know a young researcher that may be interested in being at the forefront of discovery. Please consider diabetes research as your field of focus. Pathway offers researchers mentoring, grants and much more. Who knows, maybe you're the next Frederick Banting, MD. 

More blurbs from the Pathway to Stop Diabetes website:

"Our vision is simple yet revolutionary: find a new generation of brilliant scientists at the peak of their creativity, then provide them with the freedom, autonomy, and financial and professional resources to set them on the road to breakthrough discoveries."

"Diabetes research is critically underfunded. Twice as many Americans have diabetes as have cancer. Diabetes is over 20 times more prevalent than HIV/AIDS. Yet National Institutes of Health (NIH) funding for diabetes is 1/5 that of cancer and 1/3 that of AIDS. On a per-person-affected basis, diabetes funding is a rounding error in comparison. This difference has persisted for decades." - more

Arden's Day wishes the Pathway program a very successful (but hopefully short) life!

Be well,

Scott

Alzheimer's and insulin resistance

This is an old article from Time Health but it raises interesting points about insulin's effect on Alzheimer's and I thought it was worth sharing.

When the body refuses to make insulin, the condition is called type 1 diabetes; when the body mismanages the hormone, it's known as type 2. Now, scientists report new evidence linking insulin to a disorder of the brain: when the brain prevents the hormone from acting properly, the ensuing chemical imbalance may help trigger Alzheimer's disease. The correlation is so strong that some researchers are calling Alzheimer's disease "type 3" diabetes.

In the body, insulin helps convert food into cellular energy. But the brain has other uses for insulin, namely as a means to learn and make new memories. Here's how it works: At synapses, the spaces across which brain cells communicate and where memories are conceived, neurons reserve special parking spots just for insulin. When the hormone pulls in, a connection is made that enables new memories to form. Since new memory formation is one of the first things to go awry in people with early stages of the disease, this insulin-initiated process may hold the key to decoding the mystery of Alzheimer's.

In August, a team of scientists at Northwestern University were the first to show why the brain's "memory function" fails in the face of an insulin shortage. The group's prior research had already pinpointed the culprit: toxic proteins called amyloid beta-derived diffusible ligands (ADDLs, for short), which are known to pile up in the brains of people with Alzheimer's. Scientists also knew that Alzheimer's patients' brains have lower levels of insulin and are insulin resistant. But what the Northwestern team discovered is the molecular mechanism behind that resistance: when ADDLs bind to neurons at synapses, they obliterate the receptors that are normally reserved for insulin. Without those parking spaces on the brain cells' surface, insulin has no place to connect, and memory fails.

"We now understand that the function of insulin at those synapses is to modulate and influence the underlying cellular structure of memories," says William Klein, professor of neurobiology and physiology at Northwestern University and a co-author of the study published online by the FASEB Journal. "What we have here is a striking phenomenon that may ultimately explain why the brains of people with Alzheimer's disease are insulin resistant and how that ties into memory."

Researchers hope these findings will help shape future research in Alzheimer's therapy — perhaps in the development of drugs that can make brain cells' insulin receptors more responsive to the hormone, or in the application of type 2 diabetes drugs, which address insulin resistance, to Alzheimer's.

The notion that Alzheimer's disease might be a neuroendocrine disorder, akin to diabetes, isn't entirely new; it first showed up in the scientific literature roughly 20 years ago, but the idea petered out. In 2005, Suzanne la Monte, a neuropathologist at Brown University Medical School, revisited the idea. Based on two of her discoveries — that the brain makes its own insulin and that Alzheimer's disease depletes insulin — she coined the disease process "type 3" diabetes.

Still, referring to Alzheimer's disease as "type 3" diabetes is controversial, especially within the diabetes community. Alzheimer's disease is a complication of diabetes, not a unique form of the disease, says Dr. Sue Kirkman, vice president of clinical affairs for the American Diabetes Association. "Nevertheless," she says, "this is primarily a semantic argument."

The terminology aside, both diseases share many traits and risk factors, including high cholesterol, high blood pressure, and metabolic disorders. So, de la Monte sees the semantic "splitting of hairs" as a good thing. "People are arguing about small parts of the bigger story," she says. "At the end of the day, these conversations will help us to better understand both diabetes and Alzheimer's disease."

D Science

As a general rule I don’t repost stories about the latest diabetes “cure” that seem to be “almost” ready.  I mostly avoid doing this because I remember the first time I saw an article that claimed the researchers had cracked the code and just needed a few more dollars to cure us all. That first article came to my attention just weeks after Arden was diagnosed and it took me two days to realize that these “cures” have been pro ported to be just around the corner for decades. I believe that one of them will eventually break through but for me (or you) to emotionally chase each one of them, well that’s not a good idea. All of that doesn’t mean that I don’t follow along with what the scientific world is trying to do... Today, I’m reposting an article because this one seems a little different, just slightly more hopeful. It has no anti-rejection drugs that trade diabetes for cancer and it’s backed by a philanthropist with a strong personal connection and an eye for a good idea. In short this one seems doable to me. See what you think and comment if you’re so moved.

Fromhttp://m.xconomy.com/3376/show/9afa00bb7aaa31f4ea0ec98fd59537aa/

Posted by Arlene Weintraub on Friday Jun 24th at 4:00pm

What happens when a guy who got wealthy selling cars hands millions of dollars to a scientist and tells her how to spend it? Folks attending the American Diabetes Association conference starting today in San Diego are getting a hint of the answer to that question. Denise Faustman, director of the Massachusetts General Hospital (MGH) immunobiology laboratory is presenting two abstracts from a clinical trial funded by the Boston-based Iacocca Family Foundation, established by former Chrysler CEO Lee Iacocca to support research aimed at curing type 1 diabetes.

Faustman’s data shows that low doses of an 80-year-old vaccine temporarily reversed type 1 diabetes in Phase 1 human trial. The vaccine is called bacillus Calmette-Guerin (BCG). It was developed to prevent tuberculosis and is now available as a generic drug. BCG induces the immune system to make tumor-necrosis factor (TNF), which kills the T-cells that cause the pancreas to stop producing insulin.

Faustman’s team went to Iacocca’s foundation for funding after repeatedly having the door slammed in their faces by drug companies. The MGH scientists had plenty of animal studies showing that it was possible to regenerate the pancreas, and therefore restore insulin production in diabetes models. But when MGH went to the pharmaceutical industry looking for funding to research a pancreas-regenerating drug, “everyone said, ‘you’re reversing the disease. How are we going to make money?’” Faustman says.

So MGH spent years looking for a generic drug that would stimulate the production of TNF. Iacocca’s foundation supported much of that work, which involved drawing blood from thousands of diabetes patients and proving that they could use TNF to kill the bad T-cells. “One day, Mr. Iacocca looked at me and said, ‘Denise, when are you going to cure diabetes?’” Faustman recalls.

Iacocca instructed Faustman to show the technique worked in a mouse study, so it could eventually be tried in humans. “No one had ever reversed diabetes in a mouse,” she says. “Philanthropy can take risks. He made it clear it was his money and he wanted risky therapies done.” Then the foundation put $10 million toward the Phase 1 human trial. All told, Iacocca’s group is the largest single donor to Faustman’s research.

MGH’s Phase 1 study was designed to answer four key questions about BCG, Faustman says. “Does it kill the bad T-cells? Does it induce the good T-cells? Does it change the pancreas? Does it restore insulin secretion?” The data, she says, “shows positive responses in all four outcomes.”

One caveat, Faustman says, is that the drug produces a transient effect. That means it will have to be given in repeated intervals, perhaps every four to six weeks. Still, says Faustman, “this will be the first data showing that the pancreas can be turned back on.”

Iacocca launched his foundation in 1984 in honor of his late wife, Mary, who died of complications from type 1 diabetes. The foundation declined to comment for this story. But Kathryn Iacocca Hentz—president of the foundation and Lee’s daughter–said in a statement “These results are very meaningful to the Iacocca Family. We have supported this work since the mouse studies first showed the reversal of longstanding diabetes.”

The foundation has made a gift of undisclosed size to MGH to support the Phase 2 program, which MGH is now planning. The hospital has raised $8.5 million of the $25 million it will need to support the trial over the next three years. Though Faustman says they’ll need other partners to kick in additional funding, she’s certain they couldn’t have come this far without the help of the former Chrysler CEO. “You have to wonder how a guy who built cars knew what we needed to do,” she says. “But he knew what risks to take.”

New gel could speed wound healing

In this Wednesday Aug. 4, 2010 photo a demonstration of how wound-healing gel is used on a leg wound is seen at University College London. British scientists are about to begin a final phase of testing on a new gel that heals wounds up to five times as fast as normal treatment. The gel, named Nexagon, works by interrupting how cells communicate and prevents the production of a protein that blocks healing. That allows cells to move faster to the wound to begin healing it. Though it has only been tested on about 100 people so far, experts say if it proves successful, the gel could have a major impact on treating chronic wounds, like leg or diabetes ulcers, and even common scrapes or injuries from accidents. (AP Photo/Kirsty Wigglesworth)

LONDON — For three years, Connie McPherson had debilitating leg ulcers that were so painful she sometimes couldn't sleep. Despite repeated surgery, antibiotics, steroids and other treatments, nothing helped.

Then last year, she took part in a trial for a new gel aimed at chronic wounds.

"It was the answer to my prayers," said McPherson, 58, a real estate agent in Tulsa, Oklahoma. Within weeks, McPherson said the ulcer treated was completely healed. "I tried everything possible and this is the only thing that worked."

The gel used to treat McPherson was developed by a team led by David Becker, a professor of cell and developmental biology at University College London. The gel, named Nexagon, works by interrupting how cells communicate and prevents the production of a protein that blocks healing. That allows cells to move faster to the wound to begin healing it.

Though it has only been tested on about 100 people so far, experts say if it proves successful, the gel could have a major impact on treating chronic wounds, like leg or diabetes ulcers, and even common scrapes or injuries from accidents.

In most chronic wounds, Becker said there is an abnormal amount of a protein involved in inflammation.

To reduce its amount, Becker and colleagues made Nexagon from bits of DNA that can block the protein's production. "As that protein is turned off, cells move in to close the wound," Becker said. The gel is clear and has the consistency of toothpaste.

http://www.msnbc.msn.com/id/38671775/ns/technology_and_science-science/