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Personalized medicine experiment details diabetes development
Posted By Patrick J. Skerrett On March 29, 2012 @ 2:43 pm In Diabetes,Genes,Medical Research | Comments Disabled
The term “personalized medicine” is still something of an abstract idea. In an audacious experiment, Stanford molecular geneticist Michael Snyder gave it a face—his own—and showed what it can do.
Snyder and a large team of colleagues first sequenced his DNA, revealing his complete genetic library. This information showed that Snyder was at increased risk for high cholesterol, coronary artery disease, basal cell carcinoma (a type of skin cancer), and type 2 diabetes. Next, they measured thousands of biological markers in Snyder’s blood every few weeks for two years.
During the average checkup or workup for an illness, a doctor will look at maybe 20 chemical or biological markers. This simple snapshot can be helpful. What Snyder and his colleagues did was akin to taking a 3-D movie of his inner workings on a molecular level to observe how genes, the molecules that read and decode them (RNA), the proteins they make, and other substances work together during health and how they respond to illness.
The team saw how Snyder’s body responded to a cold at the very beginning of the study. Midway through, they watched as molecular changes wrought by a respiratory infection tipped him into full-blown diabetes. The work was published in the journal Cell.
This intensive approach to health monitoring isn’t coming to your doctor’s office any time soon. It’s an expensive process that takes a lot of time and technology, and the information it generates would overwhelm most people and their doctors. But it offers new ways to identify diseases and their triggers early, and offers a peek at how personalized medicine might someday work.
The study’s eyewitness account of the development of diabetes really caught my attention. Just before the study’s midpoint, Snyder was infected by the respiratory syncytial virus, which affects the lungs. About two weeks later, measures of his blood sugar regulation stopped looking normal. Then his blood sugar level began increasing. Three months later, Snyder was diagnosed with type 2 diabetes.
The lung infection prompted Snyder’s body to make various antibodies. That’s a healthy response to an infection. But it also made autoantibodies—antibodies that attacked his own proteins. One of the autoantibodies targeted a receptor on the surface of cells that latches onto insulin, a hormone that’s needed to usher glucose (blood sugar) into cells. Interfering with that receptor makes it hard for cells to absorb sugar from the bloodstream, a hallmark of diabetes.
I was diagnosed with diabetes six years ago, right after having a severe and persistent infection. The news was an absolute shock—I’m thin, active, eat a pretty healthy diet, and there isn’t any diabetes in my family.
I’ve long thought that the infection caused, or at least triggered, my diabetes. There hasn’t been much in the medical literature—until now—to back up my suspicion. The work by Michael Snyder and his colleagues won’t do anything to help me control my blood sugar, but it does help take some of the mystery out of why I’m living with this condition.
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