The term “personalized medicine” continues to be something of an abstract idea. In a daring experiment, Stanford molecular geneticist Michael Snyder gave it a face—his own—and showed what it could do.
Snyder and a big team of colleagues first sequenced his DNA, revealing his complete genetic library. This information showed that Snyder was in danger for prime cholesterol, coronary artery disease, basal cell carcinoma (a sort of skin cancer) and sort 2 diabetes. After that, they measured 1000's of biological markers in Snyder's blood every few weeks for 2 years.
During a mean checkup or workup for a disease, a physician will have a look at perhaps 20 chemical or biological markers. This easy snapshot could also be helpful. What Snyder and his colleagues did was to take a 3-D movie of its inner workings on the molecular level to look at how genes, the molecules that read and decode them (RNA), the proteins What they make up, and other substances work together. Health and the way they reply to illness.
The team checked out how Snyder's body responded to the cold on the very starting of the study. In between, they noticed that the molecular changes attributable to the respiratory infection caused him to develop full-blown diabetes. It was work. Published in Journal Sale.
This intensive approach to health monitoring isn't coming to your doctor's office anytime soon. It's an expensive process that requires loads of time and technology, and the data it generates can overwhelm most individuals and their doctors. But it offers recent ways to quickly discover diseases and their triggers, and offers a glimpse into how personalized medicine might at some point work.
Diabetes Relation
The eyewitness account of the diabetes development study really caught my attention. Just before the center of the study, Snyder was infected with respiratory syncytial virus, which infects the lungs. After about two weeks, her blood sugar regulation measures stopped looking normal. Then his blood sugar level began to rise. Three months later, Snyder was diagnosed with type 2 diabetes.
The lung infection prompted Snyder's body to make various antibodies. This is a healthy response to infection. But it also made autoantibodies—antibodies that attack its own proteins. One of the autoantibodies targeted a receptor on the surface of cells that binds to insulin, a hormone needed for glucose (blood sugar) in cells. Interference with this receptor makes it difficult for cells to soak up sugar from the bloodstream, a trademark of diabetes.
I used to be diagnosed with diabetes six years ago, shortly after having a severe and chronic infection. The news was a whole shock — I'm slim, lively, eat a reasonably healthy weight-reduction plan, and don't have diabetes in my family.
I even have long thought that the infection caused, or no less than began, my diabetes. There hasn't been much – thus far – within the medical literature to back up my skepticism. The work of Michael Snyder and his colleagues won't do anything to assist me control my blood sugar, but it surely does help clear up a few of the mystery of why I'm living with this condition.