Cold Spring Harbor, NY At 85, Nobel laureate James D. Watson, the co-discoverer of the double-helix structure of DNA, continues to advance intriguing scientific ideas. His latest, a hypothesis on the causation of type 2 diabetes, is to appear 7 pm Thursday US time in the online pages of The Lancet, the prestigious British medical journal.
Watson's hypothesis, which is featured as the Lancet cover story in the U.S. print edition dated March 1-7, 2014, suggests that diabetes, dementias, cardiovascular disease, and some cancers are linked to a failure to generate sufficient biological oxidants, called reactive oxygen species (ROS). Watson also argues the case for a better understanding of the role of exercise in helping to remedy this deficiency.
"The prevalent view of type 2 diabetes," Dr. Watson says, "is that an excess of intracellular oxidation causes inflammation, which in turn kills cells in pancreatic tissue." Proper function of those cells, it is well understood, is critical for the maintenance of normal blood glucose levels.
Over the last several years Watson has been puzzling out an alternative view, based on facts reported in the peer-reviewed literature of medicine and molecular biology. (He makes clear that he is not a medical doctor, rather a student of science.) He does not question that pancreatic tissue in people with type 2 diabetes is indeed inflamed. But he does present a novel theory of why. "The fundamental cause, I suggest, is a lack of biological oxidants, not an excess," he says.
For years, Watson knew, doctors have been telling patients with incipient type 2 diabetes those with high blood sugar levels -- to exercise, often before putting them on a well-proven glucose-lowering drug regimen such as Metformin. Exercise seemed to Watson the key to the puzzle: what was it about exercise that served to benefit people with high blood sugar?
There were important clues, he specul
|Contact: Peter Tarr|
Cold Spring Harbor Laboratory