01 April 2014

Freedom to the radicals!

James Watson offers his hypothesis about the causes of type 2 diabetes

NanoNewsNet based on the materials of Cold Spring Harbor Laboratory:
Nobelist James Watson proposes an unconventional view of type 2 diabetes causationAt 85, Nobel Prize winner James Watson, one of the discoverers of the DNA double helix structure, continues to put forward intriguing scientific ideas.

His hypothesis about the causes of type 2 diabetes is published in the British medical journal The Lancet (Type 2 diabetes as a redox disease).

According to Dr. Watson, diabetes, dementia, cardiovascular diseases and some cancers are associated with the inability of the body to synthesize a sufficient amount of biological oxidants - reactive oxygen species (ROS).

"The conventional wisdom about type 2 diabetes," says Dr. Watson, "is that increased intracellular oxidation causes inflammation, which in turn kills pancreatic cells."

The proper functioning of these cells, and this is well known, is crucial for maintaining normal blood glucose levels.

Over the past few years, Dr. Watson has been developing an alternative view based on the facts presented in the scientific literature on medicine and molecular biology. He does not question that pancreatic tissue in people with type 2 diabetes is inflamed, but puts forward a new theory about the cause of this inflammation.

"The main reason, I believe, is the lack of biological oxidants, not their excess," explains the scientist.

Dr. Watson has long known that often before prescribing well–proven hypoglycemic medications, such as metformin, doctors recommend that patients with the initial stage of type 2 diabetes mellitus – people with elevated blood sugar levels - pay more attention to physical education. Watson considers physical exercise to be the key to this riddle. So what is it about exercise that benefits patients with high blood sugar?

Important clues, Watson suggested, can be found in the chemistry of oxidation and reduction reactions. The cells of the body cannot live without both oxidants and antioxidants. There is a delicate balance between them. Physical exercises stimulate the production of a large number of oxidants in the body – molecules called active forms of oxygen. In a cellular organelle called the endoplasmic reticulum (ER), one of the types of reactive oxygen species – hydrogen peroxide (H 2 O 2) – helps to form chemical bonds (disulfide bridges) that stabilize proteins during their folding.

When the oxidation in the ER is reduced, Watson explains, uncoiled and unable to function proteins are formed. This, he believes, causes inflammation that harms the pancreas, sometimes causing type 2 diabetes. Thus, the scientist believes, physical exercises that stimulate oxidation can probably have a beneficial effect on people with high blood sugar levels. This benefit will become less if it does not disappear altogether, Watson reflects, if such a person consumes large amounts of antioxidants. His hypothesis can be confirmed by the fact that athletes taking large amounts of antioxidants do not seem to benefit from physical exertion.

Watson draws the attention of his audience to the following: "... we should definitely have a much more serious and detailed scientific view of the mechanisms by which exercise improves our health."

At the end of this year, Dr. Watson plans to hold a scientific conference at Cold Spring Harbor Laboratory, which, he hopes, will increase the interest of scientists in his hypothesis and will trigger deeper research.

"I am not a doctor and I cannot give advice on how to treat diabetes. I offer a new idea about what causes type 2 diabetes. But I notice that almost every doctor I've ever known recommends physical exercise to every patient if he's able to do it. I think exercise helps us produce healthy functional proteins. But to demonstrate this, we really need to conduct more in–depth research," the Nobel laureate concludes.

Portal "Eternal youth" http://vechnayamolodost.ru01.04.2014

Found a typo? Select it and press ctrl + enter Print version

Related posts