James D. Watson, Ph.D.’s Nobel Prize medal is set to go up for bids Thursday, with the co-discoverer of DNA’s structure saying he hopes that his gains go beyond dollars and allow him to “re-enter public life.”
Dr. Watson and Christie’s, which is conducting the auction in New York, also hope to fetch more than the $2.27 million winning bid for the Nobel medal of his partner in DNA discovery, Francis Crick, sold last year through Heritage Auctions. That price was paid by Jack Wang, the Shanghai entrepreneur who heads China-U.S. regenerative medicine technology developer Biomobie.
Unlike Dr. Crick (1916-2004), Dr. Watson is the first Nobel laureate to sell their medal while still alive. Dr. Watson’s medal has a reserve price of $2.5 million, but could bring between that much and $3.5 million, Christie’s has said.
Also to be auctioned are Dr. Watson’s handwritten notes for his Nobel Prize acceptance speech delivered in Stockholm on December 10, 1962. Those notes are expected to bring in an additional $400,000. He will also sell his manuscript and corrected drafts for his Nobel Lecture, delivered the following day, and estimated to be worth $200,000 to $300,000.
Dr. Watson has said he will use the proceeds from the auction for a variety of purposes. They include purchasing artwork, especially a David Hockney painting; supplementing his income; and making donations to several institutions where he has studied and worked. One is the University of Chicago, where Dr. Watson received his Bachelor of Science degree in zoology in 1947. Other institutions to benefit include Clare College Cambridge, Long Island Land Trust, and Cold Spring Harbor Laboratory (CSHL)—where Dr. Watson holds the position of chancellor emeritus.
Dr. Watson joined CSHL as director in 1968, then president in 1994, and chancellor from 2003 to 2007. He retired following publication in the Sunday Times of London of comments in which he connected intelligence to race, saying that while people want to believe that everyone possesses equal intelligence, “people who have to deal with black employees find this not true.”
He also said he was “inherently gloomy about the prospect of Africa,” adding: “All our social policies are based on the fact that their intelligence is the same as ours—whereas all the testing says, not really.”
Late last month, Dr. Watson told the Financial Times: “[The Sunday Times reporter] somehow wrote that I worried about the people in Africa because of their low IQ – and you’re not supposed to say that.”
“It was stupid on my part. All you can do is nothing, except hope that people actually know what you are,” he said, adding that he was “not a racist in a conventional way.” As a result of his comments, Dr. Watson told the FT, “no one really wants to admit I exist.
“I was an un-person,” he said. “I was fired from the boards of companies, so I have no income, apart from my academic income.”
By selling his Nobel Prize medal, Dr. Watson added, he hopes the resulting publicity will enable him to “re-enter public life.” He has not been out of the public eye entirely. Earlier this year, he published an article in The Lancet in which he advanced his hypothesis that diabetes arises from a deficiency in biological oxidants—bucking conventional wisdom that holds that diabetes is caused by an excess of biological oxidants.
Drs. Crick, Watson, and Maurice Wilkins, Ph.D., shared the 1962 Nobel Prize in Physiology or Medicine for their 1953 discovery of the double-helix structure of deoxyribonucleic acid.
Because Nobel rules permit only three scientists to share credit for joint discoveries, the award omitted the key fourth person who joined them in reporting the discovery in Nature—Dr. Wilkins’ colleague Rosalind Franklin, Ph.D. (1920-1958), who took the X-ray photographs from which Drs. Watson and Crick developed their insight before she succumbed to cancer at age 37.
The Rosalind Franklin Society, whose founder and evp is GEN Publisher & CEO Mary Ann Liebert, is named for Dr. Franklin, with the purpose of advancing the contributions of women in the life sciences and affiliated disciplines.
Undeterred by conventional wisdom or his lack of physician’s credentials, Nobel laureate James D. Watson, Ph.D., co-discoverer of the structure of DNA, is forwarding a bold hypothesis—diabetesarises from a deficiency in biological oxidants. This hypothesis directly opposes the usual view, which holds that diabetes is caused by an excess of biological oxidants, or reactive oxygen species (ROS). Biological oxidants are widely believed to cause inflammation that is harmful to pancreatic cells.
Watson first presented his hypothesis in an article that appeared online February 27 in the Lancet. The article, which is entitled “Type 2 diabetes as a redox disease,” will also be on the cover of the Lancet’s U.S. print edition dated March 1–7. In this article, Watson makes it clear that he developed his hypothesis by considering the role of exercise.
“Physical exercise has long been widely regarded as essential to human health,” Watson writes. “Yet, we do not know how exercise-stressed skeletal muscle cells that generate reactive oxygen species such as hydrogen peroxide delay—if not prevent—the occurrence and severity of diseases such as type 2 diabetes (as well as dementias, cardiovascular disease, and some cancers).”
Exercise is recommended for patients with incipient type 2 diabetes—those with high blood sugar levels. In fact, patients often begin exercise before they begin receiving glucose-lowering drugs such as metformin. It struck Watson that while exercise and metformin seem to help not only patients with diabetes, but also patients with cancer, Alzheimer’s disease, and cardiovascular disease, the reasons behind the benefits remain unclear.
How could exercise, which prompts the body to make large numbers of oxidants, protect against diabetes, which presumably arises from inflammatory processes caused by an excess of oxidants? Perhaps oxidants and their role in inflammation needed a closer look. Clearly, pancreatic tissue in people with type 2 diabetes is indeed inflamed. But could the inflammation be due to something other than an excess of oxidants?
The body’s cells cannot survive without making both oxidants and antioxidants. “There is a delicate balance between the two,” Watson observes. In a cellular organ called the endoplasmic reticulum, hydrogen peroxide, a well-known ROS, helps forge chemical bonds, which stabilize proteins as they fold.
Watson suggests that when there is not enough oxidation in the endoplasmic reticulum, proteins emerge unfolded and cannot function. This, he proposes, causes the inflammation that harms the pancreas, sometimes causing type 2 diabetes.
Watson’s thinking is described by a press release issued by Cold Spring Harbor Laboratory, where Watson is chancellor emeritus: “Watson suggests [that] exercise, which promotes oxidation, plausibly can have a beneficial effect on those with high blood sugar. Such benefit would be lessened if not abolished, he speculates, if such an individual consumed large quantities of antioxidants—just as athletes who take large quantities of antioxidant supplements do not seem to benefit or benefit less from their exertions.”
The release indicates that Watson is planning a scientific meeting at Cold Spring Harbor Laboratory later this year, which he hopes will launch a larger scientific effort to investigate the mechanisms through which exercise improves health. “Just about every doctor I’ve ever known tells every patient who is capable of doing so to exercise,” notes Watson. “I think exercise helps us produce healthy, functional proteins. But we really need to have some high-quality research to demonstrate this.”