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Early life and obesity


More on cancer
James Watson Scientist
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And out of the metabolic thing, there's the interesting fact that people with diabetes get less cancer or type II diabetes, and that's because they inhibit or the - they activate or break down the glucose and an enzyme called AMP-kinase. When your ATP is depleted, your - you have more AMP. There's a kinase which is specific for it. And it turns off protein synthesis and leads - yes, as well as inhibits a pathway in the glycolytic pathway. So it stops glycolysis and the argument is you just don't want to go through cell division and fail because there's no ATP. So it's a sort of sensor as to whether you've got good supply. So the bad thing in diabetes is glucose breakdown and the bad thing in cancer is glucose breakdown. Then after I learned I had low grade prostate cancer, I read a paper that said people with cardiac glycosides who take - get less cancer. And that is very good data. And it's because it stabilizes these - stabilize the - or, that’s it. If you get cancer, you need - glycolysis has it - so destabilizes HIF, the cardiac glycoside, it's hypoxia inducing factor. And the figures were about 30% less cancer, which is sort of to me exciting because we can actually give mechanisms for these and they're non-steroidal anti-inflammatories require the HIFFA [unclear]. People- they stopped the test because, you know, Celebrex might be damaging, but I'm taking Celebrex now, just because I - it seems to be a sort of proven anti-cancer link. Now, whether that would mean I don't have to take the cardiac glycosides, but there's very little money being spent, no sense of urgency of really studying cancer prevention. In fact, sort of all cancer research sort of now, you know, I'd say no one works on Saturday or Sunday. You know, the initial war on cancer, you know, and sort of my New York Times article said we should restart the war. You know, it should be a 24-hour-a-day thing, if we were really, you know, responding to what the people of the world want. If we could do something, why aren't we doing it faster? And in part because you're - no one's going to make money by preventing cancer. You know, it could be inexpensive. But the diabetic medicine, 37 cents [unclear]. Conceivably, for $5 a day you could take a good, reduce your incidence of, well, by about maybe 50%. So, you know, that's possible. I just want some general to lead the cancer effort, you know, someone who thinks he might win and, you know, doesn't mind opposition. But we don't have a general yet. And you know, after my embarrassment when I said cancer was going to be cured in two years, they were wanting to make a public announcement that, you know, people could be - you know, are afraid to risk their reputations by saying that something can really happen and, you know, crying wolf when you can't do anything. But it'd be better to fail than do nothing. So - and you know, it's, you know, just as a matter - there's no newspaper, you know, writers who really know enough to handle the issue. You know, they can write with much greater assurance about what we should be doing in Afghanistan and you can have the pros and cons. But you never see a level of real discussion that we should be doing something or we shouldn't do it, which means we really suffer from the - not having people who can understand us. And - I mean, magazines like Nature could do it, but they don't, probably 'cause they don't want to be controversial. But you know, they could have a column by someone who, you know, the editor says he's bright but I don't agree with him. But we sort of have a belief that as scientists we should, you know, only say something when we're absolutely sure, rather than in a true life situation, you have a gut feeling maybe 80% you're going to succeed or, you know, you can sometimes see your chance of success at odds of a few percent, because of lack of knowledge. You know, you don't want to commit yourself. But I'd say, I would willingly risk losing with the thought that I could, that the odds are better than 50% I could have good results, you know, either in preventing cancer which is the best thing or in curing it once it comes into existence. Conceivably, you know, low doses of molecules that you would need to cure advance cancers, much lower doses would prevent them from ever coming into existence. But it takes a certain amount of guts to - but you know, Jonas Salk and Albert Sabin had guts. Yes, there've been failure before, so you know, they both wanted to be heroes. And I don’t think I wanted to be a hero. You know, I - because of the death of my uncle from melanoma, you know, early on I wanted to, you know, become a scientist and cure cancer. So, you know, I think it's just the horror of seeing other people suffer, not that you want the personal glory of doing it, but just to - you just don't like suffering.

American molecular biologist James Dewey Watson is probably best known for discovering the structure of DNA for which he was jointly awarded the 1962 Nobel Prize in Physiology or Medicine along with Francis Crick and Maurice Wilkins. His long career has seen him teaching at Harvard and Caltech, and taking over the directorship of Cold Spring Harbor Laboratory in New York. From 1988 to 1992, James Watson was head of the Human Genome Project at the National Institutes of Health. His current research focuses on the study of cancer.

Listeners: Walter Gratzer Martin Raff

Walter Gratzer is Emeritus Professor of Biophysical Chemistry at King's College London, and was for most of his research career a member of the scientific staff of the Medical Research Council. He is the author of several books on popular science. He was a Postdoctoral Fellow at Harvard and has known Jim Watson since that time

Martin Raff is a Canadian-born neurologist and research biologist who has made important contributions to immunology and cell development. He has a special interest in apoptosis, the phenomenon of cell death.



Listen to Martin Raff at Web of Stories



Duration: 9 minutes, 8 seconds

Date story recorded: November 2008 and October 2009

Date story went live: 18 June 2010