2009 Nobel Prize in Medicine: DNA, Chromosomes, Telomere and Chronic Stress, Aging Process, Meditation and Mind-Body Medicine
A NOTE ON THE ARTICLES ON THIS PAGE: Back to July 3, 2007, New Yerk Times published an article (read on this site) http://www.nytimes.com/2007/07/03/science/03conv.html in the science section, which was an interview conversation with Prof. Dr. Elizabeth H. Blackburn from the University of California, San Francisco, the woman awarded the 2009 Nobel Prize in Medicine, along with Dr. Carol Greider of the Johns Hopkins University School of Medicine and Dr. Jack Szostak of Harvard Medical School and Massachusetts General Hospital.
Inspiriting part of the conversation mentioned that Dr. Blackburn had been collaborated with psychologists in research on the effectiveness of stress reduction by meditation in the Chromosomes which related with aging process and modern diseases. Since then two years later, 2009 she received Medicine Nobel Prize because of this research achievement. An interview on the date of announcement of Nobel Prize, published on Nobel Prize organization website (read on this site): http://nobelprize.org/nobel_prizes/medicine/laureates/2009/blackburn-telephone.html
 This research implies that the mind-body medicine, its cultivation practice, or stress reduction practice, such as meditation, music therapy / sound healing, energy medicine, can improve healing and preventing diseases (e.g., cancer) and slowing down aging process. It seems that this is not only because of the psychological effects, but also because of association with biological and genetic processes; maintaining the telomere or preventing its shortening or loss of DNA from the chromosome end, to result in healing benefits and slowing down aging.
This strongly supports the concept of the unified relationship within the mind, body and spirit.
Another fantastic talk from Dr. Blackburn,
70 min video talk http://www.nar.uni-heidelberg.de/english/archive/colloq.html
Quoted from: http://www.mbbnet.umn.edu/doric/telomere.html
The enzyme telomerase "caps" the ends of chromosomes with a sequence of DNA (TTAGGG) that is repeated hundreds of times. These "telomeres" are believed to shorten with each division of the cell. Old cells have short telomeres. Because telomerase can rebuild telomeres, it may play a role as an "immortalizing enzyme." Animated image (c) the Geron Corporation. All rights reserved.
Declaration: All contents and images were taken from original web pages as mentioned; placement on this page is only for the convenience of MBMU faculty members and staffs or web visitors to read.
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A Conversation With Elizabeth H. Blackburn
Finding Clues to Aging in the Fraying Tips of Chromosomes
Published: July 3, 2007
http://www.nytimes.com/2007/07/03/science/03conv.html
When Time magazine named Elizabeth H. Blackburn, a cell biologist, one of this year’s “100 Most Influential People in the World,” it listed her age as 44.
“Don’t think I’m going to ask for a correction on that one,” Dr. Blackburn, 58, a biochemistry professor at the University of California, San Francisco, said in a recent visit to New York City. “If they want to turn back the clock, that’s lovely.”
Dr. Blackburn, a winner of the 2006 Albert Lasker Award for Basic Medical Research, studies aging and biochemical changes in cells that are related to the diseases of old age.
Whatever Dr. Blackburn’s own chronologic age, the buzz in scientific circles is that she is likely to be the next woman awarded the Nobel Prize in Medicine. |
Stress can have effects similar to aging in reducing an enzyme that keeps chromosome tips in shape. |
Q. What are telomeres and telomerase?
A. Telomeres are the protective caps at the ends of chromosomes in cells. Chromosomes carry the genetic information. Telomeres are buffers. They are like the tips of shoelaces. If you lose the tips, the ends start fraying.
Telomerase is an enzyme. In cells, it restores the length of the telomeres when they get worn. As the ends of the chromosomes wear down, the telomerase comes in and builds them back up.
In humans, the thing is that as we mature, our telomeres slowly wear down. So the question has always been: did that matter? Well, more and more, it seems like it matters.
Q. Is there a link between telomere length and stress?
A. In my lab, we’re finding that psychological stress actually ages cells, which can be seen when you measure the wearing down of the tips of the chromosomes, those telomeres.
A few years ago, Dr. Elissa Epel, a psychologist who studies chronic stress, came to see me. She asked, ‘Does stress have any effect on cell aging?’ There’s always been this observation that people under great stress appear to be care-worn. They look haggard, right?
So Elissa designed this study where we looked at two groups of mothers. One had normal, healthy children. The other group had a child with a chronic illness. Physiological and psychological measurements were done on everyone. With the stressed group, we found that the longer the mothers had been caring for their chronically ill child, the less their telomerase and the shorter their telomeres.
This was the first time you could clearly see cause and effect from a nongenetic influence. Genes play a role in telomerase levels, but this was not genes. This was something impacting the body that came from the outside and affecting its ability to repair itself. By the way, we found similar effects in women who were primary caregivers for partners with dementia.
Q. Is this scientific proof of the mind-body connection?
A. It’s a proof. There have been others. Researchers have found that the brain definitely sends nerves directly to organs of the immune system and not just to the heart and the lower gut. In that way, too, the brain is influencing the body.
One of the things that came out of our study of these mothers is a link between low telomerase and stress-related diseases. We looked at the measures for cardiovascular disease — bad lipid profiles, obesity, all that stuff. The women with those had low telomerase.
We also looked at low telomeres and cancer. We wondered if a cell with worn down chromosome tips might divide in some abnormal way. Our findings have yet to be published, so I can’t tell you much here, but we think we’re onto something.
Q. Is your goal to find a drug to repair the telomeres?
A. Or an intervention. We know that stress is bad for cells. What about alleviating it? We’ve been collaborating on studies looking at the telomerase levels in people who practice meditation. We are looking at whether or not telomerase changes after a three-month program of meditation. We’ll know more soon.
One of the really interesting things about doing research these days is how interdisciplinary it has become. A few years ago, I never thought that I would be collaborating with psychologists. Ten years ago, if you’d told me that I would be seriously thinking about meditation, I would have said one of us is loco.
Q. How did you develop this specialty: studying the ends of chromosomes?
A. In the 1970s, I did a Ph.D. with Fred Sanger in Cambridge who was in the process of inventing ways to map what’s inside DNA. He later won the Nobel Prize. In his lab, I noticed you could sequence — or map — the very ends of DNA molecules. However, this was still a difficult task because DNA strands are very long and with the limited technology that existed then, it was hard to locate the ends.
Later, I did a post-doc at Yale with Joe Gall, who had discovered a class of very tiny linear chromosomes in a type of single-celled protozoa. These creatures — they are pond scum, literally — had lovely, accessible chromosomes. And I thought, ‘Oh, wonderful. I’ll sequence these.’ And right away, I found these strange molecular features about their ends: telomeres.
Elizabeth H. Blackburn
The Nobel Prize in Physiology or Medicine 2009
Interview
"You want women to have access to science because it’s such a wonderful thing to do."
Telephone interview with Elizabeth H. Blackburn immediately following the announcement of the 2009 Nobel Prize in Physiology or Medicine, 5 October 2009. The interview was recorded on the morning of the announcement and the interviewer is Adam Smith, Editor-in-Chief of Nobelprize.org.
[Elizabeth Blackburn] Hello.
[Adam Smith] Good morning, may I speak to Elizabeth Blackburn please?
[EB] This is she speaking.
[AS] Hello, it's Adam Smith, calling from the Nobel Foundation web site.
[EB] Oh, yes. I was told to expect your call.
[AS] How nice. Thank you and congratulations.
[EB] Thank you.
[AS] It's terrifically early in the morning where you are, I guess?
[EB] Don't even tell me how early it is!
[AS] Had you managed to go to bed before they woke you up with the call?
[EB] Well, I had, yes. But, the night was definitely truncated – in a good way.
[AS] Indeed. I've just spoken to Carol Greider and Jack Szostak and to them I asked the same thing: you presumably had a suspicion that this was on the way, given the number of prizes that have been coming your way recently?
[EB] Well, there had been some press speculation which I had tried to ignore. But, believe me, it still was a very great surprise.
[AS] Now, the Prize has been awarded for research work you did mainly during the early 80s...
[EB] Right, right.
[AS] But, you've devoted your whole life to telomeres and I wanted to ask what was their particular fascination for you?
[EB] Well, so many aspects. First of all, just how does it work? Why are telomeres working the way they do? And, every time we looked with an experiment, we would find something ever more complicated and clever that the cell did. And, we realized the old truism from the original cytogenetics which was that the telomere is really important for protecting ends and, as you might expect, the cell actually devotes all sorts of machinery to make sure that never goes wrong, or goes wrong as little as possible. And so that intricacy, the machinery is really just a marvellous thing. And then in recent years it has become very interesting to look at what happens to telomeres in humans because they really do seem to reflect our status of heath and our risk of disease in quite a striking way that suggests that what one sees at telomeres gets integrated from a lot of different inputs but it really serves as a kind of indicator of how well cells are doing. So it's just been endlessly fascinating because the science of it is endlessly fascinating.
[AS] I want to turn to humans in a second. But, the original observations you just mentioned about the protective role of telomeres were made in the 30s by Muller and McClintock, for instance.
[EB] That's right, absolutely. And, we always have to remember that they worked from the deduction of genetics and cytogenetics with no knowledge that even the genetic material was DNA. And so, what my work had been doing was to first of all show the molecular nature of the telomeric DNA itself and then with Jack Szostak we were able to extend that and show that something strange was going on. And, then with Carol, that was when we worked together to hunt for this enzyme, or activity that we suspected existed, which was telomerase. So that put these cytogenetic observations onto a molecular footing. You know, before the telomere had sort of been the ‘blob' at the end of the chromosome.
[AS] Well, exactly. It had sort of lain there for decades, if you like. Known about, thought about, but nobody was particularly able to tease apart its function.
[EB] Right. Like so many things in science, it depended on first of all understanding what was the nature of the chromosome, which was DNA as well as proteins. And, then, thinking about, as Kornberg did, thinking about how DNA is replicated – not only thinking, he showed – and then that showed that there were problems with replication at the ends of chromosomes. And so that was one of the big impetuses for looking for telomerase, which was to try to see how the cells answer the question of how their incomplete replication problem gets solved.
[AS] In your sort of journey through telomeres, how much has been dependent on finding the right companions to work with? Because, for instance, you met Jack Szostak at a Gordon conference in 1980. Or, at least, you decided to collaborate then.
[EB] Right, right. Well, I think that's the way all science happens, right. And, I suppose there's an element of chance favors the prepared mind. But, that's the way science happens. It's a lot of meetings of minds and the concepts of telomeric DNA and the sequencing, well that was very dependent on the sequencing methodologies that were being worked out even before the now conventional methods of DNA sequencing happened. We didn't use those. I was using very unconventional methods to sequence the telemetric DNA originally. Methods devised by, for example, my husband John Sedat and Ed Ziff while we were in Cambridge in England.
[AS] That's right. Because you were post docs together with Fred Sanger, is that ...
[EB] I was a graduate student with Fred Sanger and John Sedat, who is now my husband, now, he was a post doc. So, everything builds on other technologies so I was building on ... I was curious about the ends of chromosomes and building on technologies, completely, which were methods of sequencing DNA and people like Ray Wu and Murrays in Edinburgh, all these people had been figuring out ways to sequence the very ends of chromosomes. So, it's a tremendous sort of interactive process, as I'm sure you have heard a thousand times!
[AS] But, it's nice to hear it described. Your current work is, as you said, fixed on humans and in particular on the relationship between chronic stress and telomerase ...
[EB] Yes, we're very interested in that. That's a corner of my lab. You know, we have part of our lab where we interact with clinical colleagues and one in particular at my institution, Elissa Epel, who was the person who first started to ask with us this question of chronic stress and how was it related to telomere maintenance? Actually, we still do a lot of basic research. We're still fascinated by those same questions you addressed earlier. You know, what is it that keeps you so interested in the telomere? It's so intricate and complicated and you want to know how it works. Actually, most of my lab does the very basic research. The chronic stress part, is to me, just fascinating though. Because it is really related to what a lot of humanity undergoes.
[AS] And, is it the case that telomere length and maintenance is affected directly by stress and is that, perhaps, causative of problems that then arise from stress? Or is it some kind of epiphenomenon?
[EB] There's two parts to the question. So, one is, the association of telomere shortness, and actually even poorly regulated telomerase we're finding, that association and chronic stress is very real. And, there are certain situations where our studies – and Elissa Epel has looked at cohorts of women who are caregivers of a chronically ill child, and more recently even dementia caregivers, where the dementia patient is their husband or partner – what we find is that it really does look causative. Particularly, in one study, the number of years that a mother had been in her situation was related to the extra telomere shortness and the dampening of telomerase. And, that made us really think that this is likely to be causative. Because, number of years relating to those parameters, it's very – number of years the person was in that stressful situation relating to those parameters being worse – it's very hard to imagine a scenario where it could work the other way round. That the shortness of the telomeres and the dampened telomerase was causing that mother to have been in that situation, one year, five years, twelve years, it doesn't logically follow. So that kind of evidence makes us think that there is a causality. Now, the question is, does that cause the bad, clinical effects of stress, which have been well-documented in the literature for years and years. Does the telomere shortening cause it? It's a plausible model actually. And, I'm inclined to think it does. But, you have to be very careful about what exactly is the complete mechanism by which these adverse effects of stress are mediated. But certainly we see the effects on telomere maintenance in the immune system which is, it turns out, a very good window into what's happening in terms of disease risks in the body. So we do think that there's a lot of good reason to think that it might actually be a causative chain.
[AS] And, so, your window into the immune system in that case is studying white blood cells. Is that correct?
[EB] That's the one that participants in studies give you and we now look at many, many different cohorts of various kinds. And, generally, we try to have a situation where the person is healthy so you're not confounded by disease. So, that means that healthy individuals are donating their blood samples for the studies. So, blood is one of the cell types one can look at.
[AS] I just wanted to ask you one last thing which was that it's been commented previously that telomerase and telomere research is a field which has, happily, a large number of women working in it. Do you agree with that and is that something that ...
[EB] Well, yes, and, I'll turn your comment around and say it's fairly close to the biological ratio of men and women. It's all the other fields that are aberrant.
[AS] Absolutely, yes.
[EB] So, this is the normal field, right? Because it is a much more even distribution between men and women, absolutely. No, I can't compare with other fields. You know, this is the one I know. But, it is true.
[AS] Yes, but is it something you think you have actively worked on promoting, to make it like that?
[EB] You know, I've only actively promoted what we always hope is good science. And, then it's not as if one would favor a woman researcher in the area over a man researcher in the area. But, women have come into this field perhaps because in the molecular days of the field, that is the kind of things that I've been doing and that Carol... we were women, we tended to have women students and post docs, which was not 100%. They tended to be 50-50, men and women, which is already a little higher than the usual ratios. And so there's a sort of self-perpetuating aspect to that. Because there's nothing particularly about the science per se which has any, sort of gender-like quality to it. You know what I'm saying? I think we're looking very much at sort of sociological phenomena here.
[AS] Yes, but one might hope that since it's seen to be possible in this field it could be possible in all fields.
[EB] You really do hope that when people see something like this working, that this could be seen as, that this would be, the norm. And, the different ratios of men and women researchers in other fields would be the aberrancy. That's what I'd like to see, because you want women to have access to science because it's such a wonderful thing to do. Anything that makes it more feasible for women to be in science and do the science they like, that's good.
[AS] Well, thank you, that's a good note to stop on for now. Thank you very much for giving us your time. When you come to Stockholm in December, then happily we have the chance to interview you at greater length.
[EB] Great, and hopefully, I'll be a little less sleepy!
[AS] Do you plan on trying to return to sleep tonight or is the day beginning?
[EB] Hmm. Well, I've made a couple of calls to the family and I might try and get a little sleep right now. That might be a good idea. It is after all three in the morning.
[AS] Well, good luck with it.
[EB] Nice to talk to you.
[AS] Thank you very much indeed, bye, bye.
[EB] Thank you, bye.
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