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Elizabeth Blackburn’s latest quest: to save scientific research

Her study of pond scum unlocked the secrets of ageing and won her a Nobel. Now Elizabeth Blackburn is on a bold new mission.

Elizabeth Blackburn. Picture: Boris Zharkov
Elizabeth Blackburn. Picture: Boris Zharkov

It was a book gathering dust on a shelf in her home in Launceston, Tasmania, that caught her eye. Elizabeth Blackburn was young, barely a teenager, when she studied the cover and opened it up. It was the story of Marie Curie, the Polish-born physicist who discovered radium and won Nobel prizes in 1903 and 1911. “That book had such an impact on me,” she recalls about a tale laced with triumph and tragedy. Curie was a brilliant and trailblazing scientist who faced opposition from her male counterparts, was never rewarded financially for her work and died from leukaemia caused by her research. “She was so down to earth but she made science sound like such a noble quest,” says Blackburn. “And she was a woman.”

As the young Blackburn devoured the book, she stumbled upon a quote from Curie that struck her with the force of a freight train. She recites it today: “Nothing in life is to be feared, it is only to be understood.” More than five decades on, ­Blackburn has tried her best to understand the world rather than fear it. The scientist has taken on a US president, pioneered a path for female ­scientists and received the highest honour in ­science for unlocking one of nature’s greatest secrets: how to slow down ageing.

One night 10 years ago, when the phone rang past midnight, she feared it was bad family news. Instead it was the Nobel committee calling to inform her that she was being awarded the Nobel prize in Medicine, making her Australia’s first (and only) female Nobel laureate. Then Blackburn did something else unexpected: she wrote a book for non-scientists about her discoveries, highlighting the link between ­biology, stress and ageing, and what you can do about it.

The book, The Telomere Effect: The New Science of Living Younger, co-authored with ­psychologist Elissa Epel, says: “Ageing need not be, as thought for so long, a one-way slippery slope towards infirmity and decay. Ageing and death are immutable facts of life but how we live until our last day is not. This is up to us. The relatively new field of ­telomere ­science… can help us reach this goal.”

“The book became a New York Times bestseller almost immediately,” Blackburn says, as if genuinely surprised that ordinary people want to read about her work. “People sometimes recognise me at the bus stop now,” she laughs. “They say, ‘Are you Elizabeth Blackburn?’ and then they talk to me about ageing and about stress and health. It’s amazing.”

Now 70, Blackburn sits in the lounge room of herhome in San Francisco pondering some of the twists and turns of a rich life. She has neat grey-blonde hair and is dressed all in white except for a blue shirt, making the large black Fitbit on her wrist stand out. It is an accessory she bought once she realised her discoveries might help slow down her own ageing. “I pander to it,” she says, speaking directly to her device as if it were a person. “It tells me when to get up, it monitors what I do, my sleep. It doesn’t like me much right now because I’m sitting for too long talking to you.” She speaks in an Australian accent tinged with an international flavour after years of living in the US.

Her house, which she shares with her husband and fellow scientist John Sedat, sits high on a hill overlooking the water. It is crowded with art from Japan, Central Asia, Africa and Europe, garnered from a life of scientific conventions and global travel.

Blackburn’s long journey from a childhood in Launceston to Nobel laureate has been driven at every turn by her dominant personality trait – curiosity. “Liz is someone who emanates positivity,” says her co-author Epel, who has worked with Blackburn for almost 20 years and written more than 100 academic papers with her. “She is serious and grounded but she is also bubbly and very open to new ideas and incredibly curious. She was one of the earliest scientists – and one of the few geneticists – to say, ‘Wow, our health is determined so much more by environment than by our genes’. To hear that from a scientist who has been studying genetics and cells is very powerful and very compelling. People listen.”

Elizabeth Blackburn in 1965.
Elizabeth Blackburn in 1965.

One of seven children born to parents who wereboth family doctors, Blackburn moved from Hobart to Launceston when she was four and became obsessed with animals. “I loved animals and when you are a little kid you pick things up and play with them. We had all sorts of pets… budgies, dogs, cats, chickens, rabbits and goldfish. But I also picked up stinging jellyfish, bull ants and other dangerous things and my mother claimed I would sing to them.” Her love of ­animals, her ­parents’ medical background and the ghost of her heroine Marie Curie saw her ­gravitate to the sciences. It wasn’t always an easy childhood. Her father drank heavily and her ­parents separated. Her mother, who suffered from sometimes severe depression, took all the children to Melbourne when Elizabeth was 16.

In the midst of all this Blackburn found refuge in her schoolbooks. She attended The University High School in Parkville and then obtained a ­masters in biochemistry at the University of ­Melbourne before completing her PhD at the ­University of Cambridge. It was there that she met the man she would marry, John Sedat, an ­American scientist who was also doing his PhD.

Blackburn with her husband, John Sedat, at their home in San Francisco in 2009 after her Nobel prize win. Picture: AP
Blackburn with her husband, John Sedat, at their home in San Francisco in 2009 after her Nobel prize win. Picture: AP

Blackburn recounts her life story in a ­scientific manner, rarely pausing to describe the emotion of life-changing events but rather describing them as if they were a series of unique experiments. When asked what attracted her to Sedat, she replies: “Well, he was a scientist and I guess he approached me. We started going out and that worked. We are still going out.”

She followed Sedat to Yale, where she made the first of three major discoveries that have reshaped the science of ageing. For her postdoctoral work she studied what is commonly known as “pond scum” – a single-cell organism called tetra­hymena. She describes the organism as if it were her pet, saying it is “almost adorable” with its “plump little body and hairlike projections that make it look like a fuzzy cartoon creature”.

Working in the Yale laboratory of her mentor Dr Joseph Gall, she uncovered the molecular structure of the telomere, the region at the end of the chromosome that prevents it from disintegration as the cell reproduces. Blackburn describes telomeres as akin to the plastic tip of a shoelace that keeps our genetic material from unravelling and leading to disease and premature ageing. She found that these “plastic tips” shorten with each cell division, leading to the ageing of cells and their eventual death. As they wear down and shorten, the risk of diseases of ageing – such as heart disease, diabetes, cancer and a weakened immune system – increases. Blackburn wrote the landmark paper in 1978 on this causal link between telomeres and ageing.

Computer-generated image of telomeres, the ‘caps’ at the end of DNA strands.
Computer-generated image of telomeres, the ‘caps’ at the end of DNA strands.

She then moved to San Francisco with Sedat to continue her studies on telomeres at the University of California, Berkeley. Although she still loves Australia and returns each year, she says that at that time she thought a woman had a better chance of a successful scientific career in the US than in Australia or England where the “culture” towards women scientists was less progressive. “I didn’t think the opportunities to do science were the same in Australia as in the US,” she says. “In Australia I had not felt that I was very encouraged in my work and I thought there was too much uphill in Australia. This was the late ’70s.”

It was in California that Blackburn made her second major discovery. From her pond scum work she’d figured out that tetrahymena cells never died; their telomeres didn’t shorten over time and sometimes they got longer. “Something else was at work, and that something was not in any textbook.” It suggested there was an unknown enzyme that helped to regulate the length of the telomere and control the pace of the ageing of cells. Somehow, in some healthy cells, the ­telomeres were actually being rebuilt.

Blackburn recruited a recent biology graduate, Carol Greider, and they toiled away for many months to try to identify this mysterious enzyme and determine whether it existed at all. Then, on Christmas Day 1985, Greider went into the ­laboratory to check the results of their ­latest experiment and noticed a pattern. “Carol’s mum was dead and her father had remarried so she was in the laboratory on Christmas morning,” recalls Blackburn. “She told me to come and look at this and when we both saw it we said, ‘Ah ha. I had a feeling that this was big’.”

They had discovered an enzyme, which they called telomerase, which in some cases made the telomeres longer rather than shorter, potentially reversing the ageing process. When the pond scum’s telomerase were removed, their telomeres diminished and they died. It was a bombshell ­discovery that held the scientific community in thrall and led some overeager journalists to claim it would to open the door to reversing the ageing process or even curing cancer.

But Blackburn and Greider quickly discovered that – as Blackburn says in the book – “telomerase have a dark side; think of Dr Jekyll and Mr Hyde”. They found that a certain amount of telomerase is needed to keep telomeres healthy and slow ageing, but too much telomerase fuels the kind of uncontrolled cell growth that is the hallmark of cancer.

Blackburn shared her 2009 Nobel prize with Greider and Jack Szostak, who jointly proved with Blackburn in 1982 that the telomeres’ DNA prevents chromosomes from being broken down. The Nobel committee said their discoveries “added a new dimension to our understanding of the cell, shed light on disease mechanisms and stimulated the development of potential new therapies”. The prize was a significant moment but ­perhaps the most remarkable chapter in Blackburn’s life – one that took her from the laboratory into the lives of ordinary people – was about to unfold.

Elizabeth Blackburn and Elissa Epel. Picture: Digital Vision
Elizabeth Blackburn and Elissa Epel. Picture: Digital Vision

In 2000, she received a series of emails from ­a US psychologist, Elissa Epel, who was doing post­doctoral studies in health psychology at UCSF and had heard of Blackburn’s work on ageing. Epel was investigating links between stress and coping and was studying ­mothers of children with chronic conditions. She wanted to ask Blackburn a simple question. Should they try to test the telomeres and telomerase of these mothers who were under ­prolonged psychological stress, to see if their ­telomeres were shortening? “I had to pursue Liz – she was already very famous so it was not just one email to her. I was very persistent,” recalls Epel. “For me it was a logical step to see how stress can promote biological ageing even in young people. Liz responded by saying, ‘Anything is possible. I am convinced by data so I will believe it when I see it’.”

Blackburn says Epel’s idea changed her world, leading her to look at the telomere issue through the real-life lenses of stress and pressure. “I suddenly saw telomeres from a whole new viewpoint, from a completely different mountain. She [Epel] was interested in ageing, in how people famously get haggard when they are under long stressful ­situations,” says Blackburn. “It was a great question – it was so simple but no one had asked it.”

By this stage Blackburn was a mother, ­having given birth to her only child Benjamin in 1986. She says she also wanted to do the study because she felt for the women in it. Epel and Blackburn worked together to carefully select mothers of chronically ill children and mothers of healthy children and monitor and compare their telomeres. It would be four years until the results arrived.

Elizabeth Blackburn. Picture: Boris Zharkov
Elizabeth Blackburn. Picture: Boris Zharkov

While Blackburn was conducting that experiment she found herself thrust into the spotlight of an explosive debate in the US over the ethics of stem cell research. In 2001 she accepted an ­invitation from then US president George W. Bush to serve on the President’s Council on Bioethics, whose role was “to monitor stem-cell research” and consider “all of the medical and ethical ramifications of biomedical innovation”. Blackburn supported human embryonic stem cell research, a practice Bush and the religious right opposed. But Bush wanted all views represented on the 18-member council, even if hers was a minority view in that forum. “I knew it would be a challenge,” she says. “But when I got the call to serve on the council I thought it would be good because it would help them to have science inform the policy. But my eyes were also open, I knew the context in which this [council] had been formed.”

Blackburn is not religious, although she grew up with the Church of England. “I don’t think there is some non-physical reality but I think there is something in humans that really wants some bigger something or other and I sympathise with that, I get it. We want a thing that is bigger than us.”

Blackburn served on the council but described herself as “a nag” on embryonic stem cell research. “I kept nagging and saying, ‘We’ve got to get the ­science right, if you have a policy you have to base it on the science’. My whole career has been about getting the science right.” By early 2004, she had become increasingly frustrated that politics was trumping science on the council. She protested that parts of its reports on stem-cell research and reproductive technologies had misrepresented scientific facts. Later she published her concerns, saying the reports wrongly implied that “designer babies” – the notion of selecting embryos for ­specific intelligence, or traits of temperament – would happen and was imminent. She also slammed the council for implying research into curing age-related disease would lead people to have “a lifelong obsession with immortality”.

In February 2004, she received a call from “a polite person who said, ‘I am calling from the White House’. I presumed he was calling to renew [my position] but instead he said, ‘Thank you for your service’. He was discontinuing me.”

Blackburn’s abrupt removal from the council for opposing what she believed were its politically motivated findings triggered uproar in the scientific community. More than 170 researchers across the country signed an open letter to the president protesting the decision and accusing the administration of allowing politics to trump science.

The following month, Blackburn received far better news. “I got a call from Elissa, who said: ‘Guess what?’ ” Epel says she will never forget the moment that the data from their study on stressed mothers inched out of the printer in her San ­Francisco office. “I could see from the printout that there was a relationship between feelings of stress and the length of one’s telomeres. My heart started racing so I immediately called Liz and said, ‘We are onto something.’ ”

What they found was a clear correlation. The longer the mother had been in this stressful care­giving situation, regardless of her age, the shorter were her telomeres. “And the more she perceived her situation as being more stressful, the lower was her telomerase and the shorter were her telomeres.” In other words, life experiences could change the length of someone’s telomeres. It followed, therefore, that humans could change the way they age at a cellular level depending on the life they lead.

Word quickly spread of the findings and in 2007 Time magazine hailed Blackburn as one of its “100 most influential people”. Their work ­triggered a blizzard of other studies, including by Blackburn and Epel, to test how life factors and choices affect telomeres. The studies found that lifestyles, attitude, fitness and happiness can lengthen or maintain the length of telomeres, slowing down the ageing process and age-related illnesses. “This is what really grabbed people’s attention,” says Blackburn. “Especially the issue of stress. I think a lot of women now feel, ‘Oh, I am being taken seriously because there is a serious molecular measure’ whereas previously it was like, ‘It’s psychosomatic, go home’. ”

Studies have since found correlations between telomere length and happy relationships, with divorced couples having significantly shorter telomeres than couples in healthy relationships. Shorter telomeres have also been found in people who are routinely pessimistic, who have eating disorders or post-traumatic stress disorder. Children who have had traumatic childhoods and even those who have grown up in dangerous neighbourhoods have been found to have shorter telomeres.

Blackburn does not claim you can increase life expectancy by better managing your telomeres; rather, you can delay your entry into the “disease span” from the “health span” of our lives. In other words, you can enjoy quality of life for longer as you age. Some researchers contend these links are overblown and that there is so much variation in everyone’s telomeres that it is difficult to draw firm conclusions. Others ask, what is new given that we already know we are healthier if we exercise, eat and sleep well, stay positive and reduce stress?

The key, responds Blackburn, is that we now know the biological reason that underpins the mind-body connection. This gives us an important understanding of how much control we have in the way we age. She says people often ask her how they should change their lives to better protect their telomeres. “I say, ‘Just do as your mother told you’ because all we have done is quantify that – eat well, have a good night’s sleep and a good attitude and a healthy social network.”

Blackburn says her findings have forced her to alter the way she lives. “I have definitely changed my life,” she says, beyond just wearing her Fitbit. She walks to work, does meditation and tries not to sweat the small stuff. “I also stopped multi- tasking, trying to do 50 things at once,” she says. “Now I just do one thing at a time and, shock ­horror, it is so much more effective.”

Epel says she and Blackburn decided to write the book, published in 2017, to bring the story together for the first time. “In the last 10 years telomere research has exploded all over the world and we thought there was one big story to be told from all the pieces of these studies,” Epel says. “We felt the telomere story was one of hope because we can’t change our genes but our ­telomeres are malleable – they are influenced by our living conditions, by our environment and by our behaviour. Some people are really motivated when they learn about it and they change the way they live their lives.”

Winning the Nobel prize made Blackburn’s already crowded life even busier but she knows that being a Nobel laureate gives her a unique megaphone and she is determined to use it for good. “I have stopped to think about what I can do now at this stage of my life that would make a ­difference,” she says. So she has taken up a new cause. “What I am interested in now is a global pact for science research. Should we have a ­Paris-like agreement where we can all support ­sustained ­science research internationally? What goes on in terms of science policy really matters.”

Blackburn says such a pact is needed today because governments wax and wane on scientific funding depending on political circumstance, ­giving no certainty to ongoing research. “Science is in danger because of the political winds,” she says. “Look at Brexit. There has been wonderful back and forth between science in the United Kingdom and the European Union and now Brexit has come along.” Politicians such as ­Donald Trump are another reason for such a pact. “Trump is not a friend of science,” she says of the president, who has backed deep cuts to ­science funding. “He is just pandering to whatever base he thinks will get him elected.”

Last year Blackburn presented her preliminary ideas on a global science framework at several international forums and received an enthusiastic response. She talks about HIV as a perfect example of how drugs to combat the disease were only developed after years of research. “Years of ­prolonged research paid off on HIV but we don’t know what is going to happen next [in the world].”

She is working with other scientists to draft a historic agreement on the topic called the “Lindau Declaration 2020”, which she hopes will be adopted at the group’s meeting next year. Under the plan, wealthy countries could contribute finds and resources to a global science initiative while poorer countries could contribute talented individuals. “The advocacy side is very new to me,” she says of her quest. “But a basic human right is access to knowledge. This [pact] would help to keep the basic sciences alive and accessible to everyone.”

Blackburn says every young woman should have the chance to delve into pond scum like she did and try to unlock the secrets of science. “Not to boast, but if I had not gone into science maybe some things wouldn’t have happened. We haven’t figured it all out. We have only figured out enough to know how much we don’t know.”

Cameron Stewart
Cameron StewartChief International Correspondent

Cameron Stewart is the Chief International Correspondent at The Australian, combining investigative reporting on foreign affairs, defence and national security with feature writing for the Weekend Australian Magazine. He was previously the paper's Washington Correspondent covering North America from 2017 until early 2021. He was also the New York correspondent during the late 1990s. Cameron is a former winner of the Graham Perkin Award for Australian Journalist of the Year.

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Original URL: https://www.theaustralian.com.au/weekend-australian-magazine/elizabeth-blackburns-latest-quest-to-save-scientific-research/news-story/24836e0e4f001eda362cb2e52ad3b9f8