Coleen Murphy is the James A. Elkins Jr. Professor in the Life Sciences and Professor of Molecular Biology at Princeton and director of the Lewis-Sigler Institute for Integrative Genomics and the Paul F. Glenn Laboratories for Aging Research. Her lab studies the molecular mechanisms of aging.
Last year, Murphy published a book titled “How We Age: The Science of Longevity,” where she combines personal recounts of witnessing and contributing to landmark discoveries with a comprehensive overview of key areas of aging research.
Murphy sat down with The Daily Princetonian one year after her book’s publication to discuss her interest in aging, groundbreaking research in the field, and the future of longevity science. This transcript has been edited for clarity.
The Daily Princetonian: To start off, was there a particular moment in your career that sparked your passion for understanding aging? What motivated you to write “How We Age?”
Coleen Murphy: I remember when I was a junior in college, I took a class where it was the first time that I saw primary literature instead of a textbook, and it was really cool. That’s how I became interested in research.
When I started graduate school, I studied biochemistry. There, I heard a talk by Cynthia Kenyon, and I really liked this idea with aging that you could apply all the really hardcore, in-depth methods that I had learned how to do to this big, almost philosophical question of aging. And that’s what got me interested in the first place. And then [I] also [realized] that if you slow down the rate of aging, you could have an impact on a lot of age-related diseases.
Then, I taught a lot of classes at Princeton, and I finally got to teach a class on aging. We were looking at up-to-date studies in aging. That naturally sets you up for a really nice book, because then you can go into depth with all these topics. So not just the work that my lab does, but all these different things that the entire aging field does, so then we decided to publish it.
DP: Would you say that addressing aging itself can help prevent multiple diseases simultaneously?
CM: Yeah, that’s the idea, or at least slow it down, and the reason for that is that aging is the biggest risk factor for a whole host of diseases. So you have things like metabolic disorders, cardiac issues, neurodegenerative diseases, diabetes, and lots of cancers too. If we could slow down the rate of aging, we might at least slow down the onset of all these other things.
And there’s an important concept called the compression of morbidity — this is a concept that Jim Fries developed. The idea is that even if you didn’t make people live longer, if you could delay the onset of all these different diseases, you would have a compressed time when people are disabled. And so that is, I think, a good way to think about the efforts in the field to improve health span.
DP: This concept of “health span” has become an important focus in longevity research. Can you explain this concept?
CM: We’ve had this idea for a long time that if you could separate all these behaviors, there’s longevity, but then you can actually see if C. elegans [experimental worms] are healthy or not. For example, we know there’s some longevity mutants that live long, but they’re very unhealthy, like mitochondrial mutants, whereas the insulin receptor mutants do better in every regard. They’re long-lived, but they also maintain their functions really long. And they’re super healthy. For most people, it’s immediately obvious that they don’t just want to live longer, but they want to stay healthy as long as possible. Most research in the field is really interested in helping people live healthier for a longer time.
DP: In your book, you discuss the biological mechanisms that contribute to aging. What do you believe is the most promising recent discovery in the science of longevity?
CM: It’s exciting for me that I could say 10 things that are kind of all in parallel. So I don’t think there’s going to be one answer, one pill for everything. I think there’s going to be a lot of different approaches that are going to be used combinatorially to help people.
The other thing that is not in my book because it became popular after I submitted my book is GLP-1 agonist, used in drugs such as Ozempic. That is the longevity drug that nobody was looking for. It is helping people become much healthier, and I think that we keep finding all kinds of ways that it is good. That’s probably what I’m most excited to see how it shakes out and how it affects people. Decreasing obesity also helps with ulcer, metabolic disorders, cardiovascular disease, etc, and then it turns out it affects the brain as well, so it can help with conditions like addiction. So if you could decrease people’s addiction to smoking or alcohol or opioids, that would be a way to help people that is not directly related to aging, but it definitely could increase the average lifespan.
DP: How close are we to developing effective therapeutics or treatments for slowing human aging?
CM: Really close. I can think of right off the top of my head about eight biotechs that are moving research from academic findings to developing drugs that are going through clinical trials. I don’t want the field to go just in the direction of supplements, which are unregulated. I’m very excited about the biotechs that are taking the risk here. It’s a huge investment for them.
I could find a million things in my lab, but unless it gets to a point of actually going to be made into a drug, it is not really going to help anybody. And that’s the phase of the field right now, and I think it’s really exciting. Effective drugs are gonna come within the next decade, I think.
DP: As we make advancements in extending the human lifespan, what ethical challenges do you think we should be prepared to face?
CM: I think we see one right away, for example, with Alzheimer’s disease. A couple of years ago, there was a drug that was approved for Alzheimer’s disease against actually the recommendations of a lot of the panel that was doing it. The drug is super expensive, and it’s not clear it will work, so immediately it puts families in a weird position of having to decide for themselves what they do. Do they want to give their loved one who has this disease a really expensive drug that might not work at all? I don’t think that’s what we should be doing in the field. We really need to be in a situation where we’ve tested things, we know they work, and we know that they’re safe. I think that’s the biggest ethical concern.
DP: How has your own perception of growing older changed over the years?
CM: To be honest, the older I get, the less interested in aging research I get. I know this is the opposite of most people, but I do think that there’s a lot of other very interesting and pressing problems that we need to work on. I do want to make sure that I have some positive impact on the world, and there’s a lot of different ways to do that. I think, for example, there’s no point in living a long time if there’s not a planet to live on. So we need to make sure that we’re addressing the climate crisis.
DP: Are there specific lifestyle changes or interventions from your research that people can adopt now to slow the aging process?
CM: The good advice for everyone is to exercise. That’s really good for you. For undergrads, everybody should try to get more sleep, even when you feel like there isn’t enough time to do that. Oh! And stress is not great for you.
Mahya Fazel-Zarandi is a senior News contributor for the ‘Prince.’
Please send any corrections to corrections[at]dailyprincetonian.com.
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