Speaking of Psychology - Why do some of us age faster than others? With Terrie Moffitt, PhD

Episode Date: January 15, 2025

The Dunedin Multidisciplinary Health and Development Study has been tracking the health and life experiences of more than 1,000 New Zealanders since 1972. Terrie Moffitt, PhD, a professor of psychology at Duke University and one of the leaders of the Dunedin study, discusses what researchers have learned from this remarkable study about how people age, why some of us age faster than others, and how our genes and life experiences shape our physical and mental health and the aging process. Learn more about your ad choices. Visit megaphone.fm/adchoices

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You talking to me? Kayak, got that right. More than 50 years ago, in 1972, researchers in Dunedin, New Zealand began an ambitious study. They enrolled every baby born in the city that year, more than 1,000 babies in all, in a study designed to learn more about childhood health and development. Remarkably, that study is still going on. As the participants have moved from babyhood to childhood to adulthood, data from the Dunedin study has led to more than 1,400 research papers

that have examined how people's genetics and life experiences shape their lives. Now, as the participants enter middle age, the researchers have turned their attention to the next life stage, aging. Today we're going to talk to a psychologist who's helped lead the Dunedin's study for nearly four decades about what researchers are learning about how we age, why some people age faster or slower than others, and how early intervention might help forestall some of the challenges that come with growing older. Welcome to Speaking of Psychology, the flagship podcast of the American Psychological Association

that examines the links between psychological science and everyday life. I'm Kim Mills. My guest today is Dr. Terry Moffitt, the Associate Director of the Dunedin Longitudinal Study, which she joined in 1986. She's also the Nancohean University Professor of Psychology at Duke University and Professor of Social Development at King's College London. Dr. Moffett has wide-ranging expertise in longitudinal methods, developmental theory, clinical mental health research, neuropsychology, and genomics in behavioral science.

Now her work is uncovering the consequences of a lifetime of mental and behavioral disorder on processes of aging. Dr. Moffat is the author of hundreds of scientific papers and has received many awards for her work, including APA's Early Career Contribution Award and Distinguished Career Award. She's a fellow of the British Academy, the Academy of Medical Sciences in the UK, and the National Academy of Medicine. Dr. Moffat, thank you for joining me today. Good to see you, Kim. So we're going to talk mainly about aging today, but I wanted to start by asking you to tell us a little more about your work over the years with the Dunedin study,

which you originally joined when the participants were teenagers. How did you get involved with this study and what were you interested in then? Oh, that's a great question. a historical one. I got involved with the Dunedin study fresh out of graduate school. All my friends said, don't go to New Zealand, you'll disappear. But the data were there. It was a wonderful longitudinal study.

And the team at the University of Otago invited me to collect data to my heart's content. They've been a wonderful group to collaborate with over the years. I can't say anything better about my colleagues. collaborators at Otago. So the study has gathered an amazing amount and variety of information about the participants over the years. Can you tell us something about the data that's been collected and what are some of the most interesting findings that have come out of it? Let's see. With the Denise study, you know, when I first joined, I was interested in, the reason for going there was to really study how teenagers got involved in delinquency and drug use

and risky sex and other tricky things that young people do when they're teenagers. and most importantly, to keep following the cohort as they grew out of that. So to see what happened that helped people leave crime behind and become good upstanding stivis. But what happened is that they did leave crime behind and they outgrew it. And I'm still working with the Dunedin cohort 35 years later, but we needed to really keep up with what was happening to the study members. And what started to be really the most important thing in their life was aging. So they're reaching midlife. They're concerned about the rest of their lives and so that we had to keep up with them. Is that common to leave crime behind? Do you really outgrow it in some cases? Most people who participate in crime when they

are teenagers do leave it behind in their 20s. They get the things that criminologists tell us and psychologists tell us are great for leaving crime behind. That is a good partner and a good job. So that's a normal developmental stage. There are, of course, a few adolescent delinquent offenders who aren't able to leave crime behind and who end up sinking further and further into an antisocial lifestyle. And in their case, we found that they, as they grow older, they can also get partners. They can also get jobs, but they tend to bring their antisocial behavior with them to those new situations. And so they will be getting involved in intimate partner violence. They'll be getting involved in work time. So it's been very interesting

to follow those young people as they've grown up, but they are a small, small number. How unusual is this study? Are there others like it that have studied so many participants for such a long period of time? There are a lot of cohort studies that are going on around the world, primarily in Britain, Canada, Scandinavia, now more new ones. starting up in the United States. Some are much, much bigger. Some have been going on much longer, some of the ones in Britain. But the thing about the Dunedin study, what makes it really special is the depth and breadth of the data collection. So in our study, all of the participants come into the clinic and get a day-long, in-depth clinical assessment by professional clinicians. So that's

quite different than taking part in a longitudinal, say, telephone survey or online survey. This is kind of a nuts and bolts question, but how is something like that funded over such a long period of time? Who is paying all of the money that's gone into the Dunedin study? The funding has to be renewed every five years, and there's always a mad scramble. Luckily, writing proposals is something I really love to do. It was a bit strange, but I do love it. And my collaborators in New Zealand write proposals to the New Zealand Health Research Council and the Ministry of Business and Industry. And I write proposals to the National Institute on Aging in the United States and the Medical Research Council in Britain. So those are our main funders,

and they all sort of collaborate with each other to make sure that their money goes for the topics that they're most interested in. Let's talk about the most recent focus of the study, which is aging. have developed a test called Dunedin Pace, which measures the rate of people's biological aging. Tell us more about what that means. What's biological aging? How does the test work? So one of the important things to think about biological aging is quite obvious. It's different from chronological aging. So you can have a group of people, as we have all of the Dunedin study members born in 1972, 73, they're all exactly the same age, but their biological age can range, you know, 10 or 15 years around their chronological age.

Some people are growing old very fast as compared to their peers in the cohort. Some people are growing old much more slowly and retaining their youthful vigor. So we were interested in being able to measure that. We set about doing it by using our longitudinal data, longitudinal approach, and I'll go into a bit of depth because that's really what sets our approach apart from all the other ways of measuring aging that you might be hearing of out there. So we measured the study members, 19 biomarkers tracking their organ systems, say their heart, their lungs, their teeth even, all over the body, the function of the kidneys, inflammation, their immune system. We tracked those biomarkers by drawing them at age 26, age 32, age 38, and age 45. So over 20 years, and now we're topping it up at age 52 this year, over 20 years we have a record of how each study member's biology and biological organ function has declined over the entire body.

That gives us then the capacity to track for each individual person whether they are aging faster biologically or slower biologically than the average typical person. So we have inherent norms. Psychologists understand that, and that's very important. That's what makes the measure really special. You will hear of many, many, many different aging clocks out there. It's been the holy grail to try to find how to measure age. The last five years, the research has really gotten very exciting and blown up,

and there have been lots of different clocks that are published. What says to the end pace apart from all the others is it is longitudinal. It really tracks actual change over time. All of the others, so far, are based on cross-sectional data. So they may predict mortality. They may have, they use information about smoking. They may use information about art function. They may use proteomics and other kinds of exciting omics.

But if they are based on one cross-sectional piece of data taken at one point in time, they don't actually document that a person is aging. I'm curious about how you determine all of this. So like do I, like a 23 and Me type of test where you spit in a test tube, I mean, how do you determine the age of somebody's biological systems? Right. Well, we had our model that we had built with the data from the 1,000 Daneden study members by tracking them through time by testing their biomarkers. That was great, but nobody else could do that. So like your doctor won't be able to do it when you go into a clinic. Other researchers couldn't even do it if they didn't have 20 years of longitudinal data. They wouldn't be able to actually just replicate our findings.

and we know replication is so important in psychology research. So what we had to do was we had to turn this model of individual differences among people in how fast or slow they're aging into something that can be done in a single blood test. So that's where the Dunedin-Pace idea comes in. What you do is we obtain DNA from every Denetan study member, all 1,000 study members. we subjected it to DNA methylation array. So those are the epigenetic marks that are on top of your genes. And those epigenetic marks change with age.

So we were able to then link those marks, identify the ones that best characterize people in the Dunedin cohort who were either aging fast or slow, and then use those to create a measure that if you have someone's DNA and you have a, you can just look at it and you can see very swiftly whether they're aging fast or slow. So that allowed us to export it so that other research teams, all they needed was a bit of blood to get the DNA. And it's been offered direct to consumer. So even individuals can obtain this test. And you just prick your finger, you get a drop of blood that goes onto a little

piece of filter paper and then you dry the filter paper and you send it in to the lab for the assay. Do people's biological systems tend to age in the same way at the same time or can your body be kind of all over the place where one organ is this age and another organ is older and so forth? This one is tricky because the field of geroscience says its theory is that what makes aging different from just having a disease. How do you know, like if your biomarker, if you're, say, HBA1C is elevated or your cholesterol is elevated, some kind of biomarker is elevated, your inflammation is elevated, how do you know whether that's because you just right now have a disease or are we tapping into your aging? Well, one way we know is we track it longitudinally,

and that helps us to determine whether someone is just sick at the moment or whether they're on a fast aging trajectory. If you have elevated biomarkers at one point in time, but you didn't have higher scores before and lower scores after, then you're not following a trajectory of aging. And it needs to be with all of your organ systems following the same trajectory, which is what makes it the whole body is aging. As opposed, let's say that all of your other biomarkers were normal

and just the only the inflammation one was raised, or only the respiratory one would raise. But that would tell us nothing about aging. It would tell us you probably have COVID. So what are some of the other factors that influence one's biological age? There are lots of different things turning up in the literature. And in fact, since we published the Demitin piece and put it on the algorithm on GitHub so that other researchers could use it, There've been over 160 publications from other teams, and they've shown all kinds of interesting things. So one of the things that influences how fast you're aging is obvious. All of your listeners can easily guess that's smoking.

So nothing exciting and new there. But we've also seen papers that are reporting that, let's say from the Health and Retirement study reporting that people who were in infant development during the Great Depression, those whose families were the poorest, now that they are in their 60s and 70s, they're aging the fastest. So there can be quite long-term effects, and a lot of the effects that we're seeing are from childhood adversity. There are also some papers that are reporting influences on the pace of aging from racial being a recipient of racial discrimination, so that kind of current intense stressor can also accelerate the pace of aging. No one goes to Hank's for his spreadsheets. They go for a darn good pizza. Lately, though, the shop's been quiet.

So Hank decides to bring back the $1 slice. He asks co-pilot in Microsoft Excel to look at his sales and costs. Help him see if he can afford it. Co-pilot shows Hank where the money's going and which little extras make the dollar. slice work. Now, Hank has a line out the door. Hank makes the pizza. Co-Pilot handles the spreadsheets. Learn more at M365 copilot.com slash work. Do you give all of that information to the study participants? Do they know what their biological ages are? Or would that influence the outcome? Yeah, Daneden's study participants are quite awesome and amazing 1,000 people. When they first began this study years and years ago, of course, their parents signed, them up. But the agreement at the time was that this would be a study of natural development

with no intervention and the research team would not be given feedback. Now, we do give feedback, of course, if someone is in danger, if their life is in danger. But if so long as it's not an unusual danger to life and limb, we don't typically give feedback. And the study members get that. They really understand the value of having a study of natural development. So they're hugely patient with us and very generous. So if I take a home test and I discover that my biological and chronological ages are out of sync, what can I do to put them in sync? Well, this is another thing that's coming out in the literature.

A lot of different papers starting to come out showing, you know, of course there are people in the longevity industry who are really keen on find, drugs and medications that people could take to slow their aging. But there are also health behaviors that you can do. So one of the things you can do is, you know, join a gym, lose weight, control your sleep. So there's a lot of different experimental studies that are using the Dunditin Pace-of-Aging measure as their outcome, giving it before the experimental intervention, and then taking it again after and to test whether people are able to slow their aging. One of the most famous of these studies is the calorie study in which participants in the trial arm,

the intervention arm, agreed to eat less than 1,800 calories a day for two years. And awesomely, they were able to do that. I'm not sure if I could, but they did and they were able to slow their pace of aging as compared to the people who were, were allowed to just eat whatever they wanted. What are some of the ways that this information is being used now? I mean, how are you applying the aging research to the public at large? What my team is doing is we are making sure that the measure, you know, it was developed in white New Zealanders.

Let's just say that. So one really big question that was out there for us and for everyone else in the field, too is would it work for Asian Americans, African Americans, Hispanic Americans, people of all different kinds of groups in the population? So systematically, we've been going through and finding datasets that have participants from different ethnic groups. And other teams have been doing that too. So for example, the Danin Pace has been applied in the Taiwanese bio bank of Chinese. So some very huge samples of people in different ethnic groups. So far, it's still predicting everything it should predict. It's predicting future disease risk. It's predicting dementia. It's predicting early mortality.

And it's related to factors such as childhood adversity and health behaviors in the different ethnic groups. You mentioned early on that you got involved in this study because you were looking at criminal behavior over time. And I'm wondering, what else has the Dunedin study looked at besides that and now aging? The Dunedin study has, its full name is the Dunedin Multidisciplinary Health and Development Study. That's a mouthful. But the multidisciplinary part helps to explain why the study members have to stay at the clinic for an eight-hour day. Then they sleep overnight and they return the following morning and they have a brain scan. So there's a whole neuroimaging, behavioral neuroimaging part to the study that's directed by Amad Hariri and myself. But there's a team that studies injury.

There's a team that studies respiratory medicine, asthma, allergies, lung capacity. There's a team that studies vision. There's a team that studies hearing. There's a team that studies cardiovascular health. So it really is a whole group of teams that get together. And some of them are based in New Zealand. Some are based in the United States. Historically, one of the respiratory teams was in Canada, but now they're in New Zealand.

So it's an international study, but also covering all the different aspects of life, really. And I should say also there's neuropsychological testing that takes place for a very large neuropsychological test battery, a mental health, standard diagnostic interview, and interviews about family life, work life, relationships with family members. So it's a very exhausting day. When the study members check in at 8 and they don't leave until 530, the last thing they do is give blood, they're really, really tired. And how have you managed to keep in touch with so many of them for so many years. Yeah, this is something that the team at the University of Otago in New Zealand is just awesome at. They have built up trust, faith, respect, mutual respect with the study members

over the many years of the study. We have extensive records because every time a study member comes into to take part, they give us contact information for family and friends who could help us find them next time. So they're they're keen to be found if they've moved overseas or something like that. And they help us out with that. The study is really, you know, a jewel in the crown of New Zealand science. People there are super proud of it, super proud to be part of it. And they refer to themselves as anonymously famous because we have kept their confidentiality all these years. never reveal even who's in the study. So that's kind of interesting. It's a small country, but we've been able to keep their confidentiality. Now, I mean, epigenetics is a relatively new

field. I mean, for many years, we felt like our genes didn't change over time, and now we know that they do and that they're affected by our environment and a number of other factors. When did the light bulb go off and you said, oh, my gosh, we need to apply this to what we're doing here with this cohort? You know, the first epigenetic finding, started to come out of Michael Meaney's group in Canada with rats rearing their pups and showing epigenetic changes having to do with mothering, having to do with variables that were interesting to clinical psychologists and interesting to the members of APA. That was very exciting. So we already had the DNA. We were early adopters. We were one of the first cohorts worldwide to collect DNA.

back when the study members were 26-year-olds, so that was almost 30 years ago now. So we had the DNA already in the lab, and we could then do the assays to look at epigenetic marks on top of the DNA was a natural addition for us. Once it became interesting to psychologists, we went in. How were the biological baselines established? Like, how do you know when biological and chronological systems are in sync?

Right. Well, we started out when the study members were 26 and we drew these 19 biomarkers. And I should just say there are things like cholesterol, HBA1C, your waist hip ratio, your blood pressure, your dental cavities, lung capacity. Those measures were taken when the study members came in when they were 26 years old. So that was, again, about 25 or 30 years ago. So we had those as their baseline when they were at their peak. of young adult health. And then when they came in, they were 32, we just repeated them. And when they were 38 and when they were 45. So we're able to calculate not only what is normal for a person in the sample, but what is normal for a super healthy young adult. And is that now becoming a standard in this kind of work? Is everybody sharing sort of the same? When you're 40,

this is what your biology should look like? You know, no. And the reason why most of the studies that are in this area are people of all multiple ages. So they range in their samples range in age from 18 to 80. And they only have biomarkers at one time point. So what that means is that they're not able to really say, here's our whole population representative sample, what they looked like when they were 26, what they looked like. like in their 30s, what they look like in their 40s, in their 50s. They don't have the data for that. So the Dunedin study is the one that has those data, but it's 1,000 people in New Zealand.

So what we're really hoping is that some of the larger American studies will get in the business. Now, the Baltimore Longitudinal Study on Aging is doing it. The Health and Retirement Study that is funded also by the National Institute on Aging is doing it. So, pretty, pretty much. pretty soon we'll have this nutted out for Americans. There's a lot of progress. They've already published some of their findings. It's very exciting. With the Dunedin study, so every year, you bring people in and test them again, is that correct? No, not every year. We bring them in every about five or six years now. We brought them every other year when they were little kids because they were developing so fast. So we saw them at age three and five and seven and nine.

and so every other year on their odd number birthday. But when they got into adulthood, you know, peer reviewers of our papers always say, you should be bringing these people in every year. And I say, that's great. But I haven't noticed that our funding agencies or the study members are keyed on that idea. So sometimes what would be the perfect methodology for science

is not in keeping with the availability of research fundings or with the need for privacy for the participants. So I think we push them about as hard as we can, and we raise money about as fast as we can, but about every five years seems to be what we can manage. Are there new factors you're hoping to be able to look at with this cohort? Yes, you know, when you run a longitudinal study like this, first of all, you have to keep up with what the cohort members tell you

is the most important thing in their lives. So they're starting to worry about menopause, in retirement now. So we're having to get, you know, learn about that. So we just not, you know, I started out studying juvenile delinquency and drug use and risky sex. And now I'm now I'm having to study menopause, retirement, those kinds of things. And the other thing is that we're trying to make sure that we, in our psychological data and psychological interviews, that we really collect information that is really important for understanding the behavioral and social, aspects of aging. So a lot of what's been done with this cohort seems very biological,

but in fact, that's quite a small part. So for example, we're interviewing extensively this time at age 52 about a construct called apathy. So you may imagine that apathy is interesting because it can be one of the very first signs of movement towards Alzheimer's dementia. When a person long before they show any memory problems, starts just losing enthusiasm for life. They start being a little less social. They start, you know, just being kind of tired and not full of them and vigor as they were before. So when that starts to happen, it's subtle, but you want to get data on it. So we're interviewing the study members about the constructive apathy, and we're interviewing

collecting data from their spouses and friends as well. So we have informant reports about that. How do other people see them as less lively than they used to be? Or are they still holding up with their vim and vigor? So your academic background is as a psychologist, but have you had to become a biologist, physiologist? I mean, it seems like you've had to learn a whole lot of other skills in the course of this work. You know, I have, but I also have incredible good collaborators and staff. So they're super patient with me and they bring me along.

So I would call myself a brain imaging neuroscientist, but Amad Harare is, you know, holding my hand. And he's very kind and patient about explaining everything to me and making sure I fully understand it before we write anything up or publish it. Because we do, you know, when you publish a research paper, you do have to sign something saying that you can explain and defend the findings yourself if you're going to be an author on the paper. So that's really important to me. And I work with my staff and we have bioinformitians. We have wetlam researchers, you know, statisticians on our team who help me. So what are the next big questions you're hoping to answer? Well, we want to know what happens with the pace of aging when we follow it up now at age 52.

According to theory, it should slightly start accelerating. as people age into their 50s and 60s and 70s. So the theory of aging is that it's a little bit like a snowball going downhill. So you age kind of slowly from 20 to 30, start noticing you don't look that great in a bathing suit anymore, but you're still able to do everything. And then 30 to 40 and then 40 to 50 and then it's sort of, you know, can snowball. And if an event happens in your life, like a fall with a broken hip or if your spouse passes away, that can really be the kind of shock to the psychological system that pushes aging, biological aging into a speed-up phase.

So that's one of the things that we're hoping to capture. Well, Dr. Moffin, I want to thank you for joining me today. This has been really interesting. This is a great work that you're doing. It's a great podcast. It's so fun to be on it. You can find previous episodes of Speaking of Psychology on our website at speakingof psychology.org or on Apple, Spotify, YouTube or wherever you get your podcasts. And if you like what you've heard, please subscribe and

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I'm Kim Mills.