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Guest Bio:

Kara Fitzgerald, ND, IFMCP, received her Doctor of Naturopathic Medicine degree from the National University of Natural Medicine in Portland, Oregon. She completed the first Council on Naturopathic Medicine–accredited post-doctorate position in nutritional biochemistry and laboratory science at Metametrix Clinical Laboratory. With the Helfgott Research Institute, Dr. Fitzgerald is actively engaged in clinical research and peer-reviewed publications on the DNA methylome using targeted diet and lifestyle practices. She has published a consumer book titled Younger You as well as a companion cookbook, Better Broths and Healing Tonics, and offers Younger You Programs based on the clinical studies.

Dr. Fitzgerald is the lead author and editor of Case Studies in Integrative and Functional Medicine and is a contributing author to Laboratory Evaluations for Integrative and Functional Medicine and The Institute for Functional Medicine’s (IFM’s) Textbook of Functional Medicine. She is on the faculty at IFM and lectures globally on functional medicine, longevity, and epigenetics to practitioners and consumers. She also maintains an award-nominated podcast series, New Frontiers in Functional Medicine, and an active blog on her website, www.drkarafitzgerald.com. Her clinical practice is in Sandy Hook, Connecticut.

Transcript

Kalea Wattles, ND, IFMCP:
Chronological age is determined by the year someone is born. Biological age, however, is the actual physiological age of one’s body and can be influenced by various factors, including genetics, medical conditions, and lifestyle. Epigenetic mechanisms that regulate gene expression have been associated with biological aging in humans. Lifestyle, behavioral, and environmental factors can cause DNA-level changes that affect the way genes work, and these epigenetic changes can play a role in the development of chronic disease and influence healthy aging.

Kara Fitzgerald, ND, IFMCP
Chronic disease is an age-accelerating, is a biological age–accelerating phenomenon. So when, you know, the pathologic changes that will bring about these chronic diseases are age accelerants. The aging journey itself, however, kind of lowers the bar to developing these chronic diseases. So they’re both kind of interplaying. So the aging journey changes happen physiologically that make us more vulnerable to developing cancer, or heart disease, dementia, diabetes, et cetera, et cetera. So both things are happening, and this is, you know, this is why we really wanna be vigilant, and there’s, you know, benefit in us really paying attention to the aging phenomena, like zeroing in on it. It’s a huge conversation now in our space, in functional medicine.

Kalea Wattles
On this episode of Pathways to Well-Being, we welcome naturopathic physician and clinical researcher Dr. Kara Fitzgerald to discuss epigenetics, longevity, and how diet and lifestyle-based interventions can slow biological aging and optimize the healthspan. Welcome to the show, Dr. Fitzgerald.

Kara Fitzgerald
Oh, it’s great to be here with you.

Kalea Wattles
Well, let’s just give some background to start this episode because now we’ve talked about there’s chronological age, which is a measure of time, and then there’s biological age, which is more a measure of function. I love to hear you talk on this topic. I think anyone is probably wanting to know, well, what are the things that are going to affect my biological age and cause me to maybe age more rapidly? So to get us started, will you talk to us about what are some of the general factors that might determine someone’s biological age?

Kara Fitzgerald
Yeah, god, it’s interesting, and it’s just an extraordinarily active area of investigation now. I think a lot of what we know, Kalea, like that’s been intuitive time immemorial has, you know, influenced bio age. I mean, let me just talk about blue zones, where culturally they’re consuming, you know, what’s kind of a time immemorial dietary pattern in, you know, wherever they are. And their lifestyle habits, you know, like take Sardinia, they’re walking a lot. They’re, you know, they’re just, they’re engaged in physical activity, they’re eating sort of the classic diet of the land. And, you know, I think it’s a Mediterranean-type dietary pattern and living long and really, really well. And so I think some of what we know to be really healthy turns out to be true.

There was actually a cool study looking at centenarians, French centenarians, again, eating this really healthy dietary pattern, engaged in healthy lifestyle habits. And they were biologically, I like to say that 100 is the new 70. So they weren’t quite 70, but they were just, they were aging at a much slower rate. So we know dietary patterns make a huge difference in our rate of aging. We know that, you know, again, just sort of tapping some of this information from these longevity hotspots, community, we know physical activity. We know, you know, being outside, we know, you know, lower toxin exposures, kind of a different relationship with stress. Stress is something that we’re all exposed to, but, you know, ways of kind of moderating its potentially toxic effect. All of these things really kind of page, you know, play a big difference.

I mean, there’s another study I’m thinking about out of China looking at loneliness and finding that it accelerated aging actually more so than smoking. Isn’t that phenomenal? We also know that acute stressors, pregnancy is actually a briefly pro-aging phenomena, which reverses, you know, once you deliver the baby, and there’s a, you know, a bonus with breastfeeding that it can more quickly sort of reduce, you know, or augment the biological age that had accelerated during that time. So just all sorts of cool stuff. Surgery actually can be a pro-aging experience, but then after that event, you know, it returns to baseline.

Kalea Wattles
Well, like you said, a lot of these factors are pretty intuitive. We’ve been teaching this in functional medicine forever, but I always think my family, we live on a big farm where we practice regenerative agriculture, and my husband is outside all day in the fresh air doing exercise with animals in a thing, you know, a role that gives him a lot of meaning and purpose, and his blood pressure is so healthy and all of his labs are so healthy. And I just, I have to think that this lifestyle-

Kara Fitzgerald
Yes.

Kalea Wattles
This guy’s gonna live forever.

Kara Fitzgerald
Yeah, yeah, that’s just so cool. And then juxtapose that, you know, with the profoundly pro-aging effects of, you know, the larger agriculture community where there’s a lot of pesticides and people are exposed to those who are, you know, who are harvesting that produce, et cetera. And there’s a different relationship, I think, with it. But it sounds like what you’re describing is absolutely beautiful. I haven’t visited your farm, but I would love to.

Kalea Wattles
Okay, well, you’ll come, we’ll do some longevity work here. Will you tell us a little bit, I am imagining that there is a connection between one’s biological age and their risk for chronic disease. Are there some connections there that you found in the research?

Kara Fitzgerald
Yeah, absolutely. I mean, it’s kind of a little bit of a chicken and the egg. Like, and also too, just to go back to some of the, let me just say some of the interventions, you know, some of the lifestyle factors that, you know, can attenuate bio age. I also wanna say that it, there’s a hotbed of research, obviously, on various interventions, drugs included, that can influence bio age. So maybe we’ll have time to circle back to that as well.

So chronic disease is an age-accelerating, is a biological age–accelerating phenomena. So when you know that the pathologic changes that will bring about these chronic diseases are age accelerants, the aging journey itself, however, kind of lowers the bar to developing these chronic diseases. So they’re both kind of interplaying. So the aging journey changes happen physiologically that make us more vulnerable to developing cancer, or heart disease, dementia, diabetes, et cetera, et cetera. So both things are happening, and this is, you know, this is why we really wanna be vigilant, and there’s, you know, benefit in us really paying attention to the aging phenomena, like zeroing in on it. It’s a huge conversation now, in our space in functional medicine. And I think it’s important, you know, to think about it, both not just a disease prevention but just really going in and thinking about how do I, you know, slow or mitigate the ravages of the aging phenomena that’s gonna, that’s happening to all of us.

Kalea Wattles
Right, when I think about, well, I have a little subset in that I work with fertility patients, and so I’m always thinking about what can I do to support reproductive longevity specifically. But most commonly for me, it goes back to inflammation and oxidative stress. And it seems like, you know, obviously those are the things that are associated with insulin resistance and cognitive decline in all of these chronic diseases. So I always try to make the case, the things that we do to support longevity in our health or in our fertility ultimately are associated with all of these things that prevent us from living the life that we love and deserve to have, right? So it makes so much sense to me that there’s these connecting points.

Kara Fitzgerald
Well, and these, I mean, aging starts at, you know, really, I mean, I would say conception, maybe we could say birth, but I mean, aging starts with the epigenetic, with the information being procured during the development, you know, in utero of a baby. I mean, it really starts, and actually, you know, then we go before that, right? So I start with this conversation here, you know, at conception, but then we know that the information from mom and dad, and then from generations past, like all of that is present in the epigenome, and we can define and talk about that. But that’s happening, you know, in the, in the in utero experience. And then, of course, you know, at birth, you know, early infancy and on, it’s a time of rapid, rapid epigenetic changes and age acceleration. But it’s supposed to be, I mean, that’s what’s, what’s really kind of extraordinary, you know, early development. You see kids just, you know, sprouting up and changing and growing and expanding, and it’s supposed to be this rapid period. But we, and we wanna honor that and foster that. We want, but the dysfunctional aging, the aging that will then kick in, you know, and lead to, you know, ultimately the chronic diseases of aging. We wanna be, you know, mitigating those forces, for sure.

Kalea Wattles
Yeah, so how do we know, how do we know what our biological age is? How can we measure? I’m sure anyone listening is like, “I gotta know, tell me more.”

Kara Fitzgerald
Yeah, so there’s a handful of ways that we can measure our biological age. We can, you know, it’s funny, we definitely don’t wanna be throwing out the standard biomarkers that we use in clinical practice. All of those have utility, and we know what we need to be thinking about when we see, say, a high CRP or a SED rate, when we see any nuclear antibodies, when we see abnormal, you know, complete blood counts, et cetera, et cetera. All of that is incredibly important and useful information, high blood pressure, you know, cholesterol imbalances, and all of those inform the aging journey, some with more validity than, than others.

But we are now in the era of being able to more sensitively measure, you know, the aging process as a whole using something called epigenetic clocks. So epigenetics, quite simply, is epi, above genetics, the genes. So we’re looking at the biochemical influences that turn genes on and off, and we can look at, you know, pretty sophisticated patterns, mostly exploring DNA methylation, one of the key epigenetic marks that changes gene expression. So in looking at different DNA methylation patterns, we can, you know, really accurately assess the rate of somebody’s aging, or their biological age at the time of collecting that specimen. I mean, we can get some pretty interesting information. Overall aging…we can look at the rate of aging of different organ systems. Those labs are being developed, you know, as I say this.

So it’s a really cool field. It’s growing by leaps and bounds, and yeah, these are tools that we can bring into clinical practice to inform our decision making with our patients, for sure. Do they supplant our standard tests? No, but they can enhance and inform.

Kalea Wattles
That makes good sense. One thing I noticed, I measured my biological age a few years ago, and I’ll admit I was a little disturbed by the results. It was good wake up call for me. But what I’ll say is it was so motivating to make all the behavior change and the lifestyle change that maybe I would’ve ignored otherwise. But now I had this result in front of me, so I found it to be extremely compelling.

Kara Fitzgerald
That’s awesome, you know, yeah, just like, like for some of us use food sensitivity testing and we, and I find, you know, if I do it, I was just talking to a patient yesterday who has a very high IgG reaction to dairy, and some of us in our, in functional medicine don’t use those labs at all. But for this, you know, it was highly motivating to her, so to your point, that very high finding was just really good energy to have her do a dairy elimination for a period of time. You know, likewise, if we see a biological age that we’re not really excited about, you know, we may be motivated to go in and look at things from a different lens also. So there’s no doubt, Kalea, you’re doing so much right. But then you may explore, you know, yeah, I’m sitting in my, you have huge commutes, or, you know, it’s kind of the nooks and crannies of what might be influencing our bio age.

I saw, you know, I’m in Connecticut now, but we’re living a lot of the year in Mexico, and the massive variable change for me was my heart rate, you know, my heart rate variability. So the massive, I should say, the massive variable that I observed changing was heart rate variability just really expanded because this, you know, where I live in Connecticut, I’ve got all sorts of good habits employed in a lot of fronts, but I’m in my car a lot, you know, there’s tons of traffic, there’s a certain energy and environment here that I really can’t change that I’ve noticed shift considerably, you know, in being in Mexico. So, yeah, it’s cool to have these tools to kinda get into the nitty gritty and look through a lens that we may not otherwise look at.

Kalea Wattles
It’s very cool. And I just wanna underscore something you said because I think it’s really important that doing some advanced testing is not a replacement for doing your standard evaluation, that’s gonna look at hormones, and inflammation, and metabolic health, and all of these factors. Because I always thought these things should really be combined to get the whole picture, right?

Kara Fitzgerald
Yes, yeah, I mean, I will say, when I first started thinking about epigenetics and being really excited about it many, you know, many years ago, I was bullish that they would supplant some of our standard markers. And now, you know, I’ve come full circle in that and really embrace kinda the richness of the tools that we’ve had for so long. I mean, when did we first develop the chemistry? And it’s still, or the CBC, I mean like 50s, maybe? I mean, and these are still decently useful tools. In fact, we can talk about a specific clock, the PhenoAge clock that is built on looking at some of these old school biomarkers, and it’s, you know, it’s a good solid second generation clock, that can potently predict morbidity and mortality. And it’s based on the DNA methylation patterns that are used in the clock are based on, you know, an alk phos, white blood cells, glucose, you know, creatinine. I mean, just these work, these foundational laboratories that we’re looking at day in and day out.

Kalea Wattles
Yeah, that’s so interesting. I think maybe I get a little, I have to look closely at all these different clocks. So you mentioned, I think you said pheno clock. How does that differ from something like the Horvath clock?

Kara Fitzgerald
Yeah, good question. There’s a, yeah, so again, you know, this is the, we’re in the era of clock manufacturing, you know, decidedly different than, you know, like turn of the century clocks. Yeah, they tell time very differently. Yeah, and so they’re just, we’re up to third generation and maybe some argue even beyond that. And this field will just continue to morph and morph and evolve. So we need to hold on loosely, really, and just sort of allow this to happen and have them inform our thinking. But also, you know, the other data points are essential.

So Horvath clock, which is what we used in our publication, because it was the only clock available at the time, and particularly we collected saliva, so you have to make sure the sample, you know, you’re using an appropriate clock for samples. And anyway, that was the first epigenetic clock to be released, and it came out in 2013, and it just lit the fire, you know, lit the fire of all of this. It’s amazing, and so that clock was trained to, against chronological age. That was the variable that it looked at. And it was very, it could rigorously predict chronological age, but it was not a one-to-one prediction. If it was, that’s the only thing that it would be useful for. There was a little wiggle room, it predicted it with about 0.96 degree, you know, accuracy, which is insane, you know, that’s, any other measurement prior to that, this blew out of the water. Like if we talk about telomeres, you know, they’re a distant second in the reliability of this particular clock, but because it wasn’t an exact predictor of chronological age, there was some additional information being gathered, and as they drilled into this, they could actually see that it was a better predictor of morbidity and mortality, it was a better predictor of the aging process than chronological disease. So even though it was trained against chronological age, it performed better at being able to predict disease. And that was the very first clock, you know, and it just kind of formed the start of the research and lit the movement on fire.

Then there were the second generation clocks, and the PhenoAge is what I just mentioned. That’s sort of the, one of the hallmark second generation clocks. And it is better at predicting morbidity and mortality than the Horvath clock. So clocks are just getting more refined, and you know, how they’re training them. They’ve moved away from just chronological age as the variable, the third. Oh, and so let me just say about the PhenoAge, and the, both of these clocks are still being used in research. I mean, oftentimes in studies, people will, you know, scientists will employ a handful of different clocks. I think there’s still a place for them. And you know, these clocks have, Horvath’s original clock is also referred to as the pan-tissue clock, because it’s able to do well in a variety of tissues. So for us, for example, having saliva in our original study, it was ideal for that. Whereas the PhenoAge and most of the other clocks you need blood for, but they’re working on that, working to make clocks, you know, easier to be collected in different specimens.

So second generation PhenoAge, I wanna say that those nine biomarkers I mentioned that Morgan Levine trained the PhenoAge clock on, super standard biomarkers, we collect them in practice every single day. There’s a calculator that one can use to obtain a PhenoAge calculation. So it’s not the DNA methylation test. You can save a lot of money using this algorithm that was developed, that was the original algorithm that she then went on to train against DNA methylation. So that calculator is available, and it’s an awesome, easy, super affordable way to get a pretty good biological age without the investment of, you know, the DNA methylation testing, which is reasonably pricey. And I can give you a link to the calculator that we have on our website, but you can find this, this calculator is freely available online. So that’s a second generation clock.

Third generation, so the one that we’re really excited about and using now is something called the Pace of Aging, or the Dunedin Pace of Aging. This clock is particularly cool, Kalea, because they started, there’s a pretty decent sized group of individuals. They started tracking when they were infants, they started tracking aging using a selection of biomarkers, you know, 50 plus years ago. It’s amazing, so they have this massive longitudinal dataset, and that is unique among clocks. I mean, this is like, this is gold. You know, most of the clocks are trained against massive data sets like Framingham and, you know, and NHANES, and you know, the data sets that are banked and made available to researchers. And that’s, you know, those are like single time points. Also too, let me just throw out there that some of those data sets are pretty old, and our environment has changed. You know, our exposures have changed, our dietary habits have changed. And so these clocks might lose some of their rigor because of the data sets that they’re trained on. But this Pace of Aging clock, they’re capturing these data. They have been, you know, in real time for many, many, many years, and they’re looking at some of the standard blood markers that we’re familiar with, CRP, you know, cholesterol, et cetera. Again, standard chem screen stuff. They’re also looking at gait, they’re looking at strength, they’re looking at memory. I mean, they’re just looking at, you know, a handful of different cognitive memory tests. What else are they looking at? Grip strength, which is a pretty cool marker. And, you know, and just really kind of on, they’re looking, I think they’re looking at 19 different parameters, lung function. And they’ve measured these in, you know, they’ve measured the bulk of these in this population for 50 plus years. I think the population, the original cohort start, were born in about 1972. And so they have a pretty solid data set. And this is called the Pace of Aging. And they think that the calculation that they provide is able to capture the rate of somebody’s biological age, and they’ve pinned it against one.

So if your PhenoAge, or if your Pace of Aging is, excuse me, I said PhenoAge, erase that. If your Pace of Aging is one, then you’re aging consistently with, you know, against chronological age. If your Pace of Aging is greater than one, then you’re aging at an accelerated pace relative to chronological. And of course, if you’re younger, that’s where you wanna be. Your biological age is slower than your chronological age. And we can, and this actually can change relatively quickly. So we’re, you know, again, we’re using it in our study. This is the clock that really captured the influence of caloric restriction. So the famous calorie study, the two-year caloric restriction study, it was the Pace of Aging clock that really got the change, you know, identified in these individuals. So they lost weight, some of their standard biomarker changes were noted, but they didn’t, the other biological age clocks were not significantly changed. However, the Pace of Aging was shown to have significantly slowed in this population.

Kalea Wattles
This Pace of Aging is so fascinating to me, is that, if you were to create a hierarchy of what is most meaningful to you as a clinician, is it the Pace of Aging that you’re paying the most attention to at this point?

Kara Fitzgerald
Yeah, this is, yeah, so we’re using this PhenoAge calculator in practice, and we make it available online as well, because it’s easy. And we have those data, and it does give you a number. I mean, people love it, right? As much as you didn’t like whatever your number was relative to your chronological age, it’s probably like, what, like 20 years younger and you wanted it to be 30, or no, I’m kidding. I should, you know what, let me say this to you, Kalea, that the clocks vary in how tightly they are set to predicting chronological age. I mean, some clocks are gonna have a wider span and others are gonna be, you know, more in lock step by design. So you really have to look at what, you know, clock you’re interested. And I mean, there are people who will tout online that they’re 30 years younger than their chronological age. And you know, we know that they’re looking at a clock that’s, you know, swinging pretty broad and, you know, is that reflective of what’s really happening? I mean, do we expect them to be galloping into their mid-100s with ease, you know? I mean, it doesn’t, it just doesn’t make sense. In fact, there’s been a lot of challenge and pushback from the scientific community on some of this. So yeah, it’s, you know, it’s a little bit of the wild west as we figure out how to interpret them and how to use them and what they mean.

But to your point, yeah, I think the Pace of Aging is really solid. And yes, and arguably just looking at the rate, it’s not a sexy number. It may not emotionally motivate you in quite the same way, positive or negative, but it was developed in a really powerful way. I think it’s really pretty impactful and very useful. It’s changeable. We know lifestyle interventions can change it. So yeah, it’s the tool that, that we’re using that we’re leaning on now.

Kalea Wattles
Well, I do find comfort in the fact that we can turn this around pretty quickly. And I know when you were doing your clinical research, you looked at the impact of diet and lifestyle interventions on our biological age, and you mentioned caloric restriction. What were some of the other things, other modifiable lifestyle factors that you noticed had a positive impact on whatever measurement of aging you were using at the time?

Kara Fitzgerald
Yeah, so in our study, we didn’t do caloric restriction exactly, but we had a very gentle intermittent fasting window. And intermittent fasting has for sure been shown to be beneficial on the rate of biological aging. So we, our dietary pattern is I think classically healthy in a way that, you know, we were trained in school, I think it has underpinnings of a Mediterranean-type diet, although it’s keto leaning, it’s lower carbohydrate, it’s definitely going to, you know, balance out glucose cycling and so forth. So it’s lower carb, but it’s not a ketogenic diet. It’s, you know, higher healthy fats. There is a crazy amount of good veggies, you know, just really across the board, lots of greens, lots of cruciferous, lots of colorful veg, you know, good hydration, animal protein. So the study that, the dietary pattern that we’ve researched has animal protein in it, although we do have a vegetarian and vegan version. Animal protein that we think is particularly beneficial is liver, if you’re open to eating it, because of all of the, you know, just this extraordinary compliment of micronutrients. I mean, liver is the most nutrient dense of all of the, you know, animal sources. Eggs is, you know, another really smart nutrient dense food. And then, you know, beef and chicken and you know, so on and so forth. Of course, fish, you know, it was particularly fatty fish, clean source fatty fish, important.

We did, in our dietary pattern, design it specifically around DNA methylation and thinking about optimizing it. So our nutrients are in what we term, you know, two different classes. Either they’re methyl donor rich, so that means they’ve got folate or B12 or both, or choline, anything that’s going to help the methylation cycle make that SAMe that can go on and support DNA methylation and favorable epigenetics. And then there’s this other group that we sort of loosely or colloquially defined as methylation adaptogens. And these are largely polyphenol compounds that seem to influence, or influence, I shouldn’t say seem to, I think enough data has come out to support that these cool polyphenols actually have an ability to dictate how DNA methylation is happening and, you know, generally towards a more favorable pattern.

So just for example, in our research, we didn’t show a net increase in DNA methylation, but we saw a clear rearrangement, and we’re actually show something more favorable. And our participants reflected this in their health. They lost weight, their cholesterol dropped, their triglycerides dropped, et cetera. So some of the standard measurements we saw improve, even though this was a very healthy cohort to start. And then when we looked at epigenetics, we saw that there were changes to, in something to reflect something more favorable, something more healthful that was associated also with a longer, a younger biological age.

And I wanna just say that we’re, we continue to tease out these data, so beyond just the biological age aspect of epigenetics, we can look at, you know, well beyond that, the other epigenetic patterns that we’ve changed, and we’ve been drilling into this for years now, but hopefully there’ll be a publication in the not so distant future. We do have a publication that we’ve submitted. It’s in peer review now, looking at what aspects of the dietary pattern were most impactful. You probably wanna know the answer.

Kalea Wattles
I certainly wanna know the answer, but now I know that you’re gonna keep us updated, so that’s helpful.

Kara Fitzgerald
Yeah, I can tell you now that the, those methylation adaptogens, the ones that seem to kind of rearrange what’s happening, you know, appear to be, they came in top as far as being most closely associated with epigenetic changes.

Kalea Wattles
And I love that term, methylation adaptogens, that is just beautiful.

Kara Fitzgerald
That comes from Michael Stone, that actually is Michael Stone. He and I were talking about it at, you know, many years ago at a conference. And he just threw that out in a very, you know, in a very clever Michael Stone kind of a way.

Kalea Wattles
Yes, very clever way. It occurred to me as we’re talking about all this methylation, should homocysteine be part of the panel that we do at first? And does that play a role into your kind of clinical reasoning?

Kara Fitzgerald
So it hasn’t demonstrated itself in some of these, you know, bigger, you know, data projects like associate, you know, it hasn’t demonstrated itself to be really closely associated with biological aging, via a variety of different methods of looking at biological age. You know, it didn’t make the PhenoAge calculator. And I’m quite sure that they included it in their original analysis. They looked at a lot of different biomarkers and whittled them down to these most potent nine, and they’re just such common standard biomarkers. So it didn’t make that cut. It wasn’t that strongly associated with biological aging in a clock developed only on biomarkers, no DNA methylation involved, however, so it’s got, so on that hand, it hasn’t proved itself to be a strong marker of the aging phenomena, but we know that it’s a great surrogate marker of, of course, methylation. I mean, it’s sitting right in the methylation cycle when it’s abnormal of high or low. We know that something wonky is going on with methylation, and we know from other studies, homocysteine abnormalities are linked to DNA methylation changes, even though they haven’t linked it tightly to the aging journey. You know, it ends up changing. It can certainly change DNA methylation patterns in a less favorable way. So yeah, homocysteine is still a really useful tool for sure.

Kalea Wattles
Yep, that was helpful. My final question to you is one that I have to ask, just my clinician brain that I need to pick your brain. What type of patient should I be doing biological age testing on? Is it just someone who wants it and they’re curious? Is there a persona that I should say, “Hey, I think you would really benefit from this type of evaluation?” What’s your thought?

Kara Fitzgerald
That’s a really good question. I would say that probably, so the way that I’m using it in practice these days is because, so my functional practice, I’m already doing a pretty broad battery of testing. These are extremely useful in a, you know, the biohacker longevity folks who just, who really want those data, and these are gonna speak to them and really motivate them. But I would say, you know, anybody moving into their forties is a decent candidate. And those who are in their thirties, I mean, God, you know, people are curious and interested. It’s, you know, it’s just not a bad tool to have because to your point, I think it can be incredibly informative both for you in clinical decision making and what’s going on. I mean, if you see a highly accelerated age, you know it’s gonna be concerning, and you’re going to adjust and you’re gonna speak to your patient about that in a certain way. You’re probably going to adjust your focus with them in a certain way, and it can be motivating to the patient.

So, you know, we know we can see these changes pretty young. And so if you’ve got somebody who’s open to making that investment, I mean, why not? And the other piece that you can do is use the PhenoAge calculator that I’ll give you a link for, and chances are you already have those biomarkers, and you can just plug them in and get a rough idea of where they’re at. We see the chronic diseases of aging starting in younger and younger and younger individuals, in adolescents and, you know, in kids, we see the chronic diseases of aging starting in kids, glucose changes, lipid changes. I mean, it’s nuts. So this is a real, we’re in a very accelerated aging place culturally, and I think globally. So these tools may be beneficial in younger populations. However, for me, as a clinician, you know, I’m using them in my, primarily in my middle age and up population.

Kalea Wattles
Makes great sense. Functional medicine timeline come to life.

Kara Fitzgerald
Yeah.

Kalea Wattles
Dr. Fitzgerald, it has been a pleasure being with you. I know that you will keep an eye on the research. You’ll let us know what is emerging in the field of longevity. Thank you so much for sharing all of your insights. Can’t wait to see what’s next for you.

Kara Fitzgerald
It was great to be with you. Thanks so much for having me.

Kalea Wattles
To join the conversation on this topic, visit IFM’s pages on Facebook and Instagram. For more information about functional medicine, visit ifm.org.

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