Biohacking to 100: Longevity lessons from 15 years of self-tracking ft. Michael Lustgarten, PhD
- How to optimize your diet through self-tracking
- How to measure and change your biological age
- The difference between recommended and optimal nutrient intake
- The importance of dietary acid load and uric acid to health and longevity
Our guest today is Dr. Michael Lustgarten. Michael is a scientist in the nutrition, exercise physiology and sarcopenia laboratory at the Human Nutrition Research Center on Aging at Tufts university. His research currently focuses on the role of the gut microbiome and serum metabolome on muscle mass and function in older adults. Michael is also something of a pioneer in the biohacking space, back from when it was more commonly known as Quantified Self. He’s known for his detailed self tracking of both diet and blood biomarkers, and his focus on healthy aging and longevity. Michael, thanks so much for joining us.
Of all the biohackers I’ve seen, you’re definitely one of, if not the most dedicated when it comes to this kind of tracking – in particular blood. Can you just give us an overview of what you’ve been tracking and for how long?
Sure. So I started probably 15 years ago. I had the idea that aging is a biochemical process that happens over decades, and that if I started to track my own blood tests, variables, and the stuff that’s found when you go to the doctor to get a yearly physical, the standard chem panel, the CBC, which includes things like red blood cells and hemoglobin and white blood cells and their differentials – neutrophils, lymphocytes, all that good stuff, platelets.
So I figured if I at least started off with that data and tracked it over time, I’d be able to see deviations in my physiology sooner rather than later when potentially disease and/or aging would hit me. I did that about once a year for about 10 years, and then in 2015 for whatever reason I decided to kick it up a notch. And that’s when I started tracking my nutrition and then measuring my blood four to six times a year.
And when I say measuring my nutrition, I mean tracking it with a food scale – so weighing all my food and then logging it using free online software. So I started also doing extensive literature reviews on all of those circulating analytes that are found on those – on the chem panel and CBC – so I could figure out how did these things change with age and how are they associated with risk of death from all causes.
With the logic being, the reference range is great, but it really doesn’t tell you where you should be. And back in the day out of ignorance, and I’m sure a lot of people do this, I figured “oh, the middle of the range is best”. Well that’s not true for a lot of biomarkers. So I did a deep dive, full lit reviews on everything and then I started to write about it so that other people could also benefit from my journey, and as I was tracking my diet my goal was to use my diet to optimize my circulating biomarkers and the only way to do that because if I just had one blood test result, there’s no way I can take the average diet for the whole year. I don’t have good data points.
You mentioned about reference ranges and presumably many of these when they’re originally established were about trying to stop people from getting sick rather than the idea of optimal health. How did you sort of determine from looking at the research what might be an optimal range, and did you sometimes have to think about avoiding excess intake for example, when it comes things like vitamins and minerals?
Yeah. So my approach is whole food based. I try to stay away from supplements as much as possible unless I have a biomarker that’s resistant to change through diet and fitness level and optimal body weight / body composition. So the long story short for that is full comprehensive lit reviews, looking at as many papers as possible relative to how it changes with age, what’s found in biological youth, people who are actually young, what are their biomarkers and in good health. So trying to look at athlete data and then what’s associated with risk of death for all causes.
There are some things that I do indeed go higher than the reference range or dietary intake recommended levels, and the net effect is that my biomarkers, my biological age is 15 to 20 years younger than my chronological. So I’d say I’m on the right track.
What actually is biological age? How do you measure it? I’ve had it originally people saying it’s about telomere length and I’ve had it said more recently, this is actually only part of the picture and there are many more factors to consider. So how do you see it?
Yes, so your chronological age is basically just the calendar year passes and how long you’ve been alive on earth. Biological age is actually an attempt to identify how old you are based on some metrics, whether they’re circulating biomarkers or using the microbiome or other stuff. Now you can have a biological age that’s actually older than your chronological age. You could have a biological age just that’s the same or younger.
And in studies that have looked at the correlation between biological age with chronological age, people who had a higher biological age based on whichever metric, whether it was epigenetic age or a composite of circulating biomarkers like albumin and inflammation, just the composite of those, so people who had a higher biological age based on those metrics than their chronological age had an increased all cause mortality risk, reduced frailty and physical function. I mean all the negative consequences that you can imagine, which conversely people who had younger biological ages relative to the old, the chronological age had lower all cause mortality risk and better physical function.
So in terms of the telomere question, there’s a paper published a while ago called The Hallmarks of Aging, which basically outlines nine things that happen during aging, for example, inflammation or epigenetic alterations or mitochondrial dysfunction. So these are hallmarks of aging that happen no matter what the species basically.
And then more recently, just in the last year or two, probably the best quote-unquote “metrics of quantifying biological age” is the epigenetic test. So basically you look at methylation on DNA for a few or a bunch of different genes and then they associate the methylation status of those genes with chronological age and you can predict biological age from chronological age.
But interestingly, and this is kind of why I blog about it like crazy, but the circulating biomarkers that I measure in one study, the correlation between a composite of nine of those biomarkers with chronological age or with biological age, the correlation coefficient was 0.94 which when you compare that with the correlation coefficient for the gold standard, quote-unquote “epigenetic clocks” was 0.97, so you could make the argument that they’re not too dissimilar in terms of their ability to predict biological age.
So that’s one reason I focus on the stuff that I’m measuring rather than going with the quote-unquote “gold standard” of the epigenetic clocks. As another piece of information there, the stuff that I’m measuring, it’s cheaper with the exception of C-reactive protein, which is about a $40 blood test. Just getting the standard chem panel and the CVC is about $35. So collectively we’re talking $75-80 for all the stuff that you can get a decent, or a pretty good biological age quantification.
Whereas the epigenetic test, first of all, it’s four times more, it’s $300 and that’s the epigenetic test that didn’t show an association with smoking. So I’m not sure that I will spend $300 on something that doesn’t indicate smoking as being bad for your aging process.
And that kind testing is kind of an emerging field. I think it’s only a couple of companies that are even offering those tests right now, so probably we’ll get more cost effective and sophisticated in future, right?
And there’s probably a tension for them in producing something that’s rigorous, but also something that’s cost effective enough to sell, to build a business. I mean really the genius of guys at 23andMe is that they essentially got paid to collect people’s data for drug research, right? Which is pretty amazing. How can we change our biological age? What can we do to reduce it?
So this goes back to again, multiple measurements over time. I’d say tracking diet is obviously important, but what’s interesting is a couple of papers on the subject have been published in the last few years – an increase in life expectancy of 10 to 14 years, whether you’re a woman or man, I think it was 12 for men and up to 14 for women, they had five factors.
So obviously not smoking, having a BMI that was less than 25, moderate alcohol intake, having a quote-unquote “healthy” diet (without going into the details of that), and then the fifth one was exercise, which was as little as 30 minutes a day every day. And in the data that they published, the biggest gain of those 14 or 12 years, depending on your gender, was exercise. Eight years of an increased average life expectancy came from people who exercise for 30 minutes a day. And this isn’t, strenuous weightlifting. This was as limited as just walking for 30 minutes a day.
So sure, in terms of optimizing biological age first, it’s important to measure many times a year so you get a full picture of what’s going on, or a more full picture than one time point. And obviously diet’s going to contribute to that too. But the biggest – fitness – like I said with the eight year increase in life expectancy is a huge contributor to that.
Now there are people in the calorie restriction society who take it to the extreme and get their BMI to 18 or less and think “oh well I’m CR, I’m going to live infinitely long”. And it goes back to what do your biomarkers say and what is the optimal body weight – and potentially even splitting that further, body composition – that’s optimal for your biological age. So it’s not an arbitrary, “hey, I’ll get to a BMI of 18 and then I’m going to be youthful forever”. It may be 22, it may be 24, maybe 26, it can vary. So those are the factors.
And then it’s for each individual, I don’t want to put a blanket statement and say “do this, this, this and this”. It’s for each individual to self test and to identify the factors that optimize it in them. When I first started out, I used to go completely based on the literature and the population trends and follow them.
And once I saw that some of them didn’t affect my circulating biomarkers at all, I thought, well okay, that’s great for the average population, but that may not work in me. Which is kind of what the whole purpose of epidemiology is, is to make recommendations to the average person, but have people actually integrate those changes. So that’s kind of my point is to self identify those things.
What would you say the main changes you made to your lifestyle and diet from self tracking, for example, carbohydrate restriction, the amount of protein you eat, macronutrient ratios and so on?
So when I started getting very serious about the role of diet in this process, I went full vegan and there’s actually a Tufts video that it presented, I think five years ago just showing that data. And I did that because at least five years ago the media bias was, “oh, if you go vegan and you go completely plant-based, this is optimal for your health, it’s better than everything”.
So I thought, “all right, let’s see. Let’s see what the data says”. So when I did that, my triglycerides doubled, which may seem like a lot superficially to hear that they doubled, still within range, still less than one millimolar, which is about 90 milligrams per deciliter. So less than 90 or one millimolar is associated with less risk of death from all causes in a huge meta analysis.
So granted, my triglycerides went up to about 90 but my average was about 45. If I stand in clinical medicine, I’m still within range. But to me if something’s doubling that’s a big jump. And then my HDL went down and these are things that are going in the wrong direction. So then I thought, “well okay, clearly full vegan isn’t optimal for these two biomarkers so I’m going to add fish back in”. And I knew from past measurements that when I had fish in my diet, my HDL went up probably about 25% and my triglycerides went down.
So when I added fish, which is basically sardines every day because I don’t feel like cooking – fish every day for 40 minutes, just pop it out of a tin and I’m good – exactly what I predicted happened. My triglycerides went down, HDL went up, things going in the right direction. So since then it’s a continual trial and error process. I kind of laugh when I see companies that’ll say, “oh well, send us a microbiome measurement and we’ll give you the diet that’s best for you”.
I mean, I’ve been doing this now for five years where I’ve got five years of dietary data, 1800 days of consecutively tracked dietary data, macro and micronutrients with 25 to 30 blood tests. And it isn’t a perfect thing – I’m still trying to figure out at times what’s the optimal diet, like you and I talked about through email, I noticed my creatinine levels going up, which indicates that my kidney function may be going down, which kidney function goes down with age, especially measured by eGFR as a measure of kidney function.
So in all my little dietary experiments to see how it affects my biomarkers, I started eating more meat, eggs and cheese. And this isn’t to say I didn’t need it before, maybe before I had it once a week, but now it was more often, maybe five or six times a week. And I noticed that my eGFR started to go down, which is a bad thing. I don’t want to fall into these traps where my biomarkers are following age related trends, in this case going down.
So even though my other biomarkers of kidney function didn’t change – being blood urea nitrogen, uric acid – when I look at the correlation between the sum of my meat, cheese and egg intake with creatinine, it’s a relatively strong correlation, 0.5 to 0.6. It’s not 0.8. I mean I have seven data points for creatinine with seven dietary periods, so more data will help to flush out that data.
So I don’t like seeing my eGFR values hitting 80 whereas they’re usually around 90, 95, 100 and before you know it, they could be 60. So I get your point about, maybe it’s not a kidney function thing and it’s just a creatinine thing, which is true but for these things, I tend to err on the side of caution rather than measuring myself to death with other things. But I’m going to cut my meat, cheese and egg intake, but not touching my fish or whey protein, which I put in my homemade protein shakes and then see what happens.
If indeed I’m eating too much meat, cheese, and eggs like five to six days a week, which I changed it to a few months ago – it was never that often – for my next blood test in a couple of weeks, we should expect to see my creatinine levels going back down. Now, whether that’s actually related to decreased kidney function, I don’t know, but for this instance I’d have better peace of mind knowing that my eGFR was closer to 100 rather than going in the opposite direction, but it’s a constant trial and error process.
You mentioned about your triglycerides doubling and your HDL falling on full vegan and then those numbers correcting when you added fish back in. Did you try the same experiment with say meat, cheese and egg as a source of protein, or is it something specific you think to fish oils or the nature of fish protein?
Yeah, so fish has got Omega 3s. Omega 3s can reduce inflammation, improve intestinal barrier function. There’s a lot of ways that it could lead to reductions in triglycerides and increases in HDL. This could get into the role of dietary acid load. But then again, just as an example there, I added full fat yogurt. And it’s funny because I have friends that I’d make fun of them for eating dairy because I’d say “dairy’s for babies, and once babies outgrow weaning, they don’t consume their mother’s milk”.
But had some microbiome testing done in my gut lactobacillus, which is found primarily in fermented foods like yogurt were basically zero and there’s a lot of positive health benefits of lactobacillus-related species, especially as it relates to muscle mass, the gut-muscle axis. So I added full fat yogurt into my diet and for two biomarkers, red blood cells which decreased with age (which isn’t a good thing in terms of mortality risk) and hemoglobin (which are found in red blood cells), which for biological youth for example, red blood cells are about five and hemoglobin about 15 is optimal.
So for me, no matter what I did before I added the full fat yogurt in, I couldn’t get my red blood cells back to five which I had actually seen in blood test results on my own 15 years ago. So I knew that it was possible. It just, for whatever reason, I couldn’t do it. And similarly for hemoglobin, I hadn’t been able to hit 15. I had an older blood test for a while and part of me was almost resigned to the fact, well, I guess my red blood cells are aging and I’m just aging now, and that’s just how it’s going to be.
But for whatever reason, I thought, all right, I’m going to do the experiment. And I didn’t even expect the yogurt to affect those two variables. But as soon as I added yogurt into my diet, my red blood cells haven’t been lower than five. Whereas over 15 measurements they couldn’t crack five, and hemoglobin is back up past 15. So the reason I bring up the yogurt, which goes back into the dietary acid load because from the potential renal acid load (PRAL) calculation – you know, Professor Remer’s calculator – yogurt has a lower dietary acid load.
So for that as a source of protein, I don’t include it in the group for meat, eggs and cheese, I’d say in terms of nutritional benefit, those foods may have less relative to the yogurt, which has got the lactobacillus species and the sardines which have the Omega 3s. Whereas meat, cheese and eggs for me probably have less nutrients that are positively impacting my physiology. Or maybe it’s just too much animal protein for whatever reason.
That’s the next thing. It’s…I have friends that are like, okay, sure you’ve got this correlation, but is it causing it? And to me, if I see positive changes in biomarkers on some level, I don’t care. But as long as it works and you see things going in the right direction, I’m not interested in going down the rabbit hole of doing more food based experiments to figure out what the exact mechanism is.
So it’s the net effect that the food that you eat has on producing acid in your body. Now granted your kidneys should be able to buffer it out with bicarbonate, but the idea is that too much food that can lead to a high acid burden can kind of wear out the kidney’s ability to buffer that over time leading to small deviations and increased acid levels in the blood and that isn’t good. Metabolic acidosis isn’t good for lots of different things in the body, bone loss, just as one example.
So then you could have get into the carnivore issue, right? With how would you reconcile that data. Because if you’re eating just pure meat diet, it’s just pure acid. There’s no alkaline producing fruits and vegetables there, right, so.
No, it’s a tricky topic because I had a chat with someone called Lynda Frassetto – she’s a nephrologist who’s really specialized in this area – and I really feel the waters have been muddied over for dietary acid load by this concept of the “alkaline diet”, and it’s largely since been discredited, but there were some people really trying to sell products based on the idea that “you must be alkaline all the time”.
And I think that really confused some of the good science underneath this. So we know for example that the body has to maintain a steady-state pH in the blood, and that varies very little, that acidity is removed both through the respiratory system and also the renal system and through buffers, and that extra acidity has to be excreted. When we’re young, we have very strong kidney function, so people who are in their 20s and 30s and probably 40s are not going to suddenly get sick from having a high dietary acid load.
However, we also know from looking at people at the older spectrum – because typically people in their 60s and 70s have about stage two kidney disease (CKD), so it’s not requiring treatment but a stage before that, a significant loss of function, and also actually from space as well, things like bone loss – that acid load does accelerate bone loss and also loss of kidney function. So the way I kind of say is, “look, having a high acid diet you’re probably going to be fine right now, but with more and more of us living or trying to live to 100, we know that kidney function declines with age. So let’s make an investment in our health to maximize that longevity”.
We also know there are also other potential consequences in terms of muscle function and retention, even muscle performance – acid load impairs physical performance for athletes – so that’s another benefit to being on the safe side. But I think it’s tricky because obviously for example there are many benefits from being carnivore. There is the satiety, there is the blood sugar regulation, there’s the muscle mass retention and growth. So I’m not saying it’s all bad, but it’s tricky when you get into this area because people feel very strongly about the diets they associate with, right? So how do you get that kind of trade off?
Superficially, I think most people would probably think that I would be anti-carnivore, but evolutionarily there are periods when maybe that’s all you ate, was meat for a short period of time, right? But was that optimal for health? I mean yeah, it was optimal for survival. I mean, if you ate, you had more energy to reproduce and there you go. But say, you roamed a three mile radius for all the animals that you could eat and you caught and ate them all over some period of time. Well, if there were no more animals to eat in your localized region that you could walk to everyday, you’d have to eat all this stuff.
So there are probably periods where, people ate nothing but meat for a few days or weeks or months. But then after that was gone, it was less meat and lots of other stuff. And if you look at some of Eton’s papers, he’s published, like “what was the paleolithic diet actually like?” And I think by mass and volume it was like 25% animal but then 75% plants, so when he calculated out the fiber intake of that time period it was like eating 100 grams of fiber a day but also high-protein, obviously. That’s kind of what I’m doing with the blood testing. I always say what does the data show?
Yes, I know this is associated with kidney function and uric acid levels that are too low – I think if I remember below four – and then too high – I think above eight – are not optimal in terms of risk of death for all causes, so too low, too high, increased risk of death for all causes for uric acid and then it increases with age. And I get your point, I’ve heard that argument before too that how do you reconcile that higher levels of uric acid act as an antioxidant and what I’d say is if it’s higher than eight, even though it may be acting as an antioxidant, when considering it’s associated with all cause mortality risk, the net picture is potentially bad.
And if that weren’t true you’d expect to see decreased all-cause mortality risk with the higher levels of uric acid. But that’s not what we see.
I think it also goes to the point that information needs to be looked at in context. You could have, for example, someone who has a high PRAL diet, a high acid diet, because of say high carbohydrate intake, grains, maybe even saturated fat. And that could be someone who has some nutrition deficiencies, they might be say from a low income family. And then there could be someone who is very fit and healthy naturally but actually eats a lot of steak for example. And they may both have a high PRAL but their actual mortality risk may be quite different. That’s why acid load itself is not a definitive marker of mortality risk.
So coming back to the uric acid point as well, uric acid is involved in scavenging free radicals, but at the same time it’s not surprising that it’s also associated with all-cause mortality because a diet high in purines – which can also include alcohol for example – can but not necessarily increases mortality risk. So I think that’s the point about the more data we have – but obviously in the most easy to collect, cost-effective, painless way – then we have more context, we can really understand what’s really going on.
100% agree and I try to almost never look at single biomarkers in isolation, but if we know that uric acid levels higher than eight are associated with increased all cause mortality risk, what if your inflammation, like your CRP (just as an example) is close to zero and your insulin sensitivity is as good as it can get. But you just have, like you said, just a higher level of uric acid because you’ve got a high PRAL diet.
If all of the other biomarkers look good, especially I’d probably say in that case, if the blood urea nitrogen wasn’t too high in this case, I’d say probably less than 15 somewhere between 10 and 15, and your kidney function was good, whether it’s by eGFR or cystatin C or some other measure, if you’ve got a high uric acid in that case, well maybe it’s just related to the high purine level of the diet and everything else is good, so it really doesn’t mean much, right? But it goes back to, again, the comprehensive picture like you mentioned, because most people don’t do that, they’ll think it in isolation instead of the whole picture, which tells you obviously more of the story.
All right, Michael. Well, this leads me to say thank you so much for joining us. It’s been a great discussion, I’m really glad we managed to get into the weeds and go through some of this stuff, and I’m just excited to see what you’ll be working on next.
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