Inflammation does play a causal role in accelerating the aging process. So if we can get in the sauna or go for a run or do some yoga or something that's going to activate these genes that are anti-inflammatory. When we are exposed to rush hour and traffic or whatever it is that we can't predict that's going to stress us out that were able to handle that stress better.
Aging none of us can escape like gravity it pulls on each of us. I did some of us age gracefully and others. Don't how do our bodies and Minds experience? Aging a cellular and molecular level. Why do we even age to begin with and maybe most importantly, can we do anything about
it?
My name is Gordon with go and here at the buck Institute in California. My colleagues and I are searching for, and actually finding answers to these questions and many more on this podcast. We discuss in discover the future of Aging, with some of the brightest scientific stars on the planet. We're not getting any younger yet.
Hi everyone, welcome to the show. Delighted to have Rhonda Patrick on today. Rhonda's. Really fascinating person is made this transition from being a bench scientist making discoveries to being someone. I guess we didn't even realize we needed, but we're doing that and that's someone who's a phenomenal Communicator through her podcasts about the field of aging and human health and she represents not companies. Not
Versa tease, but she represents ideas and probably knows as much about aging is anyone else on the planet. So delighted to welcome your under.
Thank you Gordon for having me. I am a huge fan of the buck
Institute. You're very kind row, and I thank you for that. You know, tell me, I think you grew up in California, but tell me about how you got into science in the first place.
I grew up in San Diego, and I was about 17 when I started getting a surfing. And I,
I was very much a nature girl, I decided that I wanted to spend my life being a marine biologist and studying creatures of
mystery to me, you know. So I spent
so much of my time in the water and then when I wasn't in the water, I was watching David Attenborough on the Nature Documentaries. Those were my original aspirations and it was like, okay, well, I want to be this biologist who goes out to the Galapagos and, you know,
No serfs out there while I study, you know, all the cool animals and so I decided I had to, you know, basically pursue science in order to get that biology degree. Little did I know that I would never leave the lab and I would never go out into the ocean or in, you know, into sub-Saharan Africa on a safari, you know. So I think it, you know, I'm probably not alone in that there are probably a lot of people that start out wanting to be filled by
Largest. So that was the start of my scientific Pursuit. And then I just decided like, okay, well, I probably should just do the hardest thing and that is chemistry and biochemistry. And I honestly just kind of got all tangled up in that and and then lost track of my field biologist dreams and just started to get into, you know, real, real hard science. So
actually that's an amazing parallel because I was a bird watcher and I
I wanted to be a field biologist as well and I went to my teachers, this was in a high school in Scotland. In a steel. Turn said I want to be a field biologist and no nobody. Nobody has ever met a field biologist and he said, you should just do microbiology if you're going to do that. So, so it's some point you find yourself in a lab and how, how was that experience? I'm and the reason I'm asking you about the lab experience is that you've transitioned into a
Different world of podcasting and science communication which will come to. But I want to talk about your lab experience first. So did you enjoy being in a lot?
I did. So, my first lab experience was when I was an intern and at the time, I was a junior in college, and I was synthesizing peptides and doing a lot of chemical chemistry work organic chemistry. And I did that for two years while I was still in school and decided that I
Really didn't enjoy it. Oh okay. It's a little thing. I didn't feel like I could relate to just the the real chemistry part of it where, you know, it's just too far removed from biology and that's when I went to work at the Salk Institute for biological sciences. I was doing some of the research that you do in your lab where I was looking under the microscope at these tiny little nematode worms, c, elegans? Yeah. And this was also an aging lab.
And so I think that's sparked, my first real excitement for aging and just sort of doing experiments with my own hands and I'm seeing that I could manipulate genes that were homologous in humans. You know seeing that basically I could genetically manipulate worms to live a hundred percent longer blew my mind. And so that was kind of it was a fun experience.
But I I decided to to kind of like go more into cell biology and cancer biology and so I did all my graduate work in cancer, biology and cancer metabolism. And a lot of animal works. I went from worm to Mouse where I was studying mitochondrial metabolism and it was I spent just like, I don't know how many months of my life under like an electron microscope looking at mitochondria and, you know,
No light microscopy as well. I mean just everything all things mitochondria for years and years and I was a bit of a mitochondria back, I still am I? But now I've got a bigger picture focused of it rather than looking at the electron level. So at that at that same time and and the you know, graduate school was stressful for sure but I also learned a lot and at the same time this is when I started to really develop my passion for health,
And fitness and applied science and the science behind the health and fitness. Because I found for me that when I understood mechanisms, I was able to, you know, basically do things in my life that were healthier and I was more motivated because I understood things better. And so I felt like that was really foundational for maybe other people to make these changes in their life, is like a understanding why like the science behind it.
It. And so it was something that I just, you know, in my in my free time I would do I would go to coffee shops and started blogging. I started a Blog and I would you know just write articles and you know try to find science that would back up. Things like vitamin D or omega-3 and what their role is in human health and and I would also, I would also Charter. I also would try to convince my family and friends, why they should be healthier and
Particularly people that were not healthy and I found that it was very challenging for me to do that because they took it very personal. And so I basically just started putting articles and making videos and sending it to them and notice that they took it a lot better because it wasn't like I was directing a lecture at them and lecturing
about. Yeah, yeah.
Yeah. It was, you know, you should listen to this or see this.
So that was the kind of start of my my passion for science communication, so so that. So that's, you know, something that that's kind of, that was kind of the start of it.
Well, I'll be that's fascinating because and I actually want to go back to the warm because, you know, many people and I always lie, I had this experience as well. Who you see a tiny little animal crawling around underneath
Bigger plate and it's supposed to be dead. And it's not it's not dead because either there's a mutation that that's extending lifespan or you've put a chemical compound on these worms that extends lifespan, and it's shocking to see that that the Aging is not this. This fixed quantity, that this plastic is my evil. You can intervene and a lot of people just stay there, right? They just for their entire careers.
Pretty much like myself stay with the were more with the drosophila, or, with the yeast. So what was it? That took you away? From the worm to cancer? And did you feel like this was? This was amazing. But it you wanted to do something more.
I think there was circumstantial things that directed me there. But I I think also, I just kind of realized that if I had stayed and and were
Worms that I may not learn as much about its kind of a very little, it's kind of a like kind of narrow to like the genetics and the similarities between humans and worms with the genetics. And there's this whole systems biology and and so I kind of just end it because you'll see I went from worms literally to doing research on mice and cancer biology to human trials, and clinical trials in nutrition. And so I I got this sort of well-rounded sampling of
Ology, you know, from from the real me from the genetic, you know? And but there was a big picture still with the genetic research with the worms because you know, the studying the aging process, I mean it's very relatable to like learning all the tools and how to do experiments and Metabolism learning a lot about metabolism in graduate school and then sort of moving on to humans and in human metabolism and and clinical trials and how to correctly do them and how to analyze
analyze data from them. And and so I think there was something just in the back of my mind that I wasn't quite aware of like like I am now that I was kind of gravitating towards whereas like I need to kind of broaden I need to broaden my tool set. You know and what I am and what I'm researching. So that's that's that's partly it. I
think I mean this is in that you made between bench science and you know running your own love and you know, coming to the buck is a faculty member or something.
And there you've taken, which is incredible. I mean, it's an amazing what you've achieved and everyone knows you and actually one of my PhD students in my lab right now is here, because of your podcasts. You know? So your influence is huge but I still want to still want to think about you know you as a bench scientist but you work in vitamin D or a did I get that wrong?
I did work in vitamin D. Well, researching, I was
Young at DNA, double-stranded breaks in peripheral blood mononuclear cells, from from participants in clinical trials, where we had obese people that were given a micro nutrient, Rich bar developed by Bruce and his colleagues. Yeah, before I came to the lab and at the time it was called The Quarry bar. Corey was the Children's Hospital, Oakland Research Institute and it was a it was a micronutrient dense bar, that had a fiber Matrix.
It was sort of mimicking, what you would find in in nature. So it wasn't just like a supplement, it was the whole package. And so, I was, I sort of had a hypothesis that, you know, obesity causes DNA damage through double-stranded breaks and that potentially, you know, because people that are obese or eating terrible diets. Obviously, there's all sorts of refined, sugar and terrible things that they're adding, but they're also not getting important things like magnesium.
IAM and other micronutrients that are important for the health of DNA and repairing DNA damage. And so I was sort of looking at double-stranded breaks in their, in their, their peripheral blood cells before. And after given these micronutrient bars, and also we were, we had other clinical trials, like Blueberry Blueberry extract, we were doing. And so I had, I was originally doing some of that work and then I got to do other interesting exploratory work and that had to do with vitamin D. And a lot of this work was was me.
Doing my favorite thing which is diving into the literature and and finding studies that often end up in a vacuum or in a black hole, you know, where they just don't get seen by anyone and you know sort of putting some dots and connecting them together all with evidence you know all evidence-based and so I did some in silico work as well. Looking at Vitamin D response elements in genes that were regulated by vitamin D and so you know I was looking specifically at the sequence of those elements and how
How a gene in the brain that converts tryptophan into serotonin. It's called tryptophan hydroxylase to is activated by vitamin D. According to the vitamin D, response element. And since I published this early work, as a review article there, have now been in vitro and in Vivo studies that have confirmed that it's. It is true. They have experimental e. Shown vitamin D does activate the tryptophan hydroxylase to Gene and that can affect serotonin and
So I had done some review articles, I guess, what you would call my publish, but they were more integrative, more perspectives. Yeah, where I sort of was putting out a hypothesis and giving evidence backed by literature and hoping that other people because I'm not, I wasn't, you know, a real research, I wasn't doing vitamin D work and in this in this case I was talking about the role of vitamin D in neuro developmental disorders like autism schizophrenia ADHD. And so I was hoping that people
People in those fields, would would then say, oh, look at this is interesting. Why don't we test some of this doing X Y or Z? So, that was some of the work that I did. But also, like, I launched the podcast officially in 2014. I was a, I was still a postdoc at the time and part of the part of my goal for launching the podcast. In addition to what I talked about which was really being passionate about everything I was talking about and this, the, the science behind, why a micronutrient insufficiencies can be.
Detrimental to health and why you may not know that now, but you may know that later. And and what we can do about it and you know, other things like running and exercise and sauna and all that stuff, right? Yeah. In addition to that, I was also using the podcast as a incubator for ideas, for new ideas and because we have a large science, you know, scientist following and it's actually worked out where people have done experiments based off of things. They've heard on the podcast. Yeah, absolutely. Yeah.
Cross-disciplinary, you're getting this cross-disciplinary effect where you know scientists that are doing research on vitamin D. Receptors are now listening to fasting your researchers on the podcast and then they start looking at the effect what happens when you fast and on vitamin D, you know. So yeah I think that's also that's one of my biggest excitements
honestly, just to Circle back. Micronutrients, can you give us a definition of
that micronutrients are around 40 or so essential?
Vitamins minerals, fatty acids and amino acids that you have to get from your diet, your body cannot make them. And so we need to get you get them from our diet. And the reason they are essential is because they run our metabolism. They run pretty much everything, you know in our body and about I think something like you know there's like twenty two percent of all the enzymes which are, you know, proteins that are doing work inside of our cells, require a micronutrient as
A cofactor. Yeah. As you know, you know, people may not know what a cofactor is, but a cofactor essentially just means like it's needed for the enzyme to function properly. So micronutrients are important and and there's there's huge insufficiencies in people. They're not getting enough. They're not eating, you know, healthy enough foods to basically you know satisfy their sufficiency for magnesium, for example, obviously. Yeah vitamin D is a big one but that's something that we normally we make from the
And there's other reasons why we're not getting that as much. We're definitely not outside and there's all sorts of problems. But
what that means is I'm sorry to interrupt that, I mean vitamin D. I mean it deficiency is really interesting because it elevates the risk for cancers for neurological disease for diabetes. It kind of looks like an accelerated aging phenotype deficiency of vitamin D and we did
tell you seen those vitamin D receptor, knockout mice.
I see other people knockout, are they, for
example, NOCO? But yeah, yeah, I think so. But yeah, I mean, is it looks like accelerated aging and we in in warms we squirted vitamin D on warms, they don't normally see vitamin D and eggs, extended their lifespan, it stopped protein aggregation, prevented a beta toxicity. So, it seems like deficiency is really, really important and as you see, I mean, many populations are subject to deficiency for not getting in there.
It in the not get. So I'm from Scotland where there's no sun and vitamin D. Deficiency is a big deal. So it is one of those things you think wow that that sent as I said almost an easy fix as a public health
issue. It is and seventh. 70% of the United States population doesn't have sufficient levels, which is defined by the endocrine society, as 30 NG or 30 nanograms per milliliter or more and there's been all sorts of
All-cause mortality, studies looking at vitamin D levels and association with all-cause mortality. I mean over decades and Decades of, you know, science that's been published. And it's pretty clear that levels above 40 or more. You know, between 40 and 60 is a really good sweet spot, 40 and 60 Nano grams per mil are associated with the lowest all-cause mortality. Yeah. And so, you know, Vitamin D supplements are one of the easiest way to correct the deficiency, you know? So again, I mean, we could go and we can talk for hours on vitamin D.
I mean, other dangers to overdoing it? Can you take too much?
So, I mean I've looked really deepen into that data and its really like the to get hypercalcemia which is like high blood calcium, which is like the major concern. Yeah. Like you literally have to take hundreds of thousands of IU a day for multiple days. It's really hard. It is really hard. It is now people do have certain conditions like kit like kidney disease and stuff and they might
Be more prone to a problem, you know. So obviously that's something to discuss with the position but by and large the The Institute of medicine. The the upper tolerable intake limit was set up 4,000 IU's a day and I'm absolutely a reasonable amount. Yeah. For people to take. Yes. It's that is not, you know, a dangerous level of vitamin D.
Let's talk about hormesis. What's her mises?
Well, I like I like to Define it as dr. Mark Matson, has eloquently put it in so many Publications. You know, that basically the not defining hormesis, but starting with basically intermittently challenging yourself with stress. Yeah. And and why? That's important and I think and I know probably mark,
Degree necessary, you know, that that basically humans have evolved with these intermittent challenges and, and those challenges are things like physical activity, you know. So before we had instacart and order our groceries on our phone and have them delivered to us, we had to go out and Hunt our food. If we were going to eat meat, we had to go out and like run and like we had to be fit to do that. Yeah, you know. So, physical activity was a stressor, you know that
That is stressful on the body. And also, you know, walking around and getting berries and picking, you know, berries and nuts and whatever it kind of plants and stuff. Also required movement. Yes. As well as you know, not having food. So if you didn't catch your prey or if they're, if it's too cold and there wasn't enough berries or whatever, you know you you were challenged by a food scarcity period, right? And that is also a type of stress or not having
Food nowadays, we have food all the time, so much food. I mean, you never have to not eat. I mean, we could be eating white why we're talking doing this podcast, right? I mean so that was another challenge that humans evolved with as well as eating. And this all this all gets credited to a beautiful paper review, paper that dr. Mark Matson wrote many years ago and also you know eating these compounds from Plants. These are phytochemicals, these are things like
Like, you know, flavanols and polyphenol things that you hear about those things also are little bit stressful on us and challenge us. So what what does that do? Well, that actually activates a variety of stress response, Pathways that are that are built into our genes. They're meant to be turned on, and when they're turned on, they are not only good at dealing with that small amount of stress, whether it's the exercise physical activity or the intermittent fasting.
Or if it's the plant compounds or in other cases, stress from heat or cold, they are active for a longer period of time where they have an antioxidant and anti-inflammatory effect that last far beyond what that little intermittent stress was, and helps you deal with the stress of Aging, normal metabolism, normal inflammatory Pathways being activated. We are aging right now. Inflammatory molecules are being released. So if you can have genetic Pathways that are basically
Toning down pro-inflammatory, cytokines and bumping up anti inflammatory Pathways, and, you know, bumping up antioxidant Pathways in our bodies, also helping with stem cell production and helping with our proteins, folding normally. So we don't have Aggregates building up, like, you can activate those Pathways by doing things like exercising and eating, you know, you know, some of these flavanols and polyphenols and also by, you know, fasting. So the idea of hormesis
Sometimes don't like to start with the the blunt definition, because it can sound scary. But if you have too much stress, too much of something that is stress, it can be bad. Yeah, and, you know, so I mean if you drink too much water that could be really bad if you if you do nothing but exercise without a break. I mean, you could cause like, like harm. So hormesis kind of refers to this this dose-response curve where the amount of stress when it's in a small dose.
Beneficial because it is activating all these stress response Pathways that have a net positive effect on the way our health and the way we age. But if you go over that like dose if you you know, if you were to drink 300, you know, grams of caffeine you would die, you know. Like so, yeah, you know. So basically it's like, it's a little bit of stress that's beneficial. And, and the idea is that we were meant to be stressed. We were meant to be stressed. We were meant to die. We have genetic pathways
Are activated by them. I mean, yeah. You know, to me it's like, it's so it's so
obvious great. You know, I've been really interested in this whole thing for a long time. I found it when we subjected these little tiny worm, C elegans to heat shock, they lived longer and 15
percent longer. I thought your work all the time. Yeah.
So you've interviewed Alyssa apple and her amazing work with Elizabeth Blackburn showing that
If you're exposed to psychosocial, stress such as parents with, you know, children who are have a particular condition like autism or something that there's a telomere attrition that happens in those parents. And so it seems like the chronic stress is really bad, but the acute stress can be really good and I guess it's finding that the boundaries now. I know you've written about this in terms of saunas and
This actually really is fascinating for me because as I say, we were talking worms and now you're talking about he's talking humans. So talk about saunas and talk about doors
first. Why him interested in sauna is just from using them. When I was in graduate school I lived across the street from a YMCA and I used to go into the sauna every day before I would go into the lab literally. I was doing it. Seven days. I was doing like seven days a week so and this is back in like 2009.
And of course, I had also through my early work in. Andy Dillon, SOB been exposed to heat, shocking worms and, and, and he, and expressing lots of heat shock proteins, which is part of that stress response pathway. I was talking about when you're, when you are exposed to heat one of the, you know, many different Pathways that are activated is is the the heat shock proteins and they are involved in helping proteins keep their three-dimensional structure inside of your cells to prevent them from
You know, aggregating and forming plaques and among other things, they also have antioxidant activity as well. But anyway, so I was kind of aware of that while I was doing the sauna, but the sauna really just started having really profound effects on my anxiety and my ability to handle stress again, which was. And this was like, mental stress, like I was able to handle a field experiment. That was a six-month setback. That would have been. Do you know? Those things are hard to deal with. Yeah. So the sauna was really helping and that's kind of where I got interested in it and the effects on the brain. But a
Of
the sauna the research that has been done on saunas and human health have come out of dr. Yar allow cannons Lab at the University of Eastern Finland and he's he has shown he's he does beautiful, you know epidemiology types of analyses and observational studies. But he's looked at sauna bathing in men and women and risk of, you know, cardiovascular disease and death from
From a variety of different, cardiovascular diseases and death from all causes and dementia and Alzheimer's. And when he's found is that there's a dose dependent manner, you know, that basically is protective so people that use saunas 427 times a week versus two to three times a week, have the most robust protective effect on all these mortalities. So for example, cardiovascular related mortality, is 50%, lower and pin men that use this on a four to seven times a
week, right? At one time a week in May
Yeah,
it's only 27 percent lower and men that use it two to three times a week, which is one. So there's a dose-dependent effect for frequency but also there's a temperature and duration effect, meaning. Most of the temperatures of the asanas were about a hundred and seventy-four degrees Fahrenheit. And if you look at the data and some other, in some of their tables, you'll see that men that spent only 11 minutes in the sauna. Even if it was four to seven times a week, they only had like an
Reduction in cardiovascular related, mortality compared to like a 50% reduction. Yeah. The 50% reduction came to pee men that stayed in the sauna for 20 minutes and and this was like true for other cardiovascular related mortality is there was like coronary heart disease. Mortality was 68 percent lower in men. That did this on a forty seven times a week. Versus one time, a week and all cause mortality was 40% lower compared to men only did it, you know, one time a week. Yeah, so with the observational data.
There's always the okay, well, that's not establishing causation. However, the dose dependent nature of it, the frequency as well as the duration in the sauna to me is very is very much reassuring that there is a more of a causality that can be established, you know, because it's just you just wouldn't see that if it was like some other effect, right? Like a it's like a having the the healthy user bias kind of effect. Not to mention they corrected for all kinds of problems, you know?
High lipids exercise socio-economic statuses anything. Yeah, they
did so many people. Leave the sauna and jump into a very cold bath or have a culture. So what's the called exposure story to
this? Yeah, that's the only common in countries that culturally use the sauna like like Finland and also in Russia they do the the Russian banyas and they also do some cold. Interestingly, there's a lot of overlap between these intermittent stressors, you know,
So, so you'll find that cold exposure also activates heat, shock proteins, you'll find that eating some plant compounds, like sulforaphane found in the Brassica family activates heat shock protein. Yes, he does it the best. But the, the idea here, is that back to that concept of, you know, intermittently challenging yourself and the genetic. You know, it's hardwired in our genes at these genes get activated by stress by like, a low-level type of good stress. Well, there, you know, there's
There's, there's definitely a lot of overlap and so cold, cold. It's kind of nice to know that, you know, cold does a lot of things that that that he'd also does and vice versa. So like there was a recent publication showing that heat, local heat application can can Brown fat is something that cold is known to do so cold, exposure, one of the main things it does is it changes the metabolism inside your adipose tissue and also can can do it in your muscle tissue and that is by a couple of mechanisms.
One is by making your body, both of them, help your body generate heat which is what you're trying to do your body trying to survive. So the stress response pathway in this case is norepinephrine is elevated, norepinephrine is a neuroendocrine hormone that's generated in the adrenal glands. It's made it, you know, it's in the plasma circulating but it's also a neurotransmitter in the brain. So it's robustly increased when you when you get into the cold and that activates a pathway inside of your fat cells called you see
P1, which essentially freaks your mitochondria out as, you know, Gordon and your mitochondria, are essentially trying to their kind of, you can think of, as a battery, and they're kind of trying to maintain a electrochemical gradient, a negative charge on the inside and a positive charge on the outside. So to speak. And what ends up happening is the, you cp1, totally takes that away. All these protons start leaking out and your mitochondria freaked out, and so they start making energy. They're not actually making a
Peter making energy in the form of heat but they're burning substrates to do it. Yeah. And so and so you end up having you know you end up actually burning more glucose or more fatty acids which is kind of a good thing. Even if it's not necessarily making ATP which is the real energetic currency of the cell. This is what runs everything in our in our body. But so that's one adaptation. And the other one is actually your body goes, wait a minute. What if I'm going to be exposed to cold again? Like how am I going to make sure? I don't die? Like
How am I going to make sure I can keep myself up and as you know Gordon the way it does that is by making more mitochondria in adipose tissue and that is also regulated by norepinephrine. It increases a protein called PGC 1 Alpha which is involved in the growth of new mitochondria it's called mitochondrial biogenesis and essentially your body has figured out a way to make more of these. Mitochondria that way when it's exposed to heat. I mean, sorry. When it's exposed to cold, they can make more heat. Yeah. So so that's that's
Kind of the those adaptations that occur. And of course, there's all sorts of science going on, thousands of labs, trying to understand Brown fat. And, and the reason this is called Brown fat, actually, I should say it's because when you have more mitochondria in and out of pipe out of sight cell and you look at it under a microscope, it looks dark. Yes. So it looks darker and so it's called the Browning of fat because it looks it looks Brown under a microscope rather than white with all the lipid droplets.
So I just thinking about
a classic paper from Nikki Holbrook many, many years ago now, and it made the connection between the molecular processes of stress response, like the induction of heat shock proteins, which are molecular chaperones, which, as you said, you know, involved in protein, folding protein shape. Something that's really, really important in aging and also really important in neurological disease. Alzheimer's Parkinson's. And so on and her experiments were two subject brats too.
A mild psychosocial stress, just basically restraining their movements and showing that actually, that was enough to turn on the expression of molecular chaperones. So is this connection between this molecular process that we do is really important. What we now know is really important in aging and age-related disease to psychosocial stress and I know you've thought about this as well, you've talked about mindfulness and cognitive behavioral therapy. And so so we're going from her.
Reese's here to these, these these areas of psychology,
can you talk about that a little bit?
What the psychosocial stress and I know like as you mentioned a lot of work has been done by dr. Elissa epel from UCSF, yes. Who was on the podcast years ago and, you know, and many others have done a lot of work on this. Just looking at the effects of psychosis with social stress, whether it's taking care of sick, family member or financial stress or relationship stress, like these things and there's been
Some research by various different groups showing that actually these, these types of stress, the psychosocial stress actually affects the release of endotoxin from our gut and endotoxin is for people. That don't know, it's also referred to as lipopolysaccharide but it's essentially the outer membrane of a bacterial cell and when when the bacteria are killed in this case, in our gut, by our immune cells, if they release endotoxin into our bloodstream, and this activates inflammatory,
Ways. And so, you end up getting this causal between this causation between stress inflammation, and then depression. And so, like there's been some studies done showing that you can actually even just inject lipopolysaccharide into healthy people and activate their inflammatory response and cause them to have depressive symptoms. And this is compared to people given a saline injection, but you can also then give those same people
Mega three in this case, it was EPA and basically pelant the inflammatory response from the lipopolysaccharide and actually prevent the depressive symptoms. And so the the connection between Health, you know, the stress Health, the way we feel the way we think, but also the, with the way we're aging. So this inflammatory process is not only affecting the way we feel in our mood but it's affecting the way we age. And so there's been so much research looking at the effect of inflammation and chronic inflammation on
Seeing whether we're talking about some of the data clinical data, looking at, you know, semi supercentenarians and supercentenarians and, and centenarians, and all the panels of biomarkers. And how, you know, basically inflammation was shown the reduction of inflammation or suppression of it was shown to be the only thing that was a determinant of going to the next stage. So becoming an actual supercentenarian and also maintaining good cognitive health. So nothing else really mattered as much as
Formation and then there's been a whole you know animal studies. All kinds of just it's pretty well-known inflammation does play a causal role in accelerating the aging process. It's not the only thing you know. So I think that anything that we can do preconditioning ourselves so if we can get in the sauna or go for a run or get on the Peloton or do some yoga or something that's going to activate these genes that that that are anti-inflammatory and activate them.
M. So that when we are exposed to rush hour and traffic or whatever it is that we can't predict that's going to stress us out that were able to handle that stress better. And I think that's the bottom line is that you can't predict when a family member is going to die or get sick. You can't predict when you're going to lose your job or when a relationship goes bad, like things happen in our life that are devastating and we have to be able to cope with them and we have to be able to deal with them and our bodies, you know, our bodies in our brains and obviously there's a whole aspect to meditation.
That's aside from activating stress response Pathways and stuff, right? There's just being able to handle stress and, you know, through mindfulness and stuff, but I think the stress response pathway activation does help. It helps blunt the inflammatory response and there's been a lot of elegant studies done in preclinical monocle models like mice where you give them, you know, sulforaphane or you give them curcumin or you make them run or you expose them to heat and then you give them a stressor
I like you cause them to have an ischemic stroke or something and they actually do better. Yeah, they have that preconditioning. Yes. And to me I always look back at those studies and I think well I want to be that Mouse like I want to be the one that has the good plant compounds. That's getting the exercise that's doing the sauna that's getting all the beneficial stress that's doing some some beneficial fasting. That way when something challenges me in a way, that's not good that I can deal with it better.
I'd like to talk about science communication, you are an amazing science communicator and have a great influence in your website, phone my fitness.com, you've talked a little bit about how you got into this, but just could you just tell us about what you think of the major challenges that we were living in an era where where science has accepted by some people but also ignored by many
Others and people like yourselves who were real real. Bona fide scientists doing experiments. Making discoveries have moved into this area of science. Communication, what do you put? How do you see the challenge right now? For in general, not just an aging communication, but in general.
Well first of all, thank you for that very nice compliment Gordon. I appreciate it. I think that their science communication, you know? Oftentimes
You'll find and there's a lot of good science journalist. You know, I don't want to like may say everything but you'll find that there's a lot of sensationalism in sometimes. There's perverse incentives that motivate people. And and so you can get a sensational istic story that makes headlines and just everyone becomes aware of it, and it might not really be true or it could be a terrible study, where you look at. You look at the statistical analysis and
You're like, wait a minute, like this isn't really significant or, you know, or you look at the data and you go, wait a minute, they didn't measure anything biochemically, they're, they're, they're looking at a clinical endpoint. How do you even know, you know, that something worked without measuring it, right? And so I for me, it's an important. It's an important role to fulfill I think is to help actually accurately analyze the data using my abilities.
To analyze science. And and look at the quality of the data and not only this, the study in isolation, but the big picture like knowing, okay, well this is a clinical study, what do we know mechanistically about this? What's the big picture here? Because that all matters, like you could have one. There's so many conflicting data out there and a lot of the conflicting data has to do with methodology. You know, it has to do with the way experiments were done the waist.
Studies were conducted. And if people don't know that they hear a headline and they get confused. So to me, I think it's important for more scientists to help communicate accurately, you know, to the public like the science of what's actually being published and what that even means. So so that's that's kind of what what I do. I have a small team that helps with that as well. Yeah.
It's a bigger problem than I can even handle. You know, I think it's, it goes back to just even scientist not communicating with each other, you know, like, yeah, you know, someone just having these tunnel vision where it's like, okay, you know, maybe I know you're a clinical person that ends always just looks at heart attacks as the endpoint, but like if you're going to give someone a vitamin D supplement measure their vitamin D levels, I mean, see if it even went up like, and that's getting better. But, you know, I started out coming out in the public.
Like this was like 2014 there was a lot of studies coming out and it was you know vitamin D does nothing and the studies literally they didn't even measure vitamin D they just gave people a 400 IU supplement and and then looked at a clinical endpoint and so you know, even data like that were yeah it was a randomized controlled trial but it's the gold standard but was it a well-conducted one like you know because let me tell you 400 IU's of vitamin D ain't much and it takes around 1,000. I used to raise blood, your blood levels by five nanograms per million.
People that don't have Snips that regulate, the vitamin E metabolism. So I guess what I'm getting at here is that the problem? There's many fold problems I think one is that we as scientists we need to sort of all get together and establish more protocols and for doing clinical research, make sure we're measuring things like that's key measuring things. Like you can't like publishing a randomized controlled trial. I think it all comes back to like drugs and, you know, randomize
Controlled trials are the gold standard for a new drug and but you know drugs you never have a drug in your body before you take the experimental drug. You know, when you're doing nutrition studies, we all have we all have different levels of vitamin D. We have genes that regulate how we metabolize it. Yeah, we have different levels of magnesium and if you don't measure those you know I get with a drug. It's like well yeah, obviously they're going to have, you know, zero and they're going to have something and it's going to do something so. But with with nutrients and nutrition, it's different. And I think there's a different standard that needs to be.
Therefore, all clinical research and nutrition. Then there's the problem of sensationalism and yeah clickbait and you know, journalists wanting to make a story and it's like, well, well is this story real science or is it clickbait, you know? So there's just there's multiple layers of problems. And so, what, what, what I really try to do with my team is, is to be cross-disciplinary, is to look at multiple, you know, types of data from from warm data to mice to,
Ocular to human and and to look at the methods and methodology and find well, maybe possible explanations for contradicting, you know, data and explain them to people.
So and your podcasts are very detailed driven. In fact, I love the way that you display scientific papers at the same time as your interview, your guests so you bring up the evidence-based data at the same time as you're talking about things that I think that's
Tastic. I think a large number of people are in absolute. Awe of what you do, you're serving the science Community especially AG community in amazing ways and thank you for that and I just want to obviously as a deep thinker about this you might have some predictions. I know we all hate these predictions questions but where do you think, where do you think the Aging field is going to be in 10 years?
I am, I am, you know, I'm certainly not sure. I'm not sure, you know, for certain but I do, I'm very excited about a lot of the interrupted cellular reprogramming work being done by people by dr. Juan Carlos, Belmonte and collaborators in. I do you know I I'm not sure I that hasn't been enough research done yet. I know there's going to be a lot more coming, but I do this idea.
You know, I always thought about it, you know, totally independently that, you know, when shinya yamanaka discovered, these four transcription factors that could essentially take a old adult cell and referred it to an embryonic like state. It was like, wow. That's like the ultimate reverse of Aging in a way. And so, I think what, you know, Juan, Carlos, Belmonte and others have done was so brilliant in, figuring out a way to kind of just
You know, pulse this, these these factors on and essentially wipe clear the the program and the epigenetic program of the of the adult old cell and make it, you know, not not as stem cell. It keeps its identity, but it wipes away, you know, the whole program and somehow all the gunk and protein aggregates, and DNA pieces, and everything goes away with it. It's amazing. So I'm really interested in that process, but I'm also really interested in
A lot of the work done by the convoys at UC Berkeley and yes and you know, essentially diluting out what other whatever Pro aging factors in our plasma are accelerating the aging process. I think they've nicely done that through a variety of experiments where they've this therapeutic plasma exchange exchange. I mean, obviously started out with you para, by parabiosis studies, where they were hooking organisms up together and a young and old and exchanging their, their, their blood and plasma.
My but we've developed since then and things have gotten a lot more interesting. So that works also really interesting to me but I'm the most excited about about the interrupted. So they reprogramming work and I think that there's a potential there for potentially really possibly reversing some aging. I don't know how it's going to be implemented. I mean you know it's going to probably have to be something that you have to continually do.
Do you know it's not like a long lasting effect because you're going to continually having cells age and stuff but you know and so finding finding all the hurdles and stuff that you're going to have to overcome to make it. Actually clinically relevant will definitely be quite a few years, but I am excited about that.
Fantastic Rhonda thanks so much for your time. Your insights are fascinating and it's been brilliant to talk to it. So thank you again. And
And keep doing what you're doing is really really valuable to the field and to human
health. My pleasure Gordon is really appreciate all those kind words and anytime you want to talk let's do it again. Excellent. Thanks to the buck Institute as well for all the research on aging and advancing our knowledge. Thank you Donna.
Thank you so much for listening. If you've enjoyed this podcast, Please Subscribe, share and give us a five star review on Apple Spotify or wherever you get your podcasts. You're not getting any younger. Yet is made possible by a generous Grant from the navigates Foundation. The navigate rendition is enhancing the lives of older people through the support of housing, health, education and Human. Services are podcast is produced by vital mind. Media Wellington bowler
Who's here with me using sign language to keep me on course and recording the podcast. Stella who I love spending time with talking about science as you know is our editor with the creative direction of Sharif as art and the bucket statutes very own Robyn Schneider as the executive producer if you are listening to this podcast you know that there's never been a more exciting time in research on Aging discoveries from our labs are moving into the clinic to help us all live better longer.
Are the buck Institute depends on the support of people like you to carry on our breakthrough, research, please visit us at Buck, institute.org to donate and to learn more.
