Essentials: Micronutrients for Health & Longevity | Dr. Rhonda Patrick
Date: 2026-01-01 | Duration: 00:35:37
Transcript
0:00 Welcome to Huberman Lab Essentials, [music] where we revisit past episodes for the most potent and actionable science-based tools for mental health, physical health, and performance. I’m Andrew Huberman and I’m a professor of neurobiology and opthalmology at Stanford School of Medicine. And now for my discussion with Dr. Rhonda Patrick. Rhonda, welcome. >> I am so excited to be here having a conversation with you. So, >> thank you. Well, I have so many questions, but I want to start off with a kind of a a new but old theme that
0:30 you’re very familiar with. So, temperature is a powerful stimulus as we know for biology. And you’ve covered a lot of material related to the utility of cold, but also the utility of heat. And as I learn more and more from your content and from the various papers, it seems that cold can stimulate a number of things like increases in metabolism, brown fat, etc., etc., but heat seems to be able to do a lot of the same things. And I wonder whether or not the
1:00 discomfort of cold, deliberate cold exposure, and the discomfort of heat might be anchoring to the same pathway. So, would you mind sharing with us a little bit about what happens when we get into a cold environment on purpose and what happens when we get into a hot environment on purpose? >> Let’s take a step back and I think you brought up a really important point here. You know, we evolved to intermittently challenge ourselves. And before we had Instacart, where you could
1:30 basically just get your food delivered to you, we were out hunting, gathering, we were moving, and we had to be physically fit. you couldn’t, you know, catch your prey if you were a sedentary slob, right? Physical activity was a part of everyday life. And caloric restriction or intermittent fasting was also a part of it. This is another type of of of challenge. You know, we we didn’t always, you know, have a prey that we caught or maybe temperatures were such that, you know, there was nothing for us to gather, right? So, food scarcity was something common as
2:00 well as eating plants. So, getting these compounds that I mentioned. So this is these these are all types of stress intermittent challenges that activate genetic pathways in our bodies. These are often referred to in science as stress response pathways because they respond to a little bit of stress. You know physical activity is strenuous. Fasting is a little bit stressful. Heat, cold, these things are all types of little intermittent challenges. There is a lot of cross talk between these
2:30 stressors and the genetic pathways that they activate. And these genetic pathways that are activated help you deal with stress and they do it in a way that is not only beneficial to help you deal with that little stressor exercise or heat. It’s it stays active and it helps you deal with the stress of normal metabolism, normal immune function happening just life aging, right? So this concept is referred to as hormesis, right? This has a very profound antioxidant, anti-inflammatory response or you know or whatever the response is.
3:00 It could be the production of more stem cells or something like autophagy. These stress response pathways are activated like by a a variety of stressors. So for example, one pathway is called heat shock proteins. And as their name would apply, one would go, “Oh, they’re activated by heat.” Well, correct. They are activated very robustly by heat. But you can eat a plant like broccoli sprouts, which is high in something called sulfurophane. And it activates heat proteins among other things. It also activates a very powerful detoxification pathway called NRF2,
3:30 which helps you detoxify things like carcinogens that you’re exposed to. Cold also activates heat shock proteins. Now, you’re going to more robustly activate heat shock proteins from heat versus cold, but there is some overlap. >> You mentioned plants as a a route to creating intermittent challenge. There’s a lot of debate, mostly online about whether or not plants are our friends or plants are trying to kill us. Um, the extreme version from the carnivore types, um, pure carnivore diet
4:00 types, is that plants are trying to kill us. >> These generalizations are kind of they’re just not useful. And I think that a lot of people online um in the blogosphere it it they gravitate towards them because it’s just easier and it’s a lot more sensational. But I do think with respect to plants, there’s just evidence that sulfurophane is a very powerful activator of the NRF2 pathway. And this is a pathway that regulates a lot of genes and a lot of genes that are related to like glutathione production. Um genes that are involved in
4:30 detoxifying compounds that we’re exposed to from our food like heteroscyclic amines. In fact, there have been GIWA studies. So, these are genetically um these are studies that are um genomewide associated studies. For people listening uh that aren’t familiar, people have a variety of versions of genes. And um we have a gene that’s able to make um heteroscyclic amines to basically de detoxify it so it’s not as harmful. Um and and people that don’t have a certain
5:00 version of that that’s doing it well are very prone to like colon cancer and increased cancer risk. But if they eat a lot of broccoli and cruciferous vegetables, it negates that risk because they’re getting sulfurophane which activates glutathione transferase and synthes. So glutathione is a major antioxidant in our brain and in our in our vascular system in our body. Basically, there’s evidence eating things like, you know, compounds that are like sulfurophane or broccoli or brocc broccoli sprouts which have like
5:30 100 up to 100 times more sulforophane than broccoli are activating glutathione in the brain. There’s human evidence of that. >> Uh, can we cook the broccoli and still get these nutrients or do we have to eat raw? I confess eating raw broccoli is really aversive to me. >> So, you do somewhat lower the sulurophane levels when you when you cook the broccoli. However, um there was a study a few years back that showed adding 1 g of mustard seed powder ground to your cooked broccoli increases the sulfurophane by four-fold.
6:00 >> Are you eating this every day or most days of the week? >> Well, I had shifted to supplementation with sulfurophane. There’s another compound and it’s actually called moringa. It’s like a cousin and it activates the NRF2 pathway similarly to sulfurophane. And so I’ve been buying this Koolie Moringa powder and I add it to my smoothies. >> So if you had to do your kind of top three, your superstars of nutrients for the brain and body, sounds like we’ve got one set. What would you put in
6:30 alongside them? >> Omega-3 uh the marine omega-3 fatty acids. So these are found in marine types of uh you know animals, fish, cold water fish, fatty fish. Uh so so there’s a there’s three fatty acids. There’s ALA, EPA, and DHA. If you get a high quality one, it’s in a triglyceride form. Um, so you’re you’ve got like a a glycerol backbone with three fatty acids and and that’s attached and those are either DHA or the EPA. And um or if you
7:00 have a lower quality fish oil supplement, then you have what’s called e ethylester form. And it’s not that ethylester is bad. It just means take it with food. >> What’s the dosage that you recommend people get? I think two grams is um is a good threshold. Now um the international fish oil standards IFSO, they have a website where they do third-party testing of a ton of different fish oil supplements from around the world. And they measure the
7:30 concentration of the omega-3 fatty acids in the actual supplement because nothing is ever what it says on the bottle. And then they also measure measure contaminants. So, mercury, PCBs, dioxins, things that you’d find potentially in fish that were harmful to humans. Uh, and they also measure mercury and then oxidized fatty acids. So, these omega-3 fatty acids are polyunsaturated fatty acids which are extremely prone to oxidation. So, please keep your fish oil in the refrigerator. They give you a total oxidation number.
8:00 It’s called toto to no to ox to tottox is what we call it for short. And um I like it to be at least under 10, ideally under six. It’s really hard to find all the right mixtures of things, but um people can go to this website and they can browse through the products. >> What are some things that getting 2 to four grams of EPA per day is going to help with in our brain and the rest of our body. I personally think it is one of the most powerful
8:30 anti-inflammatory dietary lifestyle things that we can we can get easily that is going to powerfully modulate the way you think, the way you feel and the way you age. So there’s been lots of work by Dr. Bill Harris and his collaborators looking at what it’s called the omega-3 index. So this is actually the omega-3 level in red blood cells. So red blood cells turn over about every 120 days. So it’s a it’s a long-term marker of omega-3 status. He’s done a variety of studies
9:00 uh observational studies. So measuring omega-3 index in people and then looking at their mortality risk for example or their cardiovascular disease risk. Uh and what he has found is that most f first of all um standard American diet has omega-3 index of 5%. Japan, by contrast, has an omega-3 index of around 10 to 11%. Big big difference there. And they also have about a 5year increased life expectancy compared to people in the US. What he showed in his data was
9:30 that people that had a omega-3 index of 4% or lower, so close to what the standard American is, but a little bit lower, they had a 5-year decreased life expectancy compared to people that had an 8% omega-3 index. people that are in the 4% omega-3 index range in order to get to the 8% right the 5year increased life expectancy if we’re comparing the two groups was to supplement with at least 2 grams it was about 2 grams a day uh and that and I think it was a little
10:00 bit less if it was triglyceride form but I think 2 g is a good safe number so most Americans that are not eating a lot of fish and they’re not supplementing are probably around a 4 to 5% omega-3 index >> where and how can somebody measure their omega-3 index. >> The omega-3 index is actually in the red blood cells. And red blood cells take 120 days to turn over. So, if you’re going to do a baseline test, um, if you want to know before supplementing what your level is, you have to wait 120 days before doing the second test after
10:30 supplementing to know how much you you went up because the that’s how long it takes for your red blood cell to turn over. >> How is omega-3 and some of these other related lipids, how are they having these positive effects? What are some of the purported, reported, and known mechanisms? >> Some of the the most well-known mechanisms um do have to do with the the omega-3 fatty acids being very powerful regulators of the inflammatory process in some way, shape, or form. Whether
11:00 that has to do with resolins that are produced, so these from the metabolites uh of like DHA for example, resolins play a role in resolving inflammation. like you want your inflammatory response to be activated when it’s supposed to be, but you want to resolve that inflammation in that inflammatory response in a a timely manner, right? And resolins help do that. And and so resolins are one. And then there’s these specialized um promediating molecules, the SPMs that also help resolve the inflammation. Just so many different
11:30 ways and inputs. And so when we talk about inflammation, honestly that that’s a big general term, but you’re talking about when you’re talking about serotonin release, um, you know, at the level of neurons, you know, we know that these inflammatory molecules cross the bloodb brain barrier. It’s known that omega-3 actually specifically EPA is able to help serotonin in inflammation inhibits the release of serotonin. And so EPA is actually able to blunt inflammatory responses along with DHA as
12:00 well. DHA does that through resolins and stuff and this then helps more serotonin be released because you’re you’re not having so much inflammation getting into the brain and affecting serotonin release right that’s one mechanism and then another would be well DHA itself has been shown it’s it’s a very important uh fatty acid that makes up cell membranes many cell membranes including in our neurons and as you very well know Andrew the structure and function of receptors of transporters these membranebound proteins on the
12:30 surface of of our cells including neurons are affected by the membrane fluidity you know like how rigid and how fluid the cell membrane is and DHA plays a role in that and so for example in animal studies if you make an animal deficient in DHA their serotonin receptors dopamine receptors they’re affected because the structure of them is affected through the fluidity of the membrane there’s been some animal studies and piglets and rodents as well showing that consuming phospho lipid DHA
13:00 uh during fetal brain development like gets way like 10 times more DHA in the brain. Uh if you’re supplementing with your your 2 to four grams of fish oil, I mean that you’re going to get phospholipid form anyway cuz your body’s going to make it. >> So we have these plant-based compounds, we have the omega-3s, so your PA, DHA, and then you mentioned there’s a third category. What would you place in your third category of foods or supplement-based nutrients that brain
13:30 and/or body health can really benefit from? >> I mean, I think the most obvious would be vitamin D. 70% of the US population has inadequate vitamin D levels. 70 of the wholeing US. So, this is everyone. And so, I think that insufficient levels defined as less than 30 nanogs per milliliter. Um and and that’s sort of defined by the the endocrine society. Um there’s been a lot of different metaanalyses of all cause mortality studies where vitamin D levels are are
14:00 really seem to be ideal between 40 to 60 nanogs per milliliter. So basically the point is that vitamin D is a steroid hormone meaning it actually binds to a receptor and um another receptor drizzes with it vitamin the the retinoid receptor and that complex goes into the nucleus of a cell where your DNA is and it rec recognizes little sequences of DNA called vitamin D response elements. They’re called VDRES. There are specific sequences of DNA that this complex
14:30 vitamin D re bound the vitamin D receptor goes inside and recognizes and turns on a whole host of genes, turns off a whole host of genes. I mean, this is this is important stuff. >> What sorts of things is it stimulating? >> Okay, so first of all, it’s it’s regulating more than 5% of the protein encoded human genome. One of the important things that you’ll find interesting that I published on back in 2014 was that the VDRES in tryptophan hydroxilase 2. So for people listening, tryptophan hydroxilase
15:00 is an enzyme that converts tryptophan into serotonin. So tryptophan is what we uh an amino acid that we get from our food. Um you convert serotonin, you convert tryptophan into serotonin into the gut in the gut, but you also do it in the brain. However, serotonin does not cross the bloodb brain barrier. So tryptophan has to get into your brain and then you have to convert it to serotonin in your brain. Well, the enzyme that does that in your brain is called tryptophan hydroxilase 2 and it’s activated by vitamin D. But most people
15:30 I mean this is regulating our immune immune cell immune system. It’s regulating uh our blood pressure you know all that that’s water retention you know I mean bone of course homeostasis 5% more than 5%. I mean I can’t tell you like so much. where and what is a good starting range for people to to think about D3 supplementation and again foods that can increase D3. >> Um [snorts] so vitamin D3 is a good way to supplement with it. Um there vitamin
16:00 D2 would be a plant source. You often find it fortified in like foods like milk. >> Yeah, vitamin D is naturally to some degree in fatty fish, but you’re not going to correct a deficiency with eating vitamin D. you you’re either going to correct it with sun exposure, being in the right area, having the right amount of sun, and being the right age, um because as you get old, you become very inefficient at making vitamin D3 in your skin. There have been uh a lot of these mandelian randomization studies. So, these are studies where scientists will look at
16:30 people that have these common variations of a gene that’s a little more than 1% of the population. So, it’s not a random mutation. It’s actually found in a in a a sizable percent of the population. A lot of times they’ll look at genes that are also involved in snips that basically make the conversion of vitamin either vitamin D precursor into D3 or in D3 into 25 hydroxy vitamin D or into the active steroid hormone which is 125 hydroxy vitamin D. So you’re not looking at vitamin D levels at all. You’re looking at just the snips and you know if they have it they have low vitamin D.
17:00 People randomly have these genes and it’s not like there’s no health status. So um these these mandelium randomization studies have found that people that can’t convert um into the the precursor the 25 hydroxy vitamin D which is usually what’s measured. It’s the most stable form of vitamin D in the body. Um they have a higher all-c cause mortality if they can’t do it. So people with you know that don’t have it have a lower all-c cause mortality. They have a higher respiratory related mortality. They have a higher cancer related mortality. They also are more likely to
17:30 get multiple scerosis. This has all been done with mandelian randomization. And so, um, it really does hammer home the importance of measuring your vitamin D levels and, uh, being being, uh, very proactive about that. I mean, you can you can get it done anyway. Your doctor will do it. You ask them to do it, you know. So, um, supplementation wise, um, typically, if you don’t have one of those snips for for the most part, taking 1,000 IUs of vitamin D will raise blood levels by around 5 nanogs per milliliter. So let’s say you’re
18:00 deficient, you’re 20 nanogs per milliliter and you want to get to 40. You’re going to need at least 4,000 IUs. >> So for people who are going to be stubborn and not get their D levels tested and simply say, “Oh, I’ll just take some D3.” Is that reasonable? 1,000 to 5,000 IUs for most people will be reasonably safe. If we look at the the the literature, the scientific literature, it is extremely hard to get like hypercalcemia, which would be the major concern with really high levels of vitamin D3 supplementation. I mean,
18:30 we’re talking like hundreds of thousands of IU a day for a long time. And by the way, there have been studies looking at uh people that are deficient in vitamin D. Um, in this case it was uh African-Americans that were given a 4,000 IU a day vitamin D supplement to bring them back to sufficient levels. And um this was a this was a smaller smaller study than um I would like but it reversed their epigenetic aging by like 3 years because again it’s a hormone. It’s regulating
19:00 more than 5% of your protein encoding human genome. So, if I’m taking vitamin D3, I still need to get out into the sun. Correct. Absolutely. >> Okay. Okay. So, we’ve we talked about these plant-based compounds, the omega-3s and D3. Is there anything that um that to supplement based or food based compounds that you, you know, you think are especially useful for brain and or body health? >> I do think magnesium is important in
19:30 there as well. I mean, I think, you know, again, about 40% of the US population doesn’t get enough magnesium. It’s an essential mineral we’re supposed to be getting from our diet. Magnesium is also involved in making ATP, the the energetic currency of our cells. They’re, you know, basically all of our cells need ATP to do anything. And um they’re al it’s also involved in utilizing ATP as well as DNA repair enzymes. These are enzymes that are involved in repairing damage to our DNA. I personally think that magnesium insufficiency causes an insidious type
20:00 of damage daily that you can’t look in the mirror and see like when you’re deficient in vitamin C you’re like my my gums are falling apart I have scurvy right but like you can’t see DNA damage you can’t see it but it’s happening it’s happening right now in my body and it’s happening in your body it’s happening normal metabolism it’s happening you know every day um but we repair that damage we have repair enzymes in our body called DNA repair enzymes they require higher magnesium. Magnesium is a co-actor for them. Well, magnesium is at
20:30 the center of a chlorophyll molecule. Chlorophyll is what gives plants their green color. So, dark leafy greens are high in magnesium. Basically, what is the 40% insuffic insufficiency in the US tell us people aren’t eating their greens. They’re eating their packaged food. They’re eating their processed food. The standard American diet isn’t really high in dark leafy greens. >> So, kale, what are some other examples? >> Kale, spinach, chard, like Swiss chard, rainbow chard, um romaine lettuce. So supplementation with magnesium, it can cause GI distress at like high doses. I
21:00 personally like to take around 130 or 135 milligrams. Um that way it’s not like um a huge bolus to my gut. You can take like magnesium 3 and8 for example and it doesn’t affect the gut as much. I would say malite would be the best. That has to do with the short chain fatty acids being good for the gut. I think mal malate’s awesome and I always try to eat green apples. They’re really high in malic acid. and um tart cherries. Tart cherries are really high in it as well. >> You’ve talked a lot about the use of deliberate cold exposure. What sort of
21:30 activity or stimulus do you do you think is a reasonable and particularly potent one uh to use in terms of cold? >> So today I did 3 minutes at 49° F. I have a cold tub. I definitely do cold when I’m going to do a podcast, when I’m going to give a talk or when I’m anxious. I feel good. I feel more focused which is why I usually do it before any type of public speaking. >> So the mooden enhancing effects that you report those are almost certainly a the consequence of having slowly elevating
22:00 but significantly elevated dop do dopamine that goes on for hours. That’s almost a dreamlike profile for dopamine because most everything else like an aderall, a rolin, a cup of coffee and a um and a workout drink or pre-workout drink or something is going to give you a big spike in adrenaline and dopamine and a big crash. But the advantage of not doing it too often is that you’re not cold adapted. Now, it’s very hard for anyone to get truly cold adapted. I some people start to look forward to the cold and what I think they’re looking forward to is the feeling afterward,
22:30 that dopamine rush. Uh but if you get cold adapted, then it certainly blunts the some of the effect. >> But I want to be cold adapted because that means I have more mitochondria in my atapost tissue and and perhaps even muscle like that’s been shown. Shivering is a very inefficient way to produce heat, which is what your body is trying to do when it’s exposed to cold. And your muscles are basically contracting and and and um and producing heat from that, but that’s just not very efficient. So, uh the the more eloquent
23:00 way to do it or elegant, I guess, uh way to do it is, you know, to basically have your mitochondria produce tons and tons of heat. So, mitochondria are these little organels inside of your cells that are responsible for producing energy. Usually that’s in the form of adenosine triphosphate ATP and that’s what lets everything function inside your body from your neurotransmitter production to your heart beating etc. Basically your mitochondria um they’re like a little battery. So they have a
23:30 they have well they have a double membrane first of all their structure but they have a negative charge on the inside and they have a positive charge on the inner membrane. Basically you can uncouple that that charge and so that positive charge protons start leaking out of the mitochondria and your mitochondria freak out. So this is called uncoupling it. And they start to it’s maximum respiration as we call it. They try to make as much energy. They’re like I got to get those that that that proton back that gradient the electrochemical gradient. And so they just go insane and they um in this case
24:00 it’s uncoupled energy. So the energy they’re making is actually heat not ATP. Uh [snorts] but heat is but you’re essentially burning substrate. So who cares? You’re burning you’re burning glucose. You’re burning your lipids. you know, you’re you’re basically burning things and making heat. And so, um, that’s what uncoupling does. And that is a much more efficient way of producing heat than shivering. And so, as you become more adapted, um, maybe the the the longer duration that you’ve you’ve stayed in the cold or the more times you’ve done it, you’ll no longer shiver
24:30 anymore. You will start to then just do this uncoupling type of thermogenesis as it’s called. And um another type of adaptation that occurs is you actually produce more mitochondria in your atapost tissue. And um and that actually happens also regulated by norepinephrine or noradrenaline through a protein called PGC1 alpha. And what that protein does is it makes more mitochondria in your atapost cell. So per atapost cell
25:00 you’re getting more mitochondria. It’s a beautiful way to basically make more heat when you’re it’s it’s one of those things where it’s like it’s your body’s going, “Okay, I’m going to be exposed to this cold next time. How can I make sure I don’t die? Oh, I can have more mitochondria and I’m going to make more heat.” And so you’re making more mitochondria in your atapost tissue. And and this is often referred to as like the browning of fat. And the reason for that is because if you look under a microscope at a lipid droplet, you know, basically um a fat cell, uh not a lipid
25:30 droplet, atyposite, um you’ll find that it looks darker because there’s more mitochondria in there. So, it’s referred to as browning fat. That’s awesome. You want more mitochondria in your muscle. It’s associated with um improved muscle mass, improved endurance. I mean, mitochondria are essentially they’re the making energy in your cell. And we, you know, we don’t make more mitochondria normally like you have certain inputs. Extra high-intensity interval training, exercise can do it. Your cells are turning over, you make new cells, you replace old ones where your mitochondria,
26:00 >> [snorts] >> um, you don’t really do that for the most part. You can, mitochondrial biogenesis does happen, but you have to stimulate it to happen. And, um, the way your mito like what happens with your mitochondria is they essentially are bobbing around inside of your cells and then they they fuse with other mitochondria, exchange all their content, mitochondrial DNA, and then fizz back apart. And that’s how they kind of stay youngish. But like as you age, you you keep doing that with the same pool of mitochondria and you’re going to get a bunch of old mitochondria mixing old stuff together, right? So why wouldn’t you want to like bring up new
26:30 healthy young mitochondria into that pool, right? So in my mind when I hear mitochondrial biogenesis, I’m like aging. Like that’s the first thing I think of. >> Uh so anyways, cold exposure does that. >> What sort of um cardiovascular other types of training do you do? Uh do you do hit? Imagine you are doing high-intensity interval training. >> I do a lot of highintensity interval Tabatas on a stationary cycle three times a week and I do a 10-minute just 10 uh because it’s efficient and I push
27:00 my ass. I push myself really hard. >> That’s the Tabata. >> It’s a 20 seconds on 10 seconds off and it’s 10 minutes >> and on means you’re pedaling like your life depending on >> you’re maxing it. And then um I always have my sauna on preheating up. I get it to about 189° F. I hop right in the sauna after my Pelaton. I literally like down a bunch of water and then I get in and and then I like either um read a science paper, prepare for a presentation or a podcast or I um hash over things in my mind. And it’s
27:30 interesting because I would use the uh sauna to memorize things. I don’t know if it has to do with the like the stress response like when you when you have an emotional trigger like you remember things better, right? Absolutely. The idea that being in this semi-stressful environment would aid in the learning and and retention of information is is really well substantiated by this beautiful work by a guy named James McGaw. He was at UC Irvine for a while and then [snorts] I think at uh University of Arizona as well. They have a great memory group at both places.
28:00 Very strong in learning and memory both places. and he was the one that really defined this um kind of uh inverted U-shaped function for the relationship between adrenaline and memory. Basically, if you’re too relaxed and not stressed enough, you’re not going to remember any information. At peak levels of stress, you actually are a memory machine, at least within the context of whatever it is you’re trying to learn. So, it very well what you’re describing is very well matches with that. And then
28:30 of course it tapers off as you really increase adrenaline to the point where people are starting to lose autonomic function where they’re just they’re panicking basically. The other thing that that I would like to ask you about is in the sauna of course there’s vasoddilation and profusion of blood to the brain is a wonderful way to enhance cognition. >> The vasoddilation does occur. So there’s a lot of overlap between moderate intensity aerobic exercise and heat stress. And as you can imagine when you’re exercising you’re elev elevating your core body temperature. you’re you’re sweating and um when you’re
29:00 actually in the sauna, blood does get redistributed to the skin to facilitate sweating. But much like exercise, blood flow in general is improved to the brain, to the muscles, everywhere. So um you know I think generally speaking that I and this you know there’s studies showing that sauna use is associated with a much lower risk of dementia and Alzheimer’s disease like people you know people that use it four to seven times a week have greater than 60% reduction in dementia risk and Alzheimer’s disease risk compared to people that use it only
29:30 one time a week. Um people that use it two to three times a week have something like a 20 a little greater than 20% reduction in risk. is a dose dependent effect on dementia risk and Alzheimer’s disease risk. Uh it also has a profound like there’s a there’s a big link between the cardiovascular system and the brain obviously blood flow a big one right you know like you you need to get blood to your brain. Um but cardiovascular mortality so mortality from cardiovascular disease if people
30:00 use or actually this was men if men use the sauna four to seven times a week it’s a 50% reduction in cardiovascular related mortality compared to one time a week. Uh again dose dependent manner two to three times a week is something like 24% lower um death from cardiovascular disease. There’s also lower, you know, sudden cardiac death like a heart attack that’s like 60 something greater than 60% lower if if men use it four to seven times a week versus once. Again, a dose dependent thing. And this is all work from Dr. Yari Linen. He’s in um the
30:30 University of Eastern Finland [clears throat] and just one of the the the world’s experts on sauna use. The more you do the sauna or any sort of heat stress, whether it’s a hot tub or jacuzzi, um you you become adapted. you’re you’re basically start to sweat at a lower core body temperature to cool yourself down. All these sort of physiological changes start to happen earlier. Uh and and so um I stay in for like 30 minutes like I mean so I stay a long time. That’s a lot. You have to listen to your body. Um most of the studies uh that I just talked about were
31:00 from um the the duration the time spent in the sauna when I said 50% reduction in cardiovascular disease related death. What was shown was that men that were in the sauna for only 11 minutes, even if they used it four to seven times a week, that reduction was only like 8%. Instead of 50, it had to be greater than 19 minutes. So like 20 minutes is the sweet spot at about 174° F. To me that’s a very strong data that this is more
31:30 causal than some you know corlary thing because that’s always the problem with observational studies including these which they corrected for a whole host of factors like cholesterol you know exercise just everything everything under the sun I mean they corrected for those and on top of that you have the dose dependent nature of the duration the time spent in the sauna and the frequency so to me it’s like something’s going on here plus there’s been studies intervention studies where it’s you know, comparing directly head-to-head moderate intensity aerobic exercise on a
32:00 stationary cycle to 20 minutes in a sauna, they’re they’re physiologically the same things happen. So, heart rate elevates while you’re doing the activity, blood pressure increases while you’re doing the activity, but then after heart rate decreases, resting heart rate decreases below baseline, blood pressure is improved. So, it decreases below baseline. This is happening the same in moderate intensity cycling versus sauna. So again, the sauna like this heat stress, there’s something about it that really mimics
32:30 this moderate intensity aerobic exercise, which is really great for people that can’t go for a run, that can’t even get on a bike. Um, so you know, disabled people, granted there are some safety concerns, they’re they’re pretty mild. Um, but they do exist. uh you know so people that had a recent heart attack or have some rare kind of heart disease or problem drinking alcohol never do that elderly people low uh prone to low blood blood pressure always talk to a physician before doing the sauna it is it is stressful um >> pregnant >> pregnant women oh yeah I definitely um
33:00 avoided saunas when I was pregnant so for those healthy fit people out there already exercising there’s a synergistic effect by also adding a sauna into that routine and to me that’s great and um there’s So many beneficial things happening uh with the with the heat stress. In addition to like mimicking aerobic exercise, there’s the heat shock proteins that we talked about earlier. Many animal studies have been done looking at Alzheimer’s disease uh you know like a human like Alzheimer’s disease in a
33:30 rodent and heat shock proteins protecting from it you know. So um heat shock proteins are robustly activated in humans. And this [snorts] has been shown to uh even o you know 50% higher over baseline levels after just 30 minutes at 163 degrees Fahrenheit in the sauna. So um and they stay activated at least in rodents for you know 48 hours at least. Um, so you know, having these heat shock proteins around, making sure they’re they’re properly taking care of our our
34:00 proteins so they’re not aggregating in our brains and in our in our plaques could be another potential way that sauna is protecting from Alzheimer’s disease and um other, you know, cardiovascular health as well as longevity. >> I know people are probably desperate to know what if they don’t have a sauna. I could imagine that a hot bath would work almost as well. Is that right? >> Yeah. [clears throat] So there’s been some studies looking at for example activation of heat shock proteins also brain drive neurotrophic factor increases with heat stress. Um and so uh the the hot bath at around 104 degrees
34:30 Fahrenheit which is typically what studies will use for temperature and um it’s at 20 minutes from the shoulders down and and that is like a very robust activation in heat shock proteins and in uh brain drive neurotic factor >> and then heat shock proteins are also protecting against muscle atrophy. So that’s also having to do with the protein structure and the muscle tissue as well. This has been studies in animal you know animal data um as well as some recent human data as well. It was local hypothermia or local heat treatment but um essentially it showed that it
35:00 protected I mean it was like there was a study where um they were looking at muscle disuse and it was it was something like the local heat treatment prevented like almost 40% of the muscle atrophy from disuse. >> We covered a lot of of territory but I just want to thank you again. It was extremely thorough and extremely informative. On behalf of the listeners and uh just directly from me, thank you so much for your time. I learned a ton. My pleasure. Thanks for having me on. It was really awesome conversation. So, I enjoyed it a lot. >> Let’s do it again.
35:30 >> Totally. >> Great. [music]