Optimizing Longevity with Micronutrients and Vigorous Exercise

[00:00] People in the low cardio-respiratory fitness group had a mortality risk that was either comparable or worse than smoking, having type 2 diabetes, having guess what? Being sedentary, being physically inactive is a disease.

[00:17] Smokers with a high omega-3 index had the same life expectancy as non-smokers with a low omega-3 index. So, in other words, not getting enough omega-3 was

[00:29] like smoking for life expectancy. It reduced their brain aging in the way such that it was like 2 years reduced brain aging. That is huge from Centrum Silver. Taking out just putting one pill in your mouth every day, right? So,

[00:43] today we're going to talk about some of my favorites, I would say. It's the the things that I think can have a very robust effect with little effort. And really improve the way we age, uh our quality of life, and our life

[01:02] expectancy. So, just to kind of give you a heads-up on what's coming up. We're going to talk about vitamin D, omega-3, and a simple multivitamin. I think these are what I call the low-hanging fruits in terms of

[01:15] just easy things that we can do to dramatically have an outsized effect on intake, and specifically we're going to focus on sulforaphane, and why I think

[01:28] that's very important for chemoprevention and detoxification. And then we're going to get into exercise, and specifically talk about vigorous-intensity exercise, and why vigorous-intensity exercise is important

[01:41] for cardiovascular health, reversing heart aging, and for the brain. So, let's just get in it, and talk about like the first part of the talk, which is really optimizing the micronutrient intake, and like I said, we're going to

[01:55] about a multivitamin instead of magnesium today. And I I I know a lot of you here are practitioners, and are pretty familiar with why vitamin D is so important. But for those of you that don't realize,

[02:10] vitamin D is so much more than a vitamin. It's actually converted into a steroid hormone. That means that it goes into the nucleus of our cells, and interacts with our DNA, and it activates genes that are important, and it

[02:25] deactivates genes that are important for uh in terms of the timing of this activation and deactivation. We know that vitamin D controls about 5% of the protein-encoding human genome. It's over 1,000 genes.

[02:39] And it's very important to talk about this because of the widespread vitamin D insufficiency and deficiency. In fact, about 30% of the population is considered deficient. So, that would be if you have your vitamin D levels

[02:54] measured in the form of 25-hydroxy vitamin D, which is the major circulating form of vitamin D. About um 30% of the population has levels of 20 ng/mL or below. That's deficient. And then the other 40% has levels which is

[03:09] considered insufficient. So, that would be 30 ng/mL population that is just walking around vitamin D deficient, doesn't really know

[03:21] and that solution is actually taking a vitamin D supplement. In fact, 4,000 IUs a day really can correct a lot of vitamin D deficiency. Not all, but a

[03:33] Um why vitamin D deficiency is so prevalent, many of you may already know this. We make vitamin D3 in our skin upon UVB radiation. So, that means that

[03:47] anything that blocks out the ability of UVB radiation to produce or to actually hit our skin is going to blunt vitamin D production. So, that means sunscreen, it means melanin, that's the dark pigmentation that is protects us from

[04:01] the burning rays of the sun. It also means depending on where we live and the at certain times of the year, UVB rays are not even reaching the atmosphere. So, if you're in a more northern latitude than, you know, 5 months out of

[04:16] the year, you're not even getting that UVB radiation. And then there's also age. As you get older, you're less able to make as much vitamin D3 from UVB um body fat is another factor. So, as body fat goes up, vitamin D, which is a

[04:36] fat-soluble vitamin, bioavailability goes down. In fact, there have been studies that have shown that about 50% of the vitamin D bioavailability is reduced in people that are overweight and obese. So, you're just not able to

[04:52] release vitamin D into the bloodstream to be converted into the active steroid hormone where it's going to change and regulate genes if you're uh overweight start talking about vitamin D in its role in aging by showing you this slide,

[05:10] people are not rodents, and there's a a lot of differences between us. But I think it's an important place to start because it really is visually highlights how important role vitamin D plays in the way we age. So, the two mice on the

[05:25] top, um they're 4 months of age. The the mouse that's on the left side here is a vitamin D receptor knockout animal. That means that its vitamin D receptor is

[05:38] knocked out, and so the action of vitamin D, you know, the hormonal function of vitamin D is not functioning. Um the mouse on the right is just a normal wild-type mouse. And then if if you look at the bottom panel,

[05:50] those are the same mice 4 months later. So, they're about 8 8 and 1/2 months of age. The vitamin D receptor knockout mouse is a progeria-type of aging model. So, it's accelerated aging. Um its organs are

[06:04] aging faster, its skin is aging faster, the hair is falling out, um bones are brittle. So, like pretty much every organ system is aging at a more rapid rate. And it's not a surprise because vitamin D is affecting, like I said,

[06:18] over 1,000 genes, you know, genes that are obviously involved in bone homeostasis, but also immune function, bone um brain function, just a lot of different processes that are important for regulating the aging process.

[06:32] And we know in humans, if we look at what's called Mendelian randomization. people, and correlated that with a higher all-cause mortality. However,

[06:47] there's always the argument of, well, you're just looking at, you know, people their vitamin D levels are low, and vitamin low vitamin D is just bio-

[07:00] biomarking, you know, disease. And so, that's where Mendelian randomization comes in, where we can actually use genetics to look at a specific environmental factor, and how it affects an outcome. So, in this case,

[07:14] we have genes that convert vitamin D3 into the active steroid hormone. And so, polymorphisms in in those genes where they're not working as effectively, and

[07:29] therefore people are actually they have lower levels of either the stable circulating form of vitamin D, which is 25-hydroxy vitamin D, or the active steroid hormone, which is 1,25-hydroxy vitamin D. And we know that people with

[07:41] those genes, their they have genetically low levels of vitamin D, they have a higher all-cause mortality than people that don't have those genes. They they also have a higher respiratory-related mortality, and they have a higher

[07:54] cancer-related mortality. And so, that that data really I think course, that you have you can never prove causation, and this is more of a

[08:06] way to look at actual causation because we're looking at these genes that are randomly, you know, distributed among the population, and those people with been a variety of studies. This is just one that I'm showing you here,

[08:22] um that have come out over the years showing that people that are deficient in vitamin D, they have low levels of vitamin D, they have accelerated epigenetic aging. So, if you look at the DNA, and you look

[08:35] at um these methylation groups that are kind of sitting on top of DNA, there's a pattern of these methylation groups as we age. And uh you know, Dr. Steve Horvath developed the first epigenetic clock uh that was really able to to to

[08:52] to categorize this aging. But um there's been subsequent clocks developed since that clock with also, you know, Dr. Steve Horvath and others um looking at actually your biological age. And so, you can look at your biological age, and

[09:07] it kind of gives you an idea of how well your body's aging. I I would say it's one of the factors. It's not my favorite, but it's one. So, people with vitamin D deficiency have accelerated epigenetic aging. If they take vitamin D

[09:19] in this in this case, in these people were African-American, and they were obese. They were two compounding effects in terms of causing their vitamin D deficiency. They were severely deficient. And they were given 4,000 IUs

[09:31] of vitamin D per day for about a month, and that reversed their epigenetic age by almost 2 years. So, essentially avoiding vitamin D deficiency is very important, and even if you are vitamin D deficient, you can get back to a

[09:46] sufficient level by supplementing, and that may improve your biological age, um deficiency. We also know that vitamin D deficiency

[09:59] has a pretty profound effect on the brain. We know that vitamin D activates klotho. This is one of the genes that it activates. Klotho is very important for brain function, cognitive function. It's associated with longevity and it's also

[10:12] variety of studies done looking at vitamin D deficiency and dementia. Same problem as before, correlation doesn't equal causation. There've been studies

[10:24] linking about, you know, vitamin D deficiency with an 80% increased risk of dementia. If we turn to the Mendelian randomization studies again, just looking at genetically low vitamin D, we do see that there's about a 50%

[10:36] increased dementia risk. So, clearly there's something going on here with vitamin D deficiencies deficiency increasing dementia risk. And then on the flip side of that, there have also been studies that have shown people that

[10:49] supplement with vitamin D are about 40% less likely to get dementia. So, it decreases dementia risk by 40%. And that's what you want to see. You want to we're talking about deficiency increasing the risk or supplementation

[11:05] decreasing the risk or the genetic component where it's a genes that are causing to deficiency are also doing the same thing as people that are getting their blood levels measured, right? And so, I think that um the the link

[11:18] between vitamin D deficient and dementia um is pretty solid, especially when we look at some of the structural changes that happen with vitamin D deficiency. So, there have been studies looking at the white matter part of the brain and

[11:33] your brain is very important for the communication um between between the brain regions and uh vitamin D deficiency causes this

[11:45] damage in white matter that shows up as like a white spot on an fMRI. And it's in a dose-dependent manner. So, actually, if you increase your vitamin D

[11:57] levels in a dose-dependent manner, for every 10 nanomoles per liter, I know I for every 10 nanomoles per liter increase in vitamin D levels, there was

[12:09] a decrease in the damage to their to the white matter part of the brain. So, this is also, I think, another important part of the story here where you're you know, vitamin D deficiency is affecting the brain. It's, you know,

[12:24] also evidence from randomized controlled trials that supplementing with vitamin D can actually improve cognitive function. Um there are two trials that I have here

[12:37] that I want to talk about. One was actually with Alzheimer's patients, so pretty low dose of vitamin D. They were given about 800 IUs of vitamin D per day

[12:49] performance, so memory, cognition. And it also reduced biomarkers of amyloid beta pathology as well. There was another study that was done in

[13:05] people with mild cognitive decline. Again, those individuals were given 800 IUs a day for about a year and that also and these are all both placebo-controlled studies. Um and the vitamin D also improved cognitive

[13:19] again a lower dose of vitamin D. So, I think that if you can get someone up to a more sufficient level, it it's not necessarily that vitamin D

[13:31] to correct deficiency. And I think that's the the key here. There's a lot of mechanisms by which vitamin D affects the brain. So, it

[13:44] plays a role in immune the immune modulation, the immune response. We could go on and on about that. It plays a role in neuroplasticity and also thousand genes it's regulating. Many of those genes are in the brain. And

[13:59] there's really a simple solution here. And that is you have to get a blood test. And this is key, even if you're just taking a you have to get a blood test because there are single nucleotide

[14:16] polymorphisms or variations in genes that affect people's ability to metabolize vitamin D3 and, you know, have it convert into this steroid hormone. Um and so, some people actually require a much higher dose and you'll

[14:29] never know that if you're supplementing with vitamin D and you don't get a blood test. So, blood test is the most important. And then the next thing sufficient level, which would be 30 nanograms per mil or more. I think the

[14:44] sweet spot that I've seen really is about thir- 30, if you you know, if about 60 or 70. Even can go up to 80. Uh you don't want to go too high, but I

[14:58] mean, that's a kind of a good sweet spot. If you're getting between 40 to 80 nanograms per milliliter. Okay. So, let's let's switch topics. Um I want to talk about omega-3 and this is

[15:11] a topic that's very I'm it's very important to me and I'm really obsessed with it. Like um the the uh person that introduced me mentioned that I am a associate scientist at the Fatty Acid Research Institute that was

[15:25] established by Dr. Bill Harris and I'm involved with research, particularly But I think it's really, really important uh to talk about because most people are not eating seafood or fish. I mean, it's like 90% of the global

[15:41] population does not eat enough omega-3 fatty acids or not getting enough omega-3 fatty acids from seafood. Um this is a this there was a Harvard study that was published a few years back that identified the top six

[15:55] preventable causes of death. So, in other words, things that are pretty preventable that will have a dramatic effect on your life expectancy. And there were things like avoiding hypertension, avoiding type 2 diabetes

[16:08] and cardiovascular disease, not smoking, right? Low omega-3 intake from seafood was on that top six list, along with the things I just mentioned. Uh there are three omega-3 fatty acids. The ones that are

[16:22] found in seafood are EPA and DHA. Those are the ones found in the marine sources. ALA is the plant source of omega-3. That was not part of the the equation here in term in terms of the one of the top six

[16:36] like I said, most people are not eating enough seafood, they're not supplementing with omega-3. You can measure your omega-3 levels. The way to do that would be an omega-3 index test. You want to measure your omega-3

[16:49] levels in red blood cells. That's because red blood cells take about 120 days to turn over, so they're more of a long-term marker of omega-3 versus just your plasma phospholipid. So, omega-3 index test is a a really

[17:03] good way to measure omega-3 levels. It was pioneered by Bill Harris and um one of his colleagues uh many years ago and I think it was back in 2004, about 20 years ago. And um

[17:15] low omega-3 index. The high omega-3 index is like 8% or more and the low omega-3 index is 4% or lower. And what they've one of their first publications,

[17:29] what they found was that people with a high omega-3 index of 8% or more had a 90% lower risk of sudden cardiac death. Like 90% lower risk. That means like if

[17:41] United States, you're 90% less likely to die from that heart attack if you had a attack. Um since then, Bill and his colleagues

[17:56] it's the Framingham cohort or UK Biobank data, lots and lots of big cohort data So, people with a high omega-3 index have about a five-year increased life

[18:13] correcting for all these confounding variables. Um we know that actually if you if you if you think about the average seafood intake in the US versus Japan, we know it's much higher in Japan. So, in Japan,

[18:29] their omega-3 index is about 10. Very high. In the US, our average omega-3 index is about five, 5%. So, we're on that like low low end. And Japan, they have about a five-year increased life expectancy than people in

[18:44] Um within this Framingham data, what was so interesting to me was that, you know, Bill and his colleagues had plotted they'd looked at the omega-3 index and

[18:58] non-smokers. And this is where it to me is so clear things you can do for your cardiovascular health and your heart is

[19:10] to smoke. Most people think about lung cancer. Forget lung cancer. That up like decades later. Cardiovascular disease happens like

[19:23] pretty quick. Um smoking is really bad for your heart. And we know that omega-3s are actually really good for your heart. And so, if slide. The green curve is the life expectancy

[19:38] curve, the green one. Those are non-smokers with a high omega-3 index. If you look at the red curve, people with the lowest life expectancy, those were smokers with a low omega-3 index, right? Big surprise. But what the

[19:52] biggest surprise to me was that if you look at the orange and blue, they're pretty much perfectly overlaid. I mean, I can't imagine anything being more >> Smokers with a high omega-3 index had the same life expectancy as non-smokers

[20:10] with a low omega-3 index. So in other words, not getting enough omega-3 was like smoking for life expectancy. And that is just something that I think people should think about. I mean, obviously like

[20:24] supplement and have the same, you know, be healthy." Um but really I think what we should be thinking about is that we're not eating enough seafood or to that 8% range. And we'll talk about what it takes to get there. But I think

[20:44] even stronger data uh we can turn to some of the large randomized controlled trials looking at supplementing with omega-3 fatty acids, whether it's the Vascepa, which is the purified EPA form in the Reduce-It trial where people were

[20:57] populations of people were given 4 g a day for was it 2 5 years and their cardiovascular disease risk and the risk of having a

[21:10] cardiovascular event, whether that was a heart attack or a stroke, that was reduced by 25% compared to placebo. And then there was the Strength study um that was actually stopped early because there was no

[21:23] benefit and the form that they were given these individuals was a free fatty on the gut. And then there was the VITAL study. In given about 840 mg of Lovaza. That's DHA and EPA combined.

[21:42] And and this was also a 5-year study. And the secondary outcomes, when you look at the secondary outcomes, the the the there was a reduced heart attack risk by almost 30%. Total coronary heart disease was reduced by 17%.

[21:55] low fish intake. So we have I think a lot of evidence cardiovascular health and it doesn't take a lot of omega-3. In

[22:09] fact, it only takes about two 1.5 to 2 g of a fish oil supplement per day to get achievable.

[22:22] just talk about a micronutrient in the form of a multivitamin because I think it's such a low-hanging fruit and it's and you know, I remember 10 years

[22:36] expensive urine, it's not doing anything and anything it might even be harmful. Um it turns out that was, you know, completely wrong. We know that

[22:48] US from a lot of these large national surveys that have been done called NHANES studies. So you can see here, we talked about vitamin D, that's not from the diet, that's from sun exposure. The vitamin E, 60% of the US population is

[23:03] not getting enough vitamin E. I mean, 45% of the population is not getting enough magnesium. Calcium is 35%, vitamin A 35%. I mean, it just goes on and on. Omega-3, I mentioned 80 to 90%. So people are not getting enough of

[23:18] running our metabolism, they're cofactor for enzymes, they're doing a lot of important things, regulating inflammation, changing gene expression.

[23:30] And we don't think about them. We're so focused on macronutrients that we forget know, regulating the way we age. And so I want to talk about the COSMOS studies. There was three trials that were done where older adults

[23:46] were given a daily multivitamin and and this was a very standard one I mean, it's like you can buy it in any CVS, Walmart, right? It's a it's not

[23:59] like a bougie type of multivitamin. They were given Centrum Silver for 2 years or a placebo. And it improved their cognitive function globally. So in fact, global cognitive function was improved by like 2 years.

[24:14] So it it reduced their brain aging in the way such that it was like 2 years reduced brain aging. That is huge from Centrum Silver taking it just putting one pill in your mouth every day, right? Um the what was so profound was the

[24:28] actually the effect on episodic memory. So that's the kind of memory, you know, Um that was improved. It was like reducing the aging of our episodic

[24:40] memory by almost 5 years. It's 4.8 years, which is just astronomical. Um from just taking a, you know, Centrum Silver every day. That's what I'm

[24:52] talking about. Like these micronutrients have effects on the way we're aging, on name a person in here that doesn't want to get their parents taking a multivitamin every day, right? It it's so easy. It's something they're going to

[25:07] do. They don't have to put a lot of effort in and there's outsized effects, that's kind of the the wrap-up for my micronutrient part of this talk is that

[25:19] one, you want to avoid vitamin D deficiency by getting a blood test. We know that about 4,000 IUs a day in most people, 4,000 to 5,000 IUs a day can get people to a sufficient level. There are outlier cases that have to take much

[25:32] index, I mean, I think it's pretty clear. You don't want to be smoking, right? I mean, your life expectancy, you don't want to be like a smoker that's taking a bunch of omega-3. Um it's it's so important

[25:47] about that, but I'm convinced that the data is clear. And when we're talking about going from a low omega-3 index to a high omega-3 index, we're not talking

[25:59] about a lot. 1.5 to 2 g of a high-quality fish oil supplement is easy brain brain aging, right? Easy. Super easy to do.

[26:14] I've really gone over. I'm going to I'm going to blast through this part. Um sulforaphane really it's something that is found in cruciferous vegetables like broccoli. Um it's actually not in the vegetable

[26:29] itself. The precursor to it's in it, glucoraphanin. When the vegetable is crushed or like broken, it's converted the glucoraphanin is converted into sulforaphane. Um sulforaphane is the biggest dietary

[26:41] activator of our NRF2 system. NRF2 is activating hundreds of genes. Many of them are involved in chemo prevention, preventing cancer. They're involved in detoxification. So it activates our phase two detoxification enzymes so that

[26:57] we can detoxify environmental toxins that we're exposed to on a daily basis. It deactivates phase one biotrans biotransformation enzymes. These are enzymes that will convert a procarcinogen into a carcinogen. We

[27:10] actually are eating lots of these things all the time we don't even know it. Uh the procarcinogens. And um it also activates antioxidant and anti-inflammatory systems. It's very very powerful pathway and sulforaphane

[27:22] Um this is just a mechanism by which it's activating it, which I don't think that sulforaphane does reduce DNA damage in people. So uh people that ate 85 g of

[27:38] watercress, that's a type of cruciferous vegetable per day for 8 weeks, lowered their oxidative DNA damage by like 24%. Broccoli, two 250 g a day, people that ate um broccoli for two 250 g of broccoli a day

[27:51] lowered their um oxidized DNA lesions by 41%. Brussels sprouts, 300 g a day, this lowered another marker of oxidative damage by about almost 30%. So again, um

[28:05] it's really it's DNA damage is the precursor to mutations that can lead to cancer, oncogenic mutations. So you want to lower that DNA damage cuz that's sixth, seventh decade of life, you get cancer.

[28:21] also been studies looking at people given a sulforaphane extract and reducing the basically the toxic burden. So there have been a couple of studies

[28:34] done most of them are out of China where their air pollution is very very bad. Uh and so benzene is a is a component that's found in air pollution. It's also in cigarette smoke, wildfire smoke. It's a carcinogen.

[28:47] about 40 micromoles per day and it increased the excretion of benzene through their urine by about 60% within 24 hours. So it didn't take a long time

[29:01] to start to work. I was just in China. I got back 5 days ago. I mean, I was studies showing this. It increases the excretion of benzene and acrolein, we cook foods. So um sulforaphane is really important for increasing the

[29:20] studies looking at prostate cancer recurrence. So men with low-grade prostate cancer that were supplementing with about 60 mg of sulforaphane a day slowed the doubling of their PSA antigen, which is like the major

[29:35] biomarker that's used to sort of monitor prostate cancer progression. Um it was slowed by about 86%. And then there's some studies on UV, topically putting sulforaphane on skin and also uh, lowering the inflammation

[29:49] and and that sort of effect as well. There's a lot of preclinical evidence cancer, breast cancer, colon cancer. I mean, it just it go into the literature,

[30:02] preclinical data is endless. Very clear. You It's like you can't you can't argue that sulforaphane basically is lowering metastasis, it's lowering tumor burden. So, if you give, you know, mice, for example, breast cancer stem cells, it'll

[30:16] just countless studies out there showing this. So, I think that the the take-home here is that eating cruciferous vegetables

[30:28] and adding them to your diet is important. Broccoli sprouts are the best times more of the precursor of sulforaphane, glucoraphanin, in broccoli

[30:40] sprouts compared to mature broccoli. So, um, broccoli sprouts are a great source of sulforaphane. About 45 to 100 g a day gets you about some of the doses that I talked about in these studies. If you're going to cook your broccoli, the enzyme

[30:54] that converts glucoraphanin into sulforaphane is heat sensitive. And so, example, raw broccoli. Um, however, if you add mustard seed powder to your

[31:07] cruciferous vegetable that you're kind of lightly cooking, it can increase that uh, bioavailability. It basically helps it It's ad- adding an exogenous source

[31:19] of that enzyme, myrosinase, back to the broccoli. So, you're basically by fourfold getting more of that sulforaphane. So, that's also important. sulforaphane out there, as well. Okay. I want to get to, like, my

[31:34] like, exercise. There is absolutely nothing that I have found in all of my, you know, reading of the literature that is

[31:48] more powerful and potent at delaying every related aspect to aging and age-related disease than exercise. Um, particularly vigorous-intensity I mean the kind of exercises that you're doing and you really can't have a

[32:04] you're so out of breath while you're doing that exercise. Uh, for people that wear heart rate monitors, we're talking about 80-85%

[32:16] max heart rate. You're getting you're getting into that zone or more. That is vigorous-intensity exercise. And I want to start by talking about cardiorespiratory fitness, which is

[32:28] something that it is a marker of It's it's a marker of our our, I would say, life expectancy and mortality risk. Dare to say longevity. Uh, we know we know that eventually, you know, as we're aging, we're going on this cliff. Our

[32:43] our cardiorespiratory fitness is going down. And so, you want to get as high up as you can. You want to have the highest cardiorespiratory fitness as you can because that cliff will come. And the higher up you start, the longer it's

[32:55] going to take to get to that cliff. And so, VO2 max, the maximum amount of cardiorespiratory fitness is measured. We know that people that are have a low

[33:09] cardiorespiratory fitness, if they go anywhere above being like the low, like, let's say they go to just the low normal range, that's associated with just a 2-year increased life expectancy. If they go from like below low to more of a

[33:22] high, then that's like a 5-year increased life expectancy. And there's been some researchers out there that have that have calculated each unit increase in your VO2 max, in your cardiorespiratory

[33:35] fitness, is associated So, for each unit, which would be 1 ml per kilogram per minute, that correlates to about 45-day life extension. So, for each unit expectancy. There've been a a few studies now. One

[33:51] of them here, this is the JAMA one, um, that have shown people that are in the more elite level, like, the real high cardiorespiratory fitness, again, they've got a 5-year increased life expectancy, but they also have a

[34:03] 80% lower, uh, mortality risk than people in the low cardiorespiratory even people with a high cardiorespiratory fitness, if you

[34:15] compared them to the elite, people in the elite group still had about a 20% lower mortality risk than people in the high. So, it just keeps going up. Uh, but what was so interesting to me about that study was that people in the

[34:28] low cardiorespiratory fitness group had a mortality risk that was either comparable or worse than smoking, having type 2 diabetes, having cardiovascular Being sedentary, being physically inactive, is a disease. And we need to

[34:45] start treating it as a disease because it is a disease. So, that that basically the cardiorespiratory fitness was predicting, you know, mortality risk like these other diseases that people know about as being terrible, right?

[34:58] terrible. We know, um, and this kind of brings it back to vigorous exercise. There The exercise is really, especially, you know, aerobic training, is really going

[35:13] um, when you get to a certain point, you know, people that are even doing the physical activity guidelines, so, let's say they're doing like 2 and 1/2 hours per week of moderate-intensity you know, moderate-intensity physical

[35:28] activity. So, this would be the kind of exercise that you can maybe have a conversation sort of like you're breathy, but you can sort of talk. that that hard. Um, you're still working, but not as hard as you would if

[35:42] Um, about 40% of people that are doing that, 2 and 1/2 hours a week, cannot improve their cardiorespiratory fitness unless they engage in high-intensity interval training. Unless they mix in that vigorous-intensity exercise. And

[35:57] it's not really known why that is, um, but you know, at the end of the day, the challenge that you're putting on your cardiovascular system, on your lungs, you when you increase that challenge, like you do when you're engaging in

[36:14] vigorous-intensity exercise, the adaptations to that are also greater. And so, the adaptations being you can transport oxygen, you know, to throughout your system quicker, right? To bring it to your muscles faster. And

[36:27] that basically it's just the the stress when the stress is stronger, the adaptation is is also stronger.

[36:40] protocols out there, high-intensity interval training protocols that can improve cardiorespiratory fitness. The longer the interval, the high-intensity interval training is referring to these short bursts of like

[36:57] more vigorous-intensity exercise followed by, you know, like a more light exercise recovery. There's so many protocols out there, and honestly, all like get an outsized effect, then you should going to start getting into the

[37:12] minutes-long interval. So, the Norwegian 4 by 4 is one I like to talk about because there's so many publications out there showing that it can improve cardiorespiratory fitness. So, that the Norwegian 4 by 4 was something that's

[37:25] Essentially, they're doing 4-minute interval, and it's on a stationary bike, they're not going all out cuz there's no way you can do that. But, they're just

[37:39] a 3-minute recovery where they're going super super light. They're letting their heart rate come down to recover. And then, they go back at it again. So, that's repeated four times. It's a 4 by 4. That is a really good way to improve

[37:56] cardiorespiratory fitness, but it's not the only way. You can do a minute on, a minute off. You can do 30 seconds on, 20 seconds off. You can do 20 seconds on, 10 sec- Like, Tabatas. All these things do improve cardiorespiratory fitness.

[38:10] Um, it's just the the longer the And I do want to talk about uh, Dr. Ben Levine's study on reversing cardiac aging. So, the reason 4, and also included a lot of vigorous-intensity exercise.

[38:27] And essentially, um, Ben took about, you know, 50-year-olds that were diseases, and put them on this intense training protocol for 2 years. It was

[38:39] 4. They worked their way up, right? When you have someone that's not active, and have to progressively get there. And so, by the end of like the first 6 months,

[38:55] people then started doing the Norwegian 4 by 4 once a week. They were doing 30 minutes of, I would say, you know, getting to that 75% max heart rate, um, zone for their their more vigorous, closer to vigorous-intensity exercise.

[39:10] working out about 5 hours a week. And a large portion of that was vigorous-intensity exercise. They also did a moderate-intensity exercise and a little bit of resistance training. The control group only did some kind of

[39:25] yoga- ish type of, you know, exercise. their hearts were imaged compared to their baseline. So, as we age, our hearts are aging as well. And our hearts shrink

[39:41] with age, and they also get stiffer with age. And this affects our cardiovascular disease risk. It also affects the ability of our hearts to our, you know, being able to improve cardiorespiratory fitness.

[39:53] You don't want a stiff heart, and you don't want it to keep shrinking. And so what happened after the 2 years of that intense exercise protocol is these 50-year-olds reversed the aging of their heart by essentially 20 years. So their

[40:08] hearts grew, and they became more flexible, and they looked structurally, probing and stuff that's done, they looked more like a 30-year-old's heart.

[40:20] data, but essentially the important thing is that it's not too late to start working out, and it will have a profound effect if you put in the time and the effort on the way you're aging. Not only the way your heart is aging,

[40:35] but also the way your brain is aging. So we know exercise can immediately 10-minute exercise bout can do that. I'm going to blast through some of

[40:48] these. It happens immediately. Your brain can be rewired. I mean, I I'm doing I'm a big fan of just doing 10 minutes like before any anything that talk, whatever it is, exercise before you do it. It makes a big difference.

[41:03] Speeds up reaction time, improves a lot of executive function. exercise intensely, when you work really hard, you're forcing your cells to make

[41:17] energy in a way that is producing lactate as a metabolic byproduct. Turns out it's not just a metabolic byproduct. In fact, lactate is a very important substrate not only to make energy, it's used it's actually energetically more

[41:32] favorable to use lactate than glucose to make energy. And lactate gets shuttled back into muscle and is used as energy. Um lactate's also shuttled to other parts of the body and most, I think, importantly, the brain,

[41:46] muscles to communicate with other parts of your body like your brain and say, "Hey, I'm working hard here. We got to like respond to this work, right?"

[41:58] And part of the way that it responds is by increasing brain-derived neurotrophic factor, BDNF. Um brain-derived neurotrophic factor is so important for it helps grow new neurons. It is important for learning

[42:12] and memory, neuroplasticity. So that's the ability of your brain to adapt to changing environments. Uh very important. So brain-derived neurotrophic factor is something that I would say is a youthful elixir for your brain. And we

[42:26] know vigorous intensity exercise increases it through lactate. Lactate is also working hard. Your brain has to work hard when you're exercising hard.

[42:38] exercise. Much like the improvements in cardiorespiratory fitness is the way your your cardiovascular system adapts. It also increases

[42:50] they've looked at dose-dependent in terms of exercise, moderate, light, moderate, and vigorous intensity exercise. And they looked at serotonin levels. And the more vigorous intensity the exercise, the higher the serotonin

[43:04] levels are. Serotonin levels in the plasma do correlate with brain serotonin levels. And in fact, individuals that were doing the vigorous intensity exercise had higher serotonin, and they had more they had better impulse

[43:16] control. So they had basically improved what's called inhibitory control. We know that serotonin, most of us think of it as the the neurotransmitter that's important for executive function, decision-making, and it's really

[43:32] important for impulse control. You can take someone and deplete their serotonin by giving them a a bunch of branch chain amino acids, which compete with tryptophan, which is the precursor to make serotonin. And within like an hour

[43:44] or two, their impulse control is just shot. So um it's very important for impulse control. It also increases norepinephrine. Norepinephrine is involved in focus and tension. Um so lactate again is the signaling molecule

[43:57] that is telling the brain to increase these neurotransmitters as a response to intense exercise, essentially. A lot of protocols out there for increasing BDNF, the Norwegian 4 by 4. Anything that's really going vigorous,

[44:11] that for like 30 minutes, that's a really big boost in BDNF. But there's a lot of protocols out there that can increase brain-derived neurotrophic factor. Again, the lactate's the key. To get the lactate, you have to go harder.

[44:26] And there's also this I like to to talk about this PNAS study. It's a classic study published back in 2011, I think. And um were doing more like 70-75% of their max heart rate, which is pretty good for

[44:44] someone who's 65 or older, right? Um they did this exercise for 2 years, and they not only countered the brain atrophy that happens with age. So as we age, as we get to older adult older adulthood, we start to lose

[44:59] between 1 to 2% of our our hippocampal brain region atrophies per year. Um these older adults that were engaging in the physical activity, um like I

[45:11] not experience that 1 to 2% brain atrophy in the hippocampal regions, they experienced growth. They experienced a 2% growth in their hippocampal region.

[45:25] So that's effectively restoring about 1 to 2 years of previous loss of their the hippocampal, you know, brain region. Again, brain-derived neurotrophic factor is responsible for the growth of new neurons, particularly in the hippocampal

[45:37] part of the brain. And they also had improvements in cognition that brain. already over. So I'm going to just tell you guys about exercise snacks cuz I

[45:55] think it's a wonderful thing. These are short bursts of intense exercise. You know, you're going you're going at 75-80% max heart rate. You can do anything from high knees to to bodyweight squats, jump, you know,

[46:07] to do. There have now been enough studies out there showing that exercise snacks can improve longevity. There have been like three studies that I at least Scientists can track their heart rate. And people that are doing these vigorous

[46:25] types of exercise snacks throughout the day, if they're doing it So it's between 1 to 2 minutes per bout, and they do it if they do it three times a day, they have a 40% reduction in cancer-related mortality, they have a 50% reduction in

[46:38] cardiovascular-related mortality, and a 40% reduction in all-cause mortality. So don't go to the gym. What they're doing is they're taking advantage of like

[46:50] they don't just, you know, walk up it, they sprint up them. Um or they they bike to bike to work or go fast to work or whatever. Um briskly walk to work. They're doing these, you know, short bouts of exercise snacks. Now, I'm

[47:05] uh versus the the Vilpa, which is the kind that's vigorous intermittent everyday situations. They're not necessarily stopping and doing air

[47:18] squats, but there's there's I think every reason to do them. One, it's increasing blood flow to the brain. Um two, even just doing, you know, air squats throughout your work day can improve

[47:33] like, you know, 30 air squats every 45 minutes for a 8-hour work day was able get up, and we're going to end with our with our exercise snack because you've

[47:49] all been sitting too long. And this is the best one like most fun part. We're going to do just a minute. I mean, we could do 2 minutes, but I think knees or air squats? Air squats? Okay.

[48:06] Dang, I just got back from China, and I did um I did my barbell squats like 2 days ago, and I am so sore, but I'm going to do them. All right. Okay. Wait a minute. Let me get the wrong one here.

[48:20] Ready? Here we go. And try to like put in some effort. Okay. Try to put in the effort, right? Like fast. Now, I'm able to talk. So it's not like super super vigorous,

[48:35] but I can also measure my heart rate and see. Come on. Like hurt? Are you burning?

[48:54] Okay, we're at 30 seconds. I know some of you hate me right now. Oh, whoops. Well, good thing we didn't do high

[49:08] Okay, 10 seconds. one. All right.

[49:25] I just want to see what my heart rate say my heart rate. Really? It's only 80? 145.

[49:39] feel good right now? Yes. Do them. Do them. Take a break every hour

[49:51] and do 1 minute of air squats. If you do that just three times. Right? Three a lot It's two just do 1 minute do six times a day, right?

[50:07] It's huge. It's having a huge effect. And so, with that that's my conclusion. Right? Avoid micronutrient deficiencies. Increase your sulfor- your sulforaphane cruciferous vegetables.

[50:20] intensity exercise, right? That's going to improve the way we age.