Well, 45 to 70% of dementia is

preventable through lifestyle. Is that a

defensible statement?

>> 45%

comes from the most recent edition of

the Lancet Commission report on dementia

prevention looking at different risk

factors that have a consistent

relationship with dementia risk. And

there are other studies like there was

one big study done from the UK bio bank

data by professor Yintaiu that estimated

that up to 72% of dementias were

preventable. Tommy, Tommy, Tommy, nice

to see you.

>> Nice to see you. Thanks for making the

time.

>> Thanks for having me.

>> Absolutely. And as mentioned before we

started recording, this is just going to

be like our last conversation because I

wanted to reach out to you because

cognition, cognition, cognition, boy oh

boy is that on the mind and pun intended

on one level, but we are going to bounce

all over the place and I hope to give

people including myself a lot of

tactical practical recommendations.

Also being clear where the science is

solid and where the science is maybe a

little thinner ice, right?

>> Yeah.

>> Or something is plausible but not yet

proven out.

>> And you've got me chewing xylitol gum.

You got me looking at air purifiers. But

I'm skipping ahead. Let's go back to the

beginning and I want to give the good

old Dr. Chattery a nod here because it

came up in a conversation you had with

him and I was like, "Wow, I never would

have thought of that. Why are human

babies so plump? Why are they so fat

compared to other species? If you look

at human babies compared to pretty much

every other mamalian species, we are the

only species that's born fat, even

compared to other primates. And it's

thought that the primary reason for this

is that that fat

>> is a repository for things that the

brain needs in order to develop. And the

two that are probably most interesting

to you and seems to be particularly

important are DHA, the omega-3 fatty

acid,

>> and fats as a source of ketones for the

brain. when the brain is developing in

particular and I think this is also very

relevant to recovery from brain injuries

and other states. The preferred

synthetic precursor as in the thing that

the brain uses to make structure like

fats and cholesterol and that kind of

stuff which makes up a significant chunk

of the brain. ketones are the preferred

source particularly in the developing

brain but I think also later on in you

know various states as an adult and so

in order to support that very hungry

brain which it is particularly in humans

we're born fat so that we can generate a

bunch of ketones to support that brain

developing for the first you know

especially for the first few weeks but

maybe even for months after that.

>> Mhm. also have lots of, as I understand

it, beautiful bat, brown atapose tissue.

>> Keep them warm.

>> Keep those little hairless monkeys warm.

>> Yeah.

>> All right. So, we're going to talk about

because I think the

>> in a sense the extremes inform the mean,

but not the other way around. So, we can

talk about certain maybe edge cases,

things that people might not view as

immediately relevant to themselves. But

since we're talking about newborns, I'm

curious. You've looked at therapies,

various types of research into brain

injury in in newborns.

>> What do you do? What can you do? I mean,

what's the state of the art when it

comes to treating brain injury in

newborns or in infants? There's two main

brain injuries of babies that I study

and they're probably also the two main

brain injuries that are most broadly

studied just because of their their

impact. And so the first is pre-term

brain injury. So that's a baby's born

early. The earlier you're born, the

greater the risk of neuro development

impairment or you know some other kind

of neurological disorder, cerebal palsy,

other impairments later in life

and the other is something that we call

hypoxy schemic and sephilopathy which is

essentially you get to normal fullterm

something happens not enough oxygen.

>> Exactly. Not enough blood flow, not

enough oxygen get to the brain.

something happens usually during

childirth and people think about you

know the cord is wrapped around the neck

or you can get placental abruption right

the placenta kind of tears off the

inside of the uterus or like the uterus

can completely rupture but sometimes we

don't know what happened the baby just

comes out and like something has

happened in that scenario the second one

hie as we call it those babies are

cooled down so this was something that I

studied a lot in my PhD you take that

baby and as long as you start within a

few hours of birth you cool them down to

33.5°

C for 72 hours. And that significantly

reduces death and disability.

>> That's 92.3° F for you Yankees out

there.

>> Although even in the US, many of the

cooling machines are made in Europe, so

they still run on Celsius. So those

babies get cooled down, and that's

really the state of the art. Although

now we're starting to figure out that

there are still a whole bunch of

injuries where that doesn't help,

including pre-term babies. So if you're

born pre-term, cooling doesn't help.

Actually, it can be detrimental. And in

that scenario, one of the things that

they found recently, which is probably

most beneficial, is caffeine. Really?

Yeah. Caffeine is not given for neurop

protection. It's given because babies

who are born pre-term don't breathe as

well. they have this thing called apnea

prematurity. So they they don't have

like a normal respiratory drive.

>> Mhm.

>> So you give caffeine to stimulate that.

But the trials that used caffeine to

treat apnea prematurity saw significant

improvements in cognitive function.

>> And those were durable improvements or

just during treatment with caffeine.

>> When you do these kinds of trials,

usually you follow those babies up to

something like 2 or 3 years old. That's

mainly because an NIH funded trial or an

NIH grant lasts five years. So if you're

going to do a full trial in five years,

then you have a year or two to enroll in

treat and then you you have two or three

years to follow them up.

>> And so they see significant improvement

at that age, but then also, you know,

going into childhood, which is ideal.

You really want to look out as far as

far as you can. So then there's now

renewed interest in caffeine in other

brain injuries and babies and that's

something that we've tested in my lab.

There are some trials now starting in

other brain injuries. But beyond that in

both groups really the biggest impact on

later outcomes is the home environment

that kid goes back to. So yes, my

colleagues who are practicing

neonatlogists do a whole bunch of

amazing stuff to keep these babies alive

and keep their brains in good shape as

much as they can when they're in the

intensive care unit. But actually the

home environment is where the biggest

impact happens. And so then that means

that even if you have an imperfect start

to life, there's probably a lot that you

can do as a parent to help that brain to

develop and grow, you know, as normally

as possible. All right, we're going to

continue to talk about brain injury for

a little bit and then we're going to

talk about a whole lot of sort of

multiffactorial prisms around cognition

and whether or not you can

intervene with the fates to preserve or

enhance cognition

as an adult. Right? So, we're going to

get to that. But if we make the hop from

infant to adult, right? And if you

slipped on the ice and hit the back of

your head and suffered a severe

concussion, what would you personally do

after that?

>> There are a few things that I think we

can probably do and we actually wrote a

paper about this came out last year that

covered various nutritional strategies

and most of the strategies would be

nutritional supplements I would probably

lean on. And assuming that I didn't have

any control over what happened

beforehand, ideally I'd do lots of

things to improve the health of myself,

right? because I think that's going to

affect how my brain and body then

respond to the injury. But after that

point, then there's a couple of things

that I would do. One is I would manage

fevers. This goes back to the

hypothermia that we talked about in

babies. Lots of trials have tried

hypothermia for traumatic brain injury

in older humans and adults and they

haven't really shown any benefit. What

does seem to be beneficial is preventing

hyperothermia. So if you have

significant trauma, one of the things

that happens is the immune system gets

activated is you get a fever. And that

fever increases this gap between the

metabolic demand in the brain and the

supply of energy because the

mitochondria become damaged during the

injury. So if you increase that gap

because the you know higher metabolic

rate because you're hotter

>> Mhm.

>> that seems to make that injury worse and

this has been found in some animal

models but also in some human data. So

the most important thing to do is to

prevent fevers.

>> So get your flu shots etc. Other things

>> in this scenario you know if you need to

take Tylenol to prevent a fever.

>> I see. Take a cetaminophen.

>> Yeah. Acetaminophen paracetamol

depending on where you are in the world.

>> Yeah. Where you are. Maybe even there

are some devices where you can do some

neck cooling or head cooling. They

probably don't have as much of an effect

as some people think they do. But

whatever you can do to maintain your

body temperature and so antibiotics, so

things that help prevent fevers are

going to be helpful. I would then also

manage blood sugar.

>> The main thing being probably avoiding

things that are going to cause large

glucose spikes. So avoiding refined

carbohydrates.

>> Why does that matter acutely after you

whack your head? You see again in

multiple studies and we have to do this

experimentally. So some of this comes

from animal models but if you create

diabetes or the hypoglycemic during the

injury or immediately afterwards and

some of it is driven by the injury. If

you have an acute injury you're going to

get higher blood sugar. So some is cause

some is effect but it seems that these

high glucose spikes are again stressful

in that setting of an acute brain

injury. So just minimizing that as much

as possible. That doesn't mean that you

shouldn't eat carbohydrates, but just

like I would avoid refined carbohydrates

when I sort of worked with athletes at

high risk of concussions. Like if you're

being taken off the field, a lowrisk

thing is just to not chug Powerade as

you're being like taken down the tunnel.

>> Mhm.

>> Other things that are going to become

important with varying degrees of

evidence, but still good enough that

there's a high sort of positive

asymmetry, right? High possibility of

benefit with low risk. creatine

supplementation. Creatine is probably

more beneficial if you have it on board

beforehand,

>> but there's at least one trial in

pediatric TBI that showed creatine

enhanced recovery. Omega-3 fatty acids

uh the same would certainly include

those as well. And then the next thing I

would do is I would take exit ketones.

>> Mhm.

>> I have them, you know, at home. There

are things I've played with. I don't use

them regularly.

>> Mhm. But in this setting, again, I think

there's enough promise, right, to

suggest that they're worth taking. I

didn't include that in this paper

because we don't have good evidence for

it, but if I was if I had a brain

injury, I would take those ketones.

>> Yeah, I would. I would, too. And then

there are a few other things that have

an increasing amount of evidence for

them. So, there's some studies on some B

vitamins, particularly riboflavin,

branch chain amino acids seem to be

beneficial. Mhm.

>> And that seems to be by improving sleep.

Then if you have sleep issues, melatonin

has some evidence for it as well. I

would avoid caffeine actually in this

scenario. There's a little bit of

evidence that says that again it's

probably due to increasing brain

metabolic rate in that sort of early

early window similar to high

temperature. So I would avoid caffeine

particularly early on. And then probably

the most important thing that we have

evidence for is early return to physical

activity. So low level aerobic exercise

as soon as you can tolerate it at a

level that doesn't make symptoms worse

and then increasing that over time as

you get better. That's going to be an

important part of recovery as well.

What's the

supposed mechanism of action with the

return to physical exercise and the

impact that has on the recovery from say

concussion? There's probably a few

different mechanisms. And to be honest,

I don't think anybody really knows,

right? Again, the the evidence is best

in pediatric brain injury, particularly

pediatric sports related concussions.

That's where they've done most of these

like randomized control trials. But

there's a few things that are going to

be happening. You're going to be

improving cable blood flow. Probably

going to get a whole bunch of mioines,

exac during physical activity. We know

many of those can have a beneficial

effect on the brain. And then you may

also see improvements in sleep, right?

We know that physical activity helps

support sleep. So many of those could be

going on at the same time as long as

you're not doing a level of activity

that's then making symptoms worse.

>> All right. So, we're going to take a

moment, not for a commercial break, but

just for a topical break to ask a very

important question, which is when you

came in second at Washington's Strongest

Man in 2024, and then when you came in

the top 20 in the world's first ever

fully off-road iron man triathlon,

what were your weights? What was your

body weight in both of those cases?

>> Those two competitions were more than a

decade apart, I will say. So, in 2012 is

when I did the world's first fully

off-road Iron Man. It was initially

called X-Man and then Marvel sued the

company. So, it ended up being called

XTR 24. So, when I did that, I think I

was probably something like low 80 kilo,

82, 83 kilos. So, like, you know, 185

pounds, something like that.

>> Mhm. All right. And then fast forward a

decade when I was competing in

Washington as the Strongest Man, I

was in the middleweight class and to get

into that class, I had to basically diet

down and then do a water cut to get

under 198. So I was just under 90 kilos

on the day. Although you normally I' I'd

hang out like 15 pounds higher than

that.

>> Okay. Super interesting. We may come

back to that. We're certainly going to

talk about your own personal routines

and tricks of the trade that you apply.

Before we do that, I want to tie up a

couple of loose ends. Specifically,

infant baby, this thing you mentioned,

DHA and

why that

andor omega-3s more broadly speaking are

important. Right. And I, for instance,

I'd say one meal a day is probably right

now two cans of sardines or chub

mackerel mixed with some type of oil,

like olive oil or MCT oil with a splash

of apple cider vinegar. It's shockingly

good. It sounds like cat food. It's

actually better than it sounds with some

salt. But could you explain why this

DHA, etc. is important? You also

mentioned the omega-3 in the context of

recovery from brain injury. So why is it

important and what is the prescription

so to speak? Like how can people

translate that into something they

actually do?

>> When you think about again sort of the

structure of the brain?

>> Mhm.

>> And you're trying to develop the brain

in the first place.

>> Big pile of fat.

>> Big pile of fat. And a lot of that fat

is DHA. And actually, brain, if you

don't mind eating brain, brain is a

great source of omega-3s.

>> I tried it. I tried sheep brain in

Turkey. I'm going to tell you, the

presentation could have used some work.

It was just like straight out of the

formaldahhide jar, popped onto a plate.

It was a bit much for me to be honest.

But yeah, continue.

>> You can fancy it up if you want, but

equally brain consumption is not

required. So, DHA tends to concentrate

the sinapses of neurons. It seems to be

really important for like helping to

regulate the release of

neurotransmitters like being part of the

structural component of those synapses.

It also tends to accumulate in

mitochondria and the DHA content of

mitochondria is like positively

correlated with their like capacity for

energy production.

>> Some of it could be due to some weird

like physical as in physics properties

of DHA like how electrons move through

it differently from other fats. But

anyway, it seems that particularly for

mitochondrial function as well as

synaptic function, DHA is critical. And

so it sort of preferentially accumulates

in those areas. Very important during

brain development. So much so that the

mother will sacrifice her own DHA stores

so that the baby gets enough if you know

she's sort of borderline in terms of DHA

levels. And it's also why women in

general tend to be better at converting

shorter chain omega-3 fatty acids like

ALA to DHA and EPA. It's thought that

that's because that's going to be needed

for a baby one day more so than in men.

>> So, eat brains or find someone you can

breastfeed on. Am I hearing this

correctly?

>> Yeah, I'm just kidding.

>> Are those the only two options? I'm not

sure.

>> I'm kidding. Oh, wait. I forgot about

the fish. I forgot about some fish.

Optional third. Then we also know that

DHA in particular but also uh EPA and

these are the both the longchain omega-3

fatty acids they're important precursors

for various signaling molecules that are

important as it pertains to brain

function but also recovery from brain

injury.

>> What is an example of a signaling

molecule? Actually a lot of the various

molecules that have various functions in

our body activating receptors turning

genes on and off are derived from

different fats. And so in this setting

the ones I'm thinking about are called

like resolins, moresins, protectins that

are derived from these unsaturated fatty

acids. And so neuroprotectin D1 is one

that people are very interested in. It's

being tested as you you give it

exogenously after different brain

injuries. We're not at a point where I

would recommend that people take it, but

that's something that's being studied

right now. And neuroprotectin D1 is

derived from DHA. In the setting of

brain injury, these resolins and

protectins seem to be really important

for regulating the immune response. In

particular, switching off the immune

response, right? The immune response is

important, but we also need to be able

to switch it off. And that's probably

part of the role that they're playing.

When you look at long-term omega-3

supplementation, there was a study that

was done in football players where they

randomized them to different levels of

DHA across the season, and they found

that those taking 1 to 2 g of DHA a day

saw less of an accumulation of a marker

of brain injury in the blood called

neuropilament light across the season.

The thought being that you know all

these small sort of subconcussive

impacts that the kids experience on the

field is generating this sort of low

level of injury that accumulates across

the season and omega-3s or DHA seem to

protect against that. So all of those to

say that if you want, you know, to

maintain brain function, and we see if

you're omega-3 deficient, you're at

higher risk of dementia, cognitive

decline, that's dependent on other

things like methylation status, but it's

going to be an important component of

maintaining brain structure and

function. So, I think that kind of

level, you know, 1 to two grams a day on

average at least, this is going to, you

know, if you get two or three good

servings of seafood a week or a

reasonable supplement, that's going to

be probably enough to consistently hit

those levels. The other part of it is

that your body will actively sequester

extra up to a point. So, when people are

talking about different forms of DHA,

right, should you take your omega-3s as

a phosphoippid form or a triglyceride

form? And the trigger form is more

common in seafood. The studies that look

at these over long periods of time, what

happens is if you consume a lot of the

trigger form from seafood, your adapose

tissue is used as a storage place. So it

cycles through the adapose and then it

gets released and the brain can use it

afterwards. That probably requires you

to spend periods of time where you're

accessing your adapose tissue, right?

You're not constantly eating. So

exercise or periods of fasting may help

you access that depo. But that depo, you

know, allows us to then use these other

forms of of DHA that can sort of

accumulate in our bodies over time and

then we we use them as we need them.

>> All right. I'm wondering if there's

anything else and it may end up circling

back around as well. But is there

anything else related to omega3

specifically that you'd like to comment

on? And am I I could be hallucinating

here. It's not just AI that does it, but

omega-3

does that have Oh, no. It was B complex

which you brought up before perhaps

>> or maybe there is an interaction with

omega3 and homoyine.

>> Yes,

>> I'm trying to figure out where homoyine

fits into the picture with respect to

cognitive health.

>> There absolutely seems to be this

interaction between omega-3 status and B

vitamin status, particularly the B

vitamins that are involved in

methylation. So they affect the level of

something called homocyine and this is

something you can get a blood test for

and those who have inadequate B vitamin

status or inadequate methylation status

have an elevation of homocyine. There

have been multiple trials that happened

sort of two or three decades ago, you

know, maybe even in the last decade

where people thought, oh, omega-3s are

going to be the answer to dementia

prevention or B vitamins and homiciding

are going to be the answer to dementia

prevention and then they would give

people B vitamins or omega-3s and then

they didn't see much of an effect. What

we found out later, I mean the, you

know, the scientific Wii, was that both

are required in order to see benefit. So

this was probably first seen in the

vittog trial which was run by David

Smith at Oxford and they found in

individuals with elevated homocyine. So

that was a level above 13 giving B

vitamins to reduce homoyine

significantly improved rate of brain

atrophy and cognitive function only in

those who had an adequate omega-3

status. And the same thing was seen in

the B proof trial subsequently and then

the opposite

>> which was seen in the omega trial where

they gave omega-3 fatty acids but they

found they only saw benefit in

individuals who had a low enough

homocyine.

>> It's thought to be because if you want

DHA to be in a membrane in a cell in

your brain it needs to be attached to

some kind of phosphoipid right fats

don't just like float around. They're

they're part of these phosphoippids that

sit inside the cell membrane and that

requires it to be attached to a head

group. These head groups are usually

derived from choline or an ethanolamine

although those can be converted from one

to the other. And in order to do all of

that kind of biochemical attaching and

placement requires methylation

>> that is very methylation dependent. So,

it's thought that in order for DHA to do

its job, you need adequate methylation

status so that all those processes can

run. And if you only have one or the

other, then you won't see benefit. Got

it. Yet another reminder for long-term

listeners, this will come as no

surprise, but you got to get blood

tests, comprehensive blood tests, and

really track this stuff with trend lines

over time. But that's a much longer

conversation, but suffice to say, you

need the orchestra, right? where you

need multiple legs of the stool. It's

not just one leg of the stool.

>> Mhm.

>> All right. So, let's maybe return to I'm

going to use a term it's a little

dangerous to throw around, but kind of

first principles or fundamentals maybe

is a better way to phrase it. I'm

terrified as many people are of this

thing called Alzheimer's disease. And

you could throw in dementia, cognitive

decline in general, right? and

conversely very interested in

extending health span. I'm not totally

convinced that, you know, we're going to

get to 150 years, 200 years.

>> Yeah, me either.

>> Like all the tech billionaires might

want to have us believe, but it does

seem certainly if I look at my own

health span kind of local maximum right

now for myself, it's not really low just

capacity right now compared to prior

generations. I feel very good about it.

So I feel like I can extend that runway

>> and cognition for me is just one of the

most maybe the most

>> important pillars of that because having

seen multiple people disintegrate

>> cognitively they don't just lose their

ability to remember they basically lose

their identity right they lose their

ability to emote it's a loss of the self

I mean it's a death before death almost

in a way so really would love to do

anything possible with the right risk

benefit ratio to avoid it.

>> But fundamentals, should we talk about

I'm going to [ __ ] this up.

>> August deer. Augusta Dita data. How do

you say this name?

>> Augusta, I think.

>> There we go. Yeah. All right. Who is

this person because I'm guessing most

folks will not recognize the name.

Certainly, I didn't recognize the name.

Hadn't seen it until I got a couple of

notes from you prior to hopping on. So

August detail or if you read some of the

original papers August D was Alzheimer's

index patient. So Alois Alzheimer that

Alzheimer's disease is named after was a

psychiatrist in the early 20th century

and he took a particular interest in

individuals who had sort of rare or

unusual cases of precenile dementia. So

what we now call or what now most of us

call Alzheimer's disease which is sort

of a late onset dementia or what was

called a scenile dementia which just

meant that it occurred after 65 years

old. That was not what Alzheimer

studied. He studied unusual dementias

where people who were quite young sort

of in their you know 40s or 50s

experienced significant cognitive

decline and dementia and August diet was

one of them. He then after studying them

as a psychiatrist or working with them

as a psychiatrist after they died he

then looked at their brains under a

microscope. So he was the first person

to see amaloid plarks to tangles that

are now sort of pathomotic. They're like

what we consider to be sort of required

as part of Alzheimer's disease. But it's

just interesting that what we have now

is not what he studied. Though over time

people thought that the brains of

individuals who had this sort of early

onset Alzheimer's or these early onset

dementias that Alzheimer studied and

those who had this late onset dementia

that we now call Alzheimer's disease

those brains looked very similar under a

microscope. So they were kind of lumped

together although we do still have two

kind of broad forms. the early onset

Alzheimer's which is usually a single

genetic mutation in something like a

precinel gene or the amaloid precursor

protein gene

that then you know creates a picture

that's much more like what Alzheimer's

studied or the late onset Alzheimer's

which is what most people think about

when they think about Alzheimer's

disease is probably somewhere between 95

and 99% of cases of Alzheimer's and

there is a genetic component to risk but

it seems to be much more tightly tied to

lifestyle and the environment and other

lifestyle factors that that we have some

control over hopefully. And the reason

why Augusta is interesting to me is

because I don't think she actually had

Alzheimer's disease as we would now

think of it. So there have been groups

that have taken sections of her brain

from like you know Alzheimer's old

collections and they've done genetic

studies and she didn't seem to have any

of the genes that cause early onset

Alzheimer's disease or any of the

mutations that cause early onset

Alzheimer's disease. She wasn't an

appleoe carrier. I think she was 33 if I

remember correctly. So she didn't have

any of the genetic risk factors. What

caused this and caused this so young? I

think she was in her 50s, right, is

still actually unknown. Some people

think there have been some like recent

retellings of the story. Some people

think that she may have had

neurosyphilis and neurosphilis actually

causes amaloid accumulation. It looks

very similar to Alzheimer's disease.

>> Neurosyphilis meaning she had syphilis

and

>> it got into her brain.

>> Got it.

>> Yeah.

>> Mhm. And that can look very similar

>> under a microscope, especially 100 years

ago or more than 100 years ago when we

were just sort of first starting to look

at brains under microscopes. And then

others have suggested that it could have

been more sort of psychiatric. Nutrient

deficiencies certainly very common,

could have been, you know, just like the

other components of her environment. She

was by all accounts a sort of like a

downtrodden housewife that maybe didn't

get, you know, sort of much engagement

or stimulation or you wasn't

particularly well treated at home and

that could have sort of precipitated a

bit and we don't actually know,

>> but many of these things kind of it just

seems interesting that it's probably

quite likely she she didn't have

Alzheimer's disease at all.

>> Wild. All right. So, I'm going to take

this in a few different directions and

as per usual, turn it around to be self-

serving for yours truly. But I'm going

through some of the notes that I had for

our conversation. And I'm sure I will

have mentioned this in the bio and intro

at the very top of this show, but

I have this bullet in front of me and I

just want to make sure this is something

you feel is defensible. 45 to 70% of

dementia is preventable through

lifestyle. Is that a defensible

statement?

>> Yes. As far as we think it can be

defensible.

>> Yeah. I'm not trying to put you in the

hot seat. I'm just saying like I don't

know where that number comes from.

>> I can tell you where that number comes

from.

>> That sounds great. I mean that seems

very

>> that seems like a ray of sunshine in a

pretty gloomy

>> possible conversation, right? Where

people think you're just like, "Okay,

there's genetic determinism. You got

this thing. You're screwed. If you have

a bunch of it in your family, you're

also screwed, etc. But it seems like

there's a lot you can do to write the

ship for a period of time. Okay. So,

where does 45 to 70% of dementia is

preventable from lifestyle? Where does

that number range come from? 45%

comes from the most recent edition of

the Lancet Commission report on dementia

prevention which is overseen by

professor Jill Livingston and brings

together all these different experts in

dementia and its risk factors and they

sort of scour the research for

observational studies and then as much

as possible interventional studies. So a

lot of it is you know epidemiological

data.

>> Mhm. looking at different risk factors

that have a consistent relationship with

dementia risk. And then you do these

sort of statistical calculations to look

at something called population

attributable risk, which is essentially

saying if I eliminated this risk factor

entirely from the population, what

percentage of dementias would I expect

to no longer happen?

>> That's essentially what it means. All of

these different percentages add up to

45%. So it's uh a couple of percent for

smoking. It's 7% for low level of early

education. It's like a percent for

alcohol. Then there's hypertension,

hearing loss. Oh, sorry. High blood

pressure. Hypertension is the fancy

medical word. High blood pressure,

hearing loss, obesity, low physical

activity, and all these different

percentages add up to 45%.

There are some things that are on that

list or that aren't on that list that I

think should potentially be included. So

like sleep loss or poor sleep and

insomnia is not included. Late life

physical activity was discussed in the

report but was not included even though

there seems to be some good evidence

there. So actually that suggests that

there may be more than 45% that are

preventable. And there are other studies

like there was one big study done from

the UK bio bank data by professor

Yintaiu that estimated that up to 72% of

dementias were preventable. If this was

going to happen this would require like

a complete societal overhaul, right?

Because a lot of this risk comes from

low socioeconomic status, low

educational and work opportunities, like

all these other things that are kind of

baked into societal risk for dementia.

But others are things that we have more

control over like level of physical

activity, whether we smoke, whether we

drink. So some is directly under our

control, that's probably something like

15 to 20% maybe more. And some is kind

of driven by these maybe bigger kind of

societal risk factors. But if you did

all of that and we managed to completely

change how everybody lives and all of

these risk factors, the idea is that,

you know, maybe even up to three

quarters of dementia cases could be

entirely prevented. Now, that's very

different from saying that I could

guarantee that you will not get

dementia, right? That's not the same

thing. We're talking about this stuff at

the population level. And I have to say

this because if I talk about, you know,

physical activity or sleep or nutrition

and these are really important for

dementia risk, somebody will always say,

well, my family member did all that

stuff and they still got dementia,

right? And so, we're talking about

probabilities. We're not talking about I

can definitely guarantee that somebody

will avoid dementia, but I think we can

definitely say you can stack the deck

massively in your favor through a whole

variety of actions that should you

decrease risk long term.

>> All right. So, part of the reason that I

make this very self-interested is

because I'm self-interested.

The other part is that I think the

personal is very easy for people to

concretize right for themselves.

>> Mhm.

>> So they can interrogate

how they're behaving, what they might do

differently, what they might add, what

they might subtract.

>> Yeah. So, let me tell you some of what I

am observing and then some of what I'm

doing. And I would love for you to

identify or maybe speak to things that

are lowhanging fruit or like reasonably

accessible that are missing. Right.

>> All right. So, few things.

>> Lots of folks in my family currently

caring for in one way or another

deteriorating very quickly with what has

been called Alzheimer's. Again, kind of

a tricky diagnosis. Not sure how how

much they're actually looking at

>> whether it's beta amalloid tow or

anything else. But certainly in in some

cases, these blood relatives are ApoE33.

So I'm like, huh? Also raises the

question of is there an undiagnosed

infection? Maybe it's an STI. Who knows,

right? Like I don't know what the answer

is to that. And it's kind of another

line of of testing perhaps. And so I've

been trying to do a few things for

myself, recognizing that if someone

starts to really show obvious symptoms

that can't be easily explained away,

in their 70s, let's just say the process

probably started what, decades earlier,

right? I mean, things have started like

the cars have started to pile up, the

machinery has started to break a lot

sooner.

>> Yeah. So, it would seem like the earlier

you intervene with better lifestyle

changes, etc., the better off you'll be.

So, I've got the fasting and the

ketogenic diet and all of that stuff,

right? Which I do regularly. I've got

the exogenous ketones, which like you I

use sparingly. I don't use them all the

time because particularly like before

this conversation, I took 11 mill of a

ketone monoester. But I think once all

is said and done, it's basically 51%

13b butane dial. And I have some

concerns around

>> 13b butane dial specifically in chronic

use. Yeah.

>> Right. Or at sufficiently high doses,

say 30 plus per day. I tend to use it

for special occasions like this. You

know, toast, have a glass of champagne,

have some exogenous ketones, and off to

the races. All right, so there's the

ketone piece, which I think is

non-trivial.

There's the

by I would say for the most part

avoiding crazy glucose spikes all the

time, right? Occasionally I'll have like

Christmas. Sure, I had a bunch of

cookies. Like who cares? It's Christmas.

>> It's fine. Had a bunch of pie.

>> But I have a CGM on right now. I had a

continuous ketone monitor on at the same

time for about 28 days. I'm really

interested to look at all of that. But

I'm generally following like a slow carb

diet or Mediterranean style diet. I am

getting enough omega-3. I know that

because of fish intake and also when

needed supplemental intake.

I do seem to be a poor methylator. So

I'm taking like B vitamins,

lmethylolate, all of that stuff.

Tracking blood once a quarter. So I've

got super comprehensive stuff on that

side. Zone 3 training. I do find it as

boring as watching paint dry. even when

I'm listening to a podcast or watching a

Netflix miniseries or something, but

probably doing two to three sessions a

week of let's call it 30 to 60 minutes.

Walking every day, lots of walking and

we'll come back to that.

>> Mhm.

>> Actually, yeah, I can't resist. We

probably will come back to it, but

walking 4,000 plus steps a day reduces

dementia risk 25% optimal 10,000 steps

daily. And then reverses hippocample

shrinkage 2% increase versus expected 1

to 2% decrease. That's the bullet that I

highlighted.

>> And then weight training a couple times

a week. I could keep going. I'm not

going to like bore people to death with

this Dr. evil life story, but I will say

that I've also wanted to get a snapshot

of what things look like.

>> Mhm.

>> So, I'm going to be having a call. I

won't mention the company by name

because I haven't done all of my due

diligence. They have some scientific

advisers who I think are very credible,

but have done brain MRI. I've done the

blood draws, the DNA tests, everything

else. So, I'm APOE34.

>> Mhm. and looking at the brain MRI. I

mean, I'm a muggle, right? So, I

probably shouldn't be allowed to sort of

grab the wheel when driving on the MRI

reading, but I I wanted to look at the

data. It seems like, and who knows how

defensible this is, but my MRI predicted

brain age based on hippocample volume,

etc., etc., etc., is 46 instead of 48.

So, I wasn't thrilled about that. I'm

like, well, all right. Not sure what

else I can do. Maybe a flood dose of

Ibeane. That actually is pretty

interesting data around that from Nolan

Williams, but not something I would

recommend to most people, including

myself. So, there's that. Did a whole

battery of cognitive testing through

this startup.

>> Mhm.

>> Now, that came in at brain age of 20

years predicted, 28 years younger than

your chronological age,

>> but you can kind of beat the test. like

there there's some gamification so I

don't know how heavily to weigh this

right so brain Age of 20 years man

sounds great

>> there are certain aspects that are

harder to game like reaction time

testing okay so I had like 267

milliseconds basically versus 406

milliseconds okay great

>> mhm

>> there could be some training effect like

learned training effect but

>> then there's like number span focus

>> I won't bore everybody with that. But

word pairs, names, and face pairing with

pneumonic devices, if you train

yourself,

>> yeah,

>> you can really game the test. And TBD on

like proteomics, I'm like I'm I'm

getting all sorts of stuff drawn to try

to get a an accurate baseline of where I

stand now so that I can measure all of

the the effect hopefully of these

interventions over time. Mhm.

>> What would you say are like there are 20

things I could mention, but like here

are

three or four that I would also pay

attention to.

>> First, a couple of comments on all the

stuff that you mentioned about what

you're currently doing.

>> Yep.

>> I've already mentioned that I think that

there's a lot of promise for ketones.

>> Mhm. I'm not sure that ketones

necessarily have to have a place in

prevention

>> and I'm not sure that you would

necessarily need them from a prevention

standpoint.

>> There are some you reasonably good data.

So like the medium chain work from

Steven Canane's lab is quite compelling

in the Alzheimer's disease taking MCT

oil seems to increase the C2 acetate

uptake into the brain. This is

associated with improvements in

cognitive function

and this is overcoming what looks like

an energetic deficit in individuals who

have Alzheimer's disease. And this is

something that again it's one of those

things that are pathommonic, right? We

think that we see this and this is kind

of like part of the picture of

Alzheimer's disease. We see that like

this is Alzheimer's.

>> Can I pause for one second?

>> Yes.

>> Real quick, don't lose where you are.

We're talking about MCT oil. Number one,

if people want to play with MCT oil, be

close to a bathroom when you start. And

if you combine it with double espresso

and creatine

definitely have some depends around. Uh

the second is the ketogenic diet for me

just to briefly provide a little more

context is also for its I think

plausible anti-cancer effects and just

to kind of all cause mortality plus

mental acuity. I just think a lot faster

when I have more metabolic flexibility

with something like intermittent

fasting. That's another thing I do a lot

of

>> where my body is has just got the

machinery to produce ketones. But yes, I

hear you. Okay. MCTs, the thought being

here, right? There's a difference

between what you find works really well

for you versus what the listener thinks

they should have to implement for

themselves. And so I'm now going down

the road of why I don't think we all

need to be in ketosis to prevent

dementia.

>> Yep. I think from a therapeutic

standpoint it seems to be beneficial

overcoming this energetic deficit that

we see in in Alzheimer's disease

particularly early Alzheimer's disease

or maybe it's easier to overcome earlier

on and one of the ways we look at this

with something called a PET scan right

so you do an FTG PET you give labeled

glucose molecule you inject that you see

how much gets into the brain in

individuals with Alzheimer's disease

less glucose is is getting into the

brain

>> now we've traditionally come at it from

the point of that glucose can't get in,

right? There's some kind of metabolic

disease, insulin resistance. This is

where the idea of type 3 diabetes has

come from, right? Insulin resistance in

the brain. That glucose isn't getting

in. But a PET scan cannot differentiate

between the glucose can't get in versus

the brain isn't asking for that glucose

in the first place.

And there are actually some very nice

studies that looked at brain activation

and glucose uptake in response to

cognitive stimulus in individuals with

Alzheimer's disease. And what they see

is that yes, at baseline, there's less

glucose being taken up into the brain of

individuals with Alzheimer's disease.

But if you stimulate that brain

cognitively, it can take up glucose just

fine.

>> And so that you get into the range of a

normal healthy brain in early

Alzheimer's disease. Once you get to

like advanced stage dementia, it's too

late. But at that early stage, I think

part of the reason why we're seeing less

glucose uptake is cuz those parts of the

brain are less active because we're just

not using them as much.

>> And just like glucose uptake into the

muscles, which is demand driven, right?

You work your muscles, they ask for more

glucose, they take more up. The brain

seems to be the same, at least early on.

So I think we think a lot about the

supply side right the energetic supply

side but I don't think we think enough

about the demand side how to create

energetic demand in the brain such that

we are maintaining glucose uptake

maintaining energetic state and then

doing that also maintains all the

metabolic machinery that you really care

about in terms of long-term function.

>> Can I just muggle translate for a

second?

>> Yeah.

All right. So, if I'm hearing you

correctly,

this is something I've, you know,

chatted with Dom Dagino about, but I'm

wearing this CGM, right? So, I've got

this device on my arm that tells me what

my glucose levels are at any given point

in time with whatever 3 minute sampling

or something like that.

>> You got to calibrate that with a

fingerprint, by the way, folks.

>> Mhm. But if I eat a meal and then I

don't go for a walk, right, my glucose

spikes and I might conclude, wow, my

muscles are really not accepting

glucose. My muscles are bad at accepting

glucose. But that's not actually true in

my case, right? If I go for a walk or I

do some light exercise, I guess it's

like glute for transporters or whatever,

get all jazzed up and help that glucose

to be better disposed into muscle

tissue.

>> Mhm. And like you said, in the case of

the brain and people referring to

Alzheimer's as type 3 diabetes, it's

like, wow, the brain can't use glucose

>> or it's very bad at using glucose.

But if I'm hearing you correctly, the

additional question that they should be

asking is, is it just that or is the

brain not asking for glucose? Right.

Yeah.

>> The equivalent of the glute for

transporters, right? Like is the brain

basically offline? It's a car up on

blocks, but if you take it down, like,

yeah, it's going to use gasoline just

fine.

>> Yeah.

>> If that's the case, I guess it's just a

call to action for more stimulation

>> of the brain.

>> Yeah. When I was first just coming

across your notes that you sent prior to

this conversation, I went on chat GPT

and I was like, what are the most

glucose inensive activities for the

brain?

And they gave me a bunch of mental

exercises, which isn't exactly what I

was looking for, but I could have

prompted it better. And it said, but

even still, you know, the sort of

improvement or increase might be,

you know, plus less than 10%. Right? in

terms of the the total. And then I was

like, well, are there other activities

such as physical activities that might

increase glucose uptake in the brain?

And it gave me a whole list. But rather

than regurgitate that,

like are all types of stimulation

created equal or are there some sort of

8020 analysis like okay, there are some

tools that are better for the job. when

looking at this purely in relation to

glucose uptake,

those data don't exist, right? So, we're

going to have to extrapolate further

than that.

>> Yeah. Right.

>> And I think that's important because a

decrease in glucose uptake is just a

signal that that area of the brain isn't

as metabolically active, which means

we're just not using it as much at the

simplest level. Then if you think about

various activities that we could use to

stimulate the brain which do seem to be

protective in various different ways

both they can enhance cognitive function

in the short term and then protective

against dementia in the long term.

Actually this ties very nicely into the

comment that I was going to make about

your physical activity routine because

this is where I think some things could

be layered on

when you look at the different physical

activities or exercise and and how they

affect the brain. Different types of

exercise affect the brain differently.

So you certainly need a smorggas board

of all of them to kind of get global

support for the brain. But something

that seems to be particularly beneficial

is coordinative exercise or open skill

exercise. You plus or minus things that

have a navigational component.

And these are essentially

sports or activities where you're

constantly having to respond to the

environment and adapt. That's what makes

them open skill rather than closed skill

or unimodal exercise like going for a

jog or sitting on a bike or something

like that.

>> So when they compare

sports or activities that have the same

amount of physical challenge but

different amounts of cognitive challenge

because of the open skill nature you see

greater benefits in terms of brain

structure, improvements in cognitive

function and open skill just means high

level of unanticipated variety or

variety. What is that?

>> Both. It basically has a greater amount

of complex motor skill required.

>> Some of it can be learned. So, dancing

is one example, right? So, because you

you learn the steps of a dance,

>> single strongest activity for dementia

prevention. Am I overstepping there?

>> Yeah, probably. If you look at physical

activity and the effect that it has on

cognitive function and also mental

health

>> or one of the stronger

>> Yeah. But in terms of both mental

health, so studies in depression as well

as studies looking at different

activities that people do and their risk

of dementia and studies where they

randomize people to different types of

activity including dance. Dance seems to

have the highest sort of effect size.

>> Mhm.

>> Compared to other types of physical

activity, but there's multiple

components to dance, right? So you have

to learn the steps, but there's also a

social component, there's a music

component, right? All these things are

probably like part of the magic source

together. But open skill sports also

include, you know, board sports or ball

sports or team sports where you're

having to like react to the environment

and other people around you. Do you say

bull sports like rodeo? What are we

talking?

>> Ball sport. B A L L. Oh, okay.

It's not going to be good for the TBI to

get people on top of bulls, but Okay,

got it. Although, I think bull sports

would probably be good if you could

avoid the TBI. actually probably right

up there. Similarly, martial arts also

good as long as you don't get punched in

the head a bunch or kicked in the head a

bunch

>> or choked out too much

>> or choked out too much.

>> Beyond the physical strain that these

exercises have, they seem to have an

additional aspect of, you know,

requiring reaction speed,

>> challenging processing speed, learned

complex motor skills, they seem to have

an outsized effect in terms of cognitive

function.

>> Yeah. something else. This is kind of an

aside, but just based on the the

physical activity component when you're

looking at so more aerobic or you know

even like close skill unimodal running

cycling kind of sports the benefit seems

to be intensity dependent. So yes, if

you're not doing anything, then going

for a walk and walking a certain number

of steps a day is going to be great,

beneficial, decrease dementia risk,

absolutely. But looking at hypocample

structure and function, for instance,

which you mentioned, right, you're

talking about measuring your, you know,

measuring your hypocampus on an MRI

scan, higher intensity activities seem

to be better. probably the longest study

where they've ever did something like

this. This is an Australian study where

they had people do the Norwegian 4x4

protocol three times a week for several

months. Oh my god. And so for anybody

who doesn't know what this involves,

it's four sets of 4 minutes on a

treadmill at 85 to 95% of your maximum

heart rate with 4 minutes rest. You do

that four times. It is miserable. I

mean, that's like pretend like you're

being chased by wolves through the snow

for four minutes and then take a

four-minute rest

>> and then doing it again.

>> Yeah. Okay.

>> Four times,

>> right?

>> But they saw significant improvements in

hypocample structure and function that

were maintained for several years after

the end of the trial.

>> Several years.

>> Several years after the trial,

>> so a few months. Yeah.

>> And then sustained for several years.

>> Yeah. I think they followed them up for

5 years after the end of the trial. That

makes it much more interesting.

>> I think a lot of this is driven by

lactate.

>> When we talk about the various things

that support the brain through exercise,

we often talk about BDNF, brain derived

neurotrophic factor, which is increased

with exercise.

>> Mhm.

>> But the BDNF that you produce that you

can measure in the blood that's produced

by the muscles during exercise doesn't

really get into the brain very readily.

Most of the BDNF we have in the brain is

produced locally and it's actually

driven by things like lactate. So

lactate does get into the brain. The

more lactate you have in the blood, the

more gets into the brain and then that

acts as a histone dicess inhibitor that

activates the brush of BDNF. Ketones do

the same thing. Osteocalin which is

released when we sort of load the bones

structurally right released from bones

seems to do something similar. So

generating lactate seems to be

beneficial because probably because one

of the things it's doing is it's

generating more BDNF

>> that then is associated with

improvements in hypocample structure and

function. So as long as you're doing

sports that have some high degree of

intensity so you're regularly producing

lactate and then either in the same

sport or separately doing these sort of

high skill high reaction time open skill

kind of sports. That's probably going to

be beneficial from a exercise

standpoint.

>> I'm still completely stuck on the three

times a week basically V2 max training,

right?

>> Yeah.

>> For a few months is a few months like 3

or 4 months or how many months was it?

>> The study was either six or 12 months. I

can't remember the the intervention

period. It was one or the other.

>> And with durable effects over a

follow-up period of

>> 5 years,

>> 5 years or something like that. Like

that is a great investment. That makes

it a much more compelling sales pitch

for me. And like I've done plenty of V2

max training in the past, but like it's

not necessarily fun, right? No.

>> I mean, I will say if you can again

avoid getting your arms snapped, exhibit

A right here with my elbow surgery. But

if you can avoid the breaking limbs and

getting choked out too frequently,

>> yeah,

>> something like jiu-jitsu, right, is is

actually fantastic because you might

have 3 to 5 minute rounds and then you

take a break for a round and then you go

back in and chances are depending on who

you're rolling with, it's going to be

pretty intense. Obviously depends on how

competitive the gym is. But the

durability is just remarkable. That is

really, really, really, really

interesting. Now is the threshold for

sufficient intensity I imagine it varies

tremendously from person to person

depending on lactate threshold right

>> but like for you do you need to do

something approaching the Norwegian 4x4

>> to

cross the threshold sufficiently in your

mind or does something less suffice the

problem with having just one I mean it's

one very good study but just having one

study

on this is that we get really focused on

the protocol. But

>> I think that anything that is regularly

producing

you're getting above your lactate

threshold you're generating significant

you know several millles of lactate

>> I don't think people need to measure it

but you know if you're getting 6 7 plus

something like that right you're

definitely going to be in that range

>> is there something like a people use a

talk test for instance Peter Tia talks

about this for zone 2 training where you

can kind of have a conversation and be

labored short senses, but you don't

really feel like it as an indicator that

you may be roughly sort of in zone 2. Is

there an equivalent for that range of

lactate?

>> Not that I know of.

>> 10% from puking into a bucket.

>> Yeah, it's definitely going to be misery

related.

>> So, if I think about a lot of the

training that I did as a student, I was

a rower, right?

>> Oh, brutal. You love misery. I don't

love misery enough, which is why

probably why I wasn't as good a rower as

I could have been. But there are lots of

protocols where you're doing relatively

short sprints with relatively long rest

periods that still generate large

amounts of lactate.

>> Mhm. And so in studies where they've

done this, you know, you're talking

about like 30 seconds flat out on a bike

or a rowing machine with several minutes

of rest times 6 8 10 rounds by the end,

right, you can generate a lot of lactate

without having to do something

continuously for, you know, several

minutes at a time. I think I was just

reading that one of the favorite

training protocols for one of the like

world champion rowers was 45 seconds I

mean flat out like completely flat out

on the row machine within 6 minutes of

recovery for doing that you know several

times and then at the end right you're

generating several mill of lactate so

>> I think anything like that that's going

to get you in that zone it just requires

you know maximum effort for even just

like 20 to 40 something seconds, even

with several minutes break in between,

you're going to be hitting that.

>> So imagine the gold standard, you have

some guy in a lab coat and with a

clipboard who pricks your finger or

something and does these blood draws to

determine the miller concentration of

lactate. Is there a breathable option as

there is with ketones, right? where you

can measure acetone through something

that looks like a breathalyzer as

opposed to a finger brick for BHB. Does

anything like that exist?

>> No. They're working on continuous

lactate monitors. Some people do sort of

have those. They're near being

commercially available. So, some people

do have access to those already.

>> But equally, I would argue that it

doesn't matter that much. Just like go

and do something really really hard for

a short period of time and do that a few

times over and do that relatively

regularly. Like that's probably enough

majoring in the minors that you need to

do to kind of get get that benefit.

>> Sounds like my sled assignment. I do

love my sled pushing and pulling. You

can definitely

>> wipe yourself out with that stuff. Okay.

All right. Without necessarily the

impact of me trying to run from wolves

on a treadmill or something. Okay. I do

want to take a brief commercial break,

but it's not for any sponsor. It's just

to mention that and then then we're

going to kind of dive straight back into

the programming and discussion, but you

have a book that is coming out shortly

called The Stimulated Mind. Goes through

all the stuff we're talking about and a

lot more. People should pick it up.

That's Dr. Tommy Wood obviously, but the

stimulated mind. There's so much

horseshit and charlatanism floating

around out there in the world of

anything related to cognition and

memory. It's part of the reason it's

going to segue is a little awkward but I

was like that's part of the reason I

want to have you on is not to highlight

necessarily that but the antithesis of

it which is someone with real clinical

expertise research credentials

who is also a practitioner right it's

like you walk the walk and I wanted to

ask you you mentioned supplements

earlier and of course everybody loves to

hear about supplements but what are some

that may not be on the usual list of

suspects, so to speak. I mean, one I I

would love to hear you speak to is CDP

choline.

>> People might not think of xylitol as a

supplement, but certainly you could

argue that maybe there's a place for it.

>> Do you want to add anything to that and

just expand on those?

>> Sure, I can expand on those. I think

that the supplements that we have the

best evidence for you start with those

core nutrients that we could get from

the diet but if we don't then we

definitely should supplement. So we

mentioned omega-3s, the B vitamins

especially those involved in

methylation. So that's vitamin B12,

folate which is B9, rioplavin which is

B2 and then B6. Vitamin D obviously

critical iron supplementation

>> particularly if people are anemic. So

that requires a whole assessment for

like why are you anemic in the first

place but often particularly more common

in women and many of the symptoms that

women may experience around permenopause

are associated with inadequate iron

status. So getting your iron status

checked and addressed is really

important. Magnesium certainly critical

as well. If we're thinking about other

things that do seem to have both an

acute and long-term benefit in terms of

cognitive function, then all the kind of

antioxidant polyphenols are very

interesting, particularly those that

come from berries, but related ones and

coffee, tea, on the skins of roasted

nuts and seeds, they have similar

effects. And then so you mentioned

choline and right at the beginning when

we were talking about omega-3s I think

choline is critical because of

its importance as a head group for fats

to be attached to in membranes.

>> That's maybe one of the reasons why it's

important for the brain. And various

estimates suggest that we're becoming

increasingly choline deficient as you

know we stop eating things like eggs and

liver which are our richest sources of

dietary choline. But there were

randomized control trials in two

different settings that we've talked

about already. So one in older adults

already experiencing some degree of

cognitive decline where supplementing

with CDP choline which is also called

citicoline

seems to improve certain aspects of

cognitive function. And then again after

traumatic brain injury

there are met analyses that show that

supplementing with CDPC choline can

improve some neuroscychological outcomes

in particular after TBI. So I think most

of us can probably get choline from the

diet but in some of these cognitively

degraded states you might call them you

know something like 500 to,000 milligs a

day of choline seems to be beneficial.

>> Do you take it or do you just get it

from eggs and so on? No, I get it from

eggs and liver and some seafood.

Sardines have some choline in as do some

whole grains like oats have some, quinoa

has some.

>> Mhm.

>> So, all of it kind of adds up. I don't

supplement choline. I do supplement with

creatine. I don't have the perfect trial

that creatine is going to prevent

dementia, but I think we've seen enough

interesting data across

depression again, sleep deprivation.

>> Sleep deprivation. How many grams do you

take daily? What's your standard daily

dose?

>> I take 10 grams every day.

>> Single dose or divided, doesn't matter.

>> So, I take it all in one go in the

morning. There's some evidence that

suggests that once you get above 5 g,

you probably start to saturate creatine

up to transporters. So, maybe you don't

take all of it up. But the reason why I

take it all in one go is because I

remember to take it all of it in one go.

Another reason is that I find creatine

to be quite stimulating, like cognitive

stimulating for me. So, you took your

ketones. I took my creatine before I got

on this call. I took five grams of

creatine, too. And so, if I take

creatine later in the day, I don't sleep

as well. It's very noticeable for me,

but it's not that's not the case for

everybody.

>> Some people take creatine and they don't

notice a cognitive effect. They doesn't

affect their sleep. So, it's very

different from person to person. And so

those are the reasons why I just take it

all in one go in the morning. But

especially if you're going to take over

10 grams, 20 30 grams, you're probably

best splitting it up into several doses

so that you absorb more of it.

>> Yeah. Or 30 g at one go also is tempting

the guts to smite you with a really bad

bathroom situation. Yeah. So yeah, and a

lot of people do mention GI side effects

from creatine. I think some of that is

due to the quality of the supplement

that you're taking.

>> Yep, I agree.

>> So, if you're taking Creapure, creatine

monohydrate, that's what most studies

that have tested creatine have used. And

there was actually a systematic review

meta analysis that just came out that

found that across all the studies they

could find compared to placebo creatine

didn't have any additional GI side

effects.

>> But also, those studies use high quality

creatine. Also, not all of those studies

use 30 g. So you could certainly get to

a point where you're going to start to

have GI effects based on dose.

>> I think it also has to do with the fact

that my like polyarm in the morning when

I'm just getting booted up. It's like I

might be having the coffee plus the

creatine plus you know

>> the MCT oil

>> sardines with MCT oil. Yeah. I mean

there's a lot going into the cocktail of

potential disaster which you do

acclimate to. Quick question before I

forget. On lactate,

>> is there any argument to be made for

anything that you would ingest or

otherwise put into your body not to

avoid doing the intense exercise, but to

increase the amount of lactate that you

uptake into the brain? or is is that

something that people have looked at or

is that just risky business and to be

avoided because you'll end up in like I

don't know some type of acidosis or some

other problem. People have looked at

exogenous lactate itself, right? Usually

as lactate salts just like people have

looked at ketone salts.

>> You can bump up blood lactate a little

bit but similar to ketone salts that you

don't get nearly the the increases you

do with other compounds. You don't need

to do anything to increase brain uptake

of indogenous lactate because the brain

will generally just take up as much as

you've got similar to ketones, right?

>> Yeah, I think I misspoke when I was

asking the question.

>> Yeah,

>> I guess it was just increasing the

amount of circulating lactate so your

brain just sucks it up like a vacuum.

>> I think you can make plenty of lactate

yourself.

>> So, you know, another way to do it,

blood flow restriction is another great

way to produce lactate with low load.

And there were some studies where well

they had them do leg presses but like

sets of 20 leg presses wearing blood

flow restriction cuffs. Oh man,

>> that will get you up there as well.

Again, several mill of lactate lag. It's

not fun.

>> I think I'd rather do the Norwegian 4x4.

Uh yeah. Oh wow, that's intense.

>> That's another way to do it. If you for

whatever reason don't want to do sprints

on a row machine or you can you can

probably get up there

>> with some blood flow restriction under

low load and high rep. But no, I don't

think there's anything that I would take

to increase lactate.

>> Okay, got it.

>> Just because you can make it so easily

yourself.

>> All right, I want to hop on the blood

flow restriction. What make model do you

use? What's your kind of tool of choice

for the BFR stuff?

>> I use the B Strongs.

>> Excuse me.

>> The company is called B Strong.

>> Be strong Strong.

>> No, no. Capital B Strong.

>> Okay, got it.

>> I have no real

>> affiliation. I have no affiliation with

them other than like I know some of the

guys who work there, but I paid for my

device myself.

>> So, it has leg and arm cuffs, but it

comes with like a spigma monometer,

right? One of those blood pressure

things to kind of pump it up to get the

pressure. Those the ones I use.

>> Yeah. Nice and simple. I'm testing a few

different ones right now. So, when you

travel, right, people think of exercise

as this thing that involves potentially,

right, all sorts of machines and you

need your kit. There can be a lot of

excuses or things that people imagine as

obstacles that are not in fact

obstacles.

>> So talk to me about your exercise when

traveling with blood flow restriction.

What does it look like?

>> As my wife calls it, I have my gym in a

bag which I take everywhere I go when I

travel. And it is a set of blood flow

restriction cuffs and a set of bands. I

use the Black Mountain Products bands

which come with handles. And I like them

because they come with a lifetime

warranty. Like I break them and snap

them all the time and you just like

email them be like, "Hey, this broke and

they just send you a new one."

>> Yeah.

>> And they cost 40 bucks or something like

so super cost effective. Can I pause you

for a second just for people who are not

looking at Tommy? I mean, you're

freaking gigant. I mean, you look

gigantic. You're wearing like a very

thick sweatshirt and I can still see

your pecs moving around for God's sake.

What's What are your dimensions here?

Not to turn you into like a Playboy

playmate or something, but

>> So, I'm 6'2. usually 220 pounds. I

usually hang out somewhere around 12%

body fat.

>> Strong unit. Okay. But the reason that I

brought that up is not to flirt with

you, although I'm not against that

either.

>> I appreciate it. Yeah, I'm not against

it. Yeah.

>> No, the reason I want to bring it up is

people might think there's somebody out

there who's like an internet keyboard

jockey on Reddit who who's like living

in a basement and squats 135 and is

like, "Oh, that guy must be some pencil

neck dab." And it's like, "No, actually

not. He's pretty big." And yet like you

can get sounds like a decent workout

with bands that cost 40 bucks and blood

flow restriction. How's that possible?

What do you do

>> when I travel? Because I'm usually at

work, conferences, I'm doing podcasts or

whatever. Like I don't have 2 hours to

go to the gym, which I like to have if

I'm at home. I might do 10 to 15

minutes. And right, you put on the

cuffs, legs and arms. I'll do some

lunges, like body weightight lunges,

squats, presses, push-ups, and then

bicep curls and tricep extensions. And

that's probably it. So, a pretty

standard protocol, which is

essentially in 3 to 4 minutes, you

accumulate somewhere between 75 and 100

reps. So, 30 20 20 or 20 15

something like that with 30 seconds of

rest in between. try and do one body

part at a time, but you can superset

them if you're kind of short on time.

That's it. And kind of to your point,

when we moved into this house, this was

now 8 years ago.

I built my own gym here, but for a long

period of time, I didn't have a gym and

I was working from home and all I had

was bands and BFR cuffs. And then it

wasn't even the Beat Strongs. It was

like these really cheap ones that kind

of look like something that somebody

would use to kind of like draw your

blood.

>> Yeah. Like train spotting. Yeah.

>> Yeah. Exactly. It looks like a toric

like tie off your leg if you've like

blown off your foot. And again, they

cost like 20 bucks. They're probably not

the best, but anyway. So, I had some of

those and some like 40 buck bands. And

that was all I used to work out for like

four or five months. And I didn't lose

any muscle mass or strength. Like I just

got straight back into it afterwards. So

like you can maintain and gain pretty

well as long as you, you know, you have

to do some hard. It's not like BFR can

be, you know, a little bit painful if

you sort of push it, but also very very