Welcome to the Huberman Lab Podcast,
where we discuss science
and science-based tools for everyday life.
I’m Andrew Huberman,
and I’m a professor of neurobiology and ophthalmology
at Stanford School of Medicine.
Today, my guest is Dr. Lane Norton.
Dr. Norton is one of the foremost experts
in protein metabolism, fat loss, and nutrition.
He did his degrees in biochemistry and nutritional sciences
and is considered one of the world experts
in understanding how we extract energy from our food
and how exercise and what we eat combine
to impact things like body composition and overall health.
Today, we discuss an enormous number of topics
under the umbrella of nutrition and fitness,
including, for instance, what is energy balance?
That is, how do we actually extract energy from our food?
We also discuss the somewhat controversial topic
of artificial sweeteners,
whether or not they are safe or not,
and whether or not they are an effective tool
for weight loss, in particular for people suffering
from obesity and different types of diabetes.
We also talk about gut health, that is the gut microbiome,
and how it’s impacted by food
and how it can actually impact the metabolism
of the foods that we eat.
We also discuss fasting, or so-called intermittent fasting,
or time-restricted feeding, what it does
and what it does not do in terms of how effective it is
for weight loss and perhaps even for health and longevity.
We also talk about protein and define very clearly
how much protein each and all of us need,
depending on our daily activities and life demands.
We discuss the various types of diets
that you’ve probably heard about,
including ketogenic diets, vegan diets, vegetarian diets,
and pure carnivore diets,
as well as more typical omnivore diets,
and how to make sure that you get all
of the essential amino acids that are critical
for healthy weight maintenance, weight loss,
or directed muscle gain.
We also talk about supplements, in particular,
the supplements for which there is an immense amount
of science pointing to their safety and efficacy
for fitness and for overall body composition.
What I’m sure will become clear to you
as you hear Lane talk about each and every one
of these topics is that he has an incredible ability
to both understand the mechanistic science,
but also the real-world applications
of the various discoveries that are made
in particular papers, and in particular,
in the randomized controlled trials.
That is, when a given scientific hypothesis has been raised,
he’s extremely good at understanding why it was raised,
but also at evaluating whether or not it works
in the real world, which is what I believe
most everybody out there is concerned with.
I think this is one of the things
that really distinguishes him from the other voices
in the nutritional landscape.
I assure you that by the end of today’s discussion,
you will have a much clearer understanding
about what the science says about nutrition, about fitness,
and about how different diets and fitness programs combine
to achieve the results that you want.
Before we begin, I’d like to emphasize
that this podcast is separate from my teaching
and research roles at Stanford.
It is, however, part of my desire and effort
to bring zero cost to consumer information about science
and science-related tools to the general public.
In keeping with that theme,
I’d like to thank the sponsors of today’s podcast.
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And now for my discussion with Dr. Lane Norton.
Lane, Dr. Norton, thank you so much for being here.
This is a long time coming,
and I have to say I’m really excited
because I’ve seen you in the social media sphere.
I’ve also listened to a number of your other podcasts,
and as a fellow PhD scientist,
I feel a great kinship with you.
I know you have tremendous experience
in fitness and nutrition, a number of areas.
We also got a lot of questions from our audience,
and I’m really looking forward to talking with you today.
Yeah, I’m excited too.
I mean, like you said, it’s been something
we’ve been talking about for a long time,
so I was glad we were able to make it happen.
Yeah, indeed, and I think some of the audience
has requested a debate or a battle,
and I can tell you right now, it’s not gonna happen.
Actually, one of the things that brought Lane and I together
in conversation online and then via text, et cetera,
was the fact that I love to be corrected,
and that’s what happened.
I did a post about artificial sweeteners,
which we will talk about a little bit later in the episode,
and Lane pointed out some areas of the study
that I had missed or maybe even misunderstood,
and I revised my opinions, and I think it’s wonderful,
and other studies have come out since then,
so hopefully, our conversation will serve as a message
of how science and actionable science can be perceived
and that it doesn’t always have to be a battle,
but hey, if we get into it, we get into it.
It won’t get physical because we know you would win.
So in any case, I’d like to start
with something that’s rather basic
and yet can be pretty complex,
and that’s this issue of energy balance
and energy utilization.
I think most people have heard of a calorie.
I’m assuming that most people don’t actually know
what that is in terms of how it works, what it represents,
and so maybe you could just explain for people
what happens when we eat food of any kind
and how is that actually converted into energy
as a way of framing up the discussion around weight loss,
weight maintenance, weight gain, and body composition.
So a great question, and like you said,
this is one of those things where people use the term
calories in, calories out,
and they say, well, that’s way too simplistic.
And I’m like, if you look at what actually makes up
calories in, calories out,
it’s actually very complicated, right?
So let’s deal with what you mentioned first.
What is a calorie?
Because I think a lot of people don’t quite understand this.
So a calorie just refers to a unit of energy,
of heat specifically.
And so, well, what does that have to do with food?
What does that have to do with what we digest and eat?
Really, what you’re talking about
is the potential chemical energy
that is in the bonds of the macronutrients of food, right?
And by digesting, assimilating,
and metabolizing those nutrients,
we are able to create energy.
And the end product of that mostly is ATP,
which is your body’s energy currency.
So to understand ATP, just try to think about
if you’re trying to power
these various reactions in your body,
and we’re talking about tens of thousands of enzymes
that require ATP,
it doesn’t make sense that you would have to create
a bunch of micro explosions, right?
You want something that can transfer high energy phosphates
to power these reactions,
to give up essentially its energy,
to power something that might otherwise be unfavorable.
So a lot of metabolism is simply creating ATP,
which the end of the line of that,
I’m gonna kind of work backwards,
is what’s called oxidative respiration.
So that happens in the mitochondria.
Everybody’s heard mitochondria, powerhouse of the cell.
And that is done through essentially creating
a hydrogen ion gradient across the mitochondria,
which powers the production of ATP
by converting free phosphate plus ADP to ATP.
Now, the way that hydrogen ion gradient is created
is through creating hydrogen ions
that can be donated through the Krebs cycle.
Now, the Krebs cycle is linked to glycolysis.
So if we talk about carbohydrate metabolism,
basically other than fructose,
get converted into glucose,
which can go into glycolysis,
and you can produce some ATPs through glycolysis,
and then it boils down to pyruvate,
then acetyl-CoA, which goes through the Krebs cycle,
produces a lot more ATPs from that.
If you talk about protein,
protein’s a little bit different
because protein gets converted to amino acids,
which can be used for muscle protein synthesis
or protein synthesis in other tissues,
but it also can be converted
through gluconeogenesis to glucose.
And there also are some ketogenic amino acids as well.
And so you can have a few different ways
to get to the Krebs cycle,
either being through acetyl-CoA
or through glucose going through the glycolysis to pyruvate.
Then you have fatty acids,
which are able to create energy
through what’s called beta-oxidation,
where essentially you’re taking these fatty acids
and you’re lopping them off two carbons at a time
to produce acetyl-CoA,
which again can go into the Krebs cycle,
produce those hydrogen ions
that can then power the production of ATP.
So that’s kind of like at the cellular level
of how this stuff works.
But stepping back and taking it back out,
like what does that have to do
with weight loss or weight gain, right?
Well, when you think about the balance
of energy in versus energy out,
sounds very simple,
but let’s look at what actually makes up
energy in versus energy out.
First of all, you’ve got to realize
that the energy inside of the equation
is more difficult to track than people think, right?
So one, food labels, which we like to think
as being, you know, like from upon high,
can have up to a 20% error in them.
So a hundred calorie,
is something listed as a hundred calories per serving,
it could, what’s actually in there,
it could be 80 or 120.
So that’s one aspect of it.
The second aspect is there’s what’s called your energy,
but then there’s also metabolizable energy, right?
So if you have a food stuff
with say a lot of insoluble fiber,
typically insoluble fiber is not really digestible.
And so you could have, you know,
quite a bit of carbohydrate, you know,
but if you can’t extract the energy from it,
and typically this is because insoluble fiber
from like plant material,
the carbohydrate or, and even some of the protein
is bound up in the plant structure,
which makes it inaccessible to digestive enzymes.
And so this is what like adds bulk
to your stool and whatnot.
But again, reduces the metabolizable energy in there.
And there’s some evidence
that based on people’s individual gut microbiome,
that some people may actually be better
at extracting energy out of fiber compared to other people.
So just starting off right there, okay,
there’s quite a bit of play in the energy inside of things.
Now, one of the things people will say is,
well, see, that’s why you shouldn’t worry
about tracking calories,
because you know, if the food labels can be 20% off,
and what I’ll say is, okay,
that’s a, that’s, I understand where you’re coming from,
but typically if it’s off, it’s gonna be consistently off.
And if you’re consistent with how you track it,
eventually you’ll be able to know
kind of what you’re taking in.
And it’s kind of, that’s kind of like saying,
well, don’t worry about tracking, you know,
if you’re, I like to use financial examples.
You know, we know that to save money,
or you have to earn more money than you spend.
Well, you can’t exactly know how much money
you’re earning at a time, you know,
cause there’s inflation and then there’s,
if you have investments, those can be, you know,
different interest rates and whatnot.
So, okay, but you’re, you know, if you have a budget,
you have a reasonable idea of what it’s gonna be,
you know, and you make certain assumptions,
but you can relatively guess.
Yeah, that’s a good example.
So now let’s look at the energy outside of the equation,
which is actually way more complicated, right?
And so your energy out is a few different buckets.
The first one and the biggest one
is your resting metabolic rate, so your RMR.
And that for most people is anywhere from 50 to 70%
of your total daily energy expenditure.
Now, people use the term metabolic rate
and energy expenditure kind of interchangeably,
but they’re not the same thing.
So your total daily energy expenditure
is the summation of all the energy you expend in a day.
Walking upstairs, exercise if you do it.
Plus your resting metabolic rate.
Right, so resting metabolic rate is a big part of that,
but it’s not the only thing.
So that’s usually about 50 to 70%.
And sedentary people will be on the higher end of that,
so it’ll be a bigger proportion,
whereas people who are more active,
it’ll be a little bit lower,
not because their metabolic rate is lower,
but because they’re expending a greater percentage
of their calories from physical activity.
Then you have something called the thermic effect of food,
which is a relatively small percentage
of your total daily energy expenditure.
It’s about five to 10%.
And very difficult to measure,
and usually what researchers do
when they’re kind of looking at this stuff
is they just kind of make an assumption about it.
They use a constant.
But that’s about five to 10%
of your daily energy expenditure.
And that refers to the amount of energy it takes
to extract the energy out of food.
So think about your body kind of like a car, right?
You don’t just have gas in your tank
and it spontaneously starts up, right?
Like you have to have a battery,
so you put in energy so you can get the energy
out of the petrol that you have in your car.
Similar with food, you can’t just eat food
and then it just appears in your cells
and you start doing stuff.
It has to be systematically broken down
and put into forms that can actually produce energy.
And so you have to put some energy in to achieve that.
And a lot of times people will say something like,
well, not all calories are created equal.
That’s not true because calories
just a unit of measurement, right?
That would be like saying not all seconds
on a clock are created equal.
Yes, they are.
All sources of calories may have differential effects
on energy expenditure and appetite.
So if we look at something like fat, for example,
the TEF of fat is about zero to 3%,
meaning if you eat 100 calories from fat,
your net will be about 97 to 100.
So the process of breaking down that fat
essentially subtracts some of the calories away
because you used it in creating energy
by breaking those chemical bonds to create ATP.
So you have like, for example,
some enzymes that require ATP to run these processes.
Now, fat is actually the easiest thing
to convert into energy.
Then you have carbohydrate,
which has a TEF of like five to 10%.
So you eat 100 calories from carbohydrate.
And obviously like the fiber content
makes a big difference on this.
But if you eat 100 calories, you’ll net 90 to 95.
Protein is about a 20 to 30% TEF.
So if you eat 100 calories from protein,
you’re only netting 70 to 80.
Now you’re still net, you know, people say,
well, you can’t eat too much protein.
Well, you know, people will ask,
well, can protein be stored as fat?
The carbons from protein,
it’s unlikely it’s gonna wind up in adipose tissue.
But if you’re eating a lot of protein
overall as part of a lot of calories,
it does, it has to be oxidized
and it can provide a calorie cushion
for other things to be stored in fat.
But protein itself does provide, you know,
a net positive for calories,
but less so than carbohydrate or fat
and tends to be more satiating.
So again, when people talk about, you know,
are all the calories created equal?
Yes, but all sources of calories
may have differential effects
on energy expenditure and appetite.
So that’s the TEF bucket and the BMR bucket.
Then we go to physical activity
and physical activity is essentially two parts.
which is kind of your purposeful movements.
Like you go out for a walk,
you do a training session, I mean, whatever,
any purposeful activity.
And then you have what’s called NEAT,
which is non-exercise activity thermogenesis,
which I think is actually really cool.
Yeah, it is.
So it’s, I was actually hanging out
with somebody last night and I was noticing them.
They were fidgeting their feet and their fingers.
And I said, you know,
have you always like been pretty lean?
And they were like, yeah,
I never really had a problem maintaining leanness.
And when you look at the obese resistant phenotype,
people think they have high BMR or, you know,
they exercise a lot.
And really what it seems to be is NEAT.
They tend to, if they overeat,
they just spontaneously increase their physical activity.
Now people get NEAT confused.
I’ve heard people say,
well, I’m going to go out for a walk to get my NEAT up.
That’s not NEAT.
NEAT is not something you can consciously modify.
What you’re doing there, if it’s purposeful, it’s exercise.
So for example, if I, when I’m talking,
if I’m waving around my hands,
if I’m tapping my feet, if I’m whatever, that’s NEAT.
But, you know, trying to like get yourself,
well, I’m just going to tap my foot more.
Well, now if I’m consciously having to do this,
then my focus, I mean, you know how the brain works.
Very hard to do.
You know, you don’t really do two things at once.
You kind of switch quickly between tasks, right?
Can I quickly ask,
was the person that you’re referring to our friend,
No, no, but he is fidgety too.
Amazing online fitness channel.
He’s a freakishly strong individual.
And I can’t remember whether or not Ben,
you’re a fidgeter or not, but anyway,
I’ll have to go check and we’ll measure your fidgeting.
About non-exercise induced thermogenesis, NEAT,
my understanding of the old papers on this,
old being, I guess, back to the mid nineties,
is that the calorie burn from NEAT
is actually pretty significant.
We’re not talking about a hundred calories
or 200 calories per day.
We’re talking about in some cases, hundreds of thousand,
excuse me, hundreds to maybe even close
to a thousand calories per day.
Could you elaborate on that?
Yeah, so there was actually a really classic study,
I think from, I want to say it’s from Levine in 1995.
It was a metabolic ward study.
And hopefully I don’t butcher the study
because I’m trying to, you know, pull it out of my brain.
I don’t expect you to have PubMed in your head,
although I must say you have a quite extensive
PubMed ID grab bag in there.
I try to bring the receipts.
I try to bring the receipts.
We will put a link to this study in the show note captions
so people can peruse it if they like.
So I believe they had people overeat.
And I think it was by like a thousand calories a day,
I think for six weeks.
And I mean, this is the metabolic ward.
So they are, this is very tightly controlled.
It’s as tight as you get.
And what was interesting is of course,
on average people gained weight and gained fat mass,
but some people gained more than expected.
And there was one person in particular
who only gained like just over half a kilo, right?
They should have gained like,
I think it was something like three to four kilos
it was predicted.
And what they found is this individual
just spontaneously increased their physical activity.
Like he didn’t purposely do it.
It just happened.
And I mean, you know, anecdotally,
I’ve seen people who are, again, you know, very lean,
even eat a meal, sit down and start sweating, you know,
and be very fidgety.
There was a natural bodybuilder back in the day
named Jim Cordova.
And this guy was just very lean all the time.
And he was exactly that phenotype.
You know, he would walk up a flight of stairs
and all of a sudden he’s sweating,
sit down, eat a meal, he’s sweating.
You know, he just-
He’s a furnace.
Just expending energy.
And what’s very interesting about NEAT
is that seems to be the most modifiable.
I mean, exercise is very modifiable
because you can be intentional with that.
But of, you know, BMR, TEF and NEAT,
NEAT seems to be far more modifiable.
So even a body weight reduction of 10%,
they’ve observed a decrease in NEAT
of almost 500 calories a day
for a 10% reduction in body weight.
Now, you also do get a decline in BMR when you lose weight.
One, because you’re just in a smaller body now.
And so it takes less energy to locomote.
But also there’s what’s called metabolic adaptation,
which is a further reduction in your BMR
than expected from the loss of body mass.
And that’s on average, usually around like 15%.
But it does seem to be,
there’s new evidence coming out
on the metabolic adaptation from BMR.
And it seems to be a little bit
kind of in the transition phases.
So if you start a diet, within the first few weeks,
you will have a reduction in BMR
that then kind of just thereafter,
any further reduction is mostly
from the amount of body mass you lose.
And then if you, like for example, finish a diet
and move your calories to maintenance,
within a few weeks, BMR kind of starts to come back up.
There is still a small reduction,
but I used to be somebody who thought the BMR,
the metabolic adaptation was a big reason
why people stopped losing weight or plateaued.
And now I think it’s much more to do with NEAT.
And you’ve said that it can’t be conscious
because that will distract us from other activities.
I don’t know if you’ve had a chance to look at this study
and I’ll send it to you.
Maybe it’d be fun to do a kind of an online journal club
about this at some point soon.
But there’s a study that came out
at University of Houston recently,
having people do, now this is a long period of time,
four hours a day of basically a soleus pushup,
which is basically a heel raise,
kind of a seated calf raise with one foot, not weighted.
And then they looked at a bunch of things
about glucose metabolism
and glucose clearance and insulin levels.
And they didn’t conclude
that people burned a ton of calories,
but what they concluded was
that blood sugar regulation improved greatly.
And I think there was a lot of excitement
about this at some level,
but based on everything you’re telling me,
this fits perfectly with what’s known about NEAT.
So this sort of fell somewhere in between with,
in between, excuse me, sort of deliberate exercise
and spontaneous movement.
I guess they’ve tried to make that spontaneous movement
a little bit more conscious.
Well, what I’ll tell people is if you’re worried about NEAT,
one thing you can do, like these watches, for example,
a lot of people are like,
oh, well, it told me I burned this many calories.
They are not accurate for energy expenditure.
I mean, it is like, there was a meta-analysis in 2018,
I wanna say, between a 28 and 93% overestimation
of energy expenditure by these watches.
So for those of you listening,
we’re not gonna name the brand,
but fitness trackers, so wrist-worn fitness trackers.
And this is across the board.
So like depending on the brand,
it could be more or less,
but they all overestimated the amount of,
the calories you burn from exercise.
So this is actually a great example where people go,
well, calories in, calories out doesn’t work for me
because I ate in a calorie deficit and I didn’t lose weight.
And when I talked to them, usually it’s,
they went to an online calculator.
It’s a few things.
They went to an online calculator,
put in their information,
it spat out some calories to eat
and they ate that and didn’t lose weight.
And it’s like, well, what do you think is more likely,
that you’re defying the laws of conservation of energy
or that you might’ve not gotten the right number for you?
The measurement tool was off.
The next thing is a lot of people weigh very sporadically.
And I’ll tell people like,
if you’re gonna make an intentional weight loss a goal,
and again, this can be different for different people,
but typically I tell people,
weigh in first thing in the morning
or after you go to the bathroom,
do it every day and take the average of that for the week.
And then compare that to the next week’s average.
Can I ask one quick, sorry to interrupt,
but one quick question about that.
When you say go to the bathroom,
not to get too detailed here for unnecessarily,
but are you talking about urination and emptying your bowels?
Ideally, because you can eat a big meal the night before.
Yeah, got it.
Wake up, use the bathroom in all forms that you’re ready.
And then get on the scale, take that measurement,
average that across the week.
And then maybe every Monday you take that value
and see how you progress.
And the reason I recommend doing that is
if you’re just kind of sporadically weighing in,
as somebody who weighs themselves pretty regularly,
I mean, my weight will fluctuate five, six pounds
and not seemingly changing much.
And that’s just, you know,
those short-term changes are fluid.
So I’ve had it before where week to week,
my average didn’t change,
but between the lowest weigh-in from a previous week
and the highest weigh-in
might’ve been like eight pounds, right?
So if you’re somebody who just randomly is weighing in
and you’re eating in a calorie deficit
and you just weigh in one day where you’ve just,
whatever reason holding some more fluid,
then you go, oh, see, this isn’t working.
When in reality, your average might be dropping.
So that’s one of the reasons.
And actually, believe it or not,
weight fluctuations are actually identified
as a major reason why people get discouraged
from weight loss.
That it kind of stops the buy-in, you know,
when they have a fluctuation up.
So that’s one of the reasons early on
that low carb diets tend to work really well
is because people lose a lot of water weight really quickly
and they get that buy-in, right?
So, oh, this is working.
Yeah, we can return to that in a little bit
because I have theories as to how that, you know,
when people eat less carbohydrate,
they screep more water and they’ll see, you know,
for the first time,
they’ll see some definition in their abs
and they’ll go, oh my God, this diet’s amazing.
And the fluid loss does hold that promise.
I think fluid loss can do some other things
that might make people literally feel lighter,
although it can have some negative effects.
I do have one quick question
and we’ll return to Neat in a moment.
But when you say the caloric burn
as a consequence of exercise,
I want to ask about the caloric burn during that exercise.
So for instance, somebody is on the treadmill
and they’ll see, okay, they burn, you know, 400 calories.
Actually, I think this is a month
where a number of prominent podcasters
like Bert Kreischer, Tom Segura, Joe Rogan,
others are doing, they call it sober October,
but in addition to avoiding alcohol,
they’re burning 500 calories per day during the exercise.
They’re measuring it.
A lot of people do this.
They think they take track of whether, excuse me,
take stock of how many calories they burned.
My understanding is that
if that particular form of exercise
is a muscle building form of exercise,
that at some point later,
there might be an increase in muscle.
If you did everything right, do everything right,
and then you will burn more energy
as a consequence of adding that tissue.
That’s a long process as you know, and we will discuss.
But I have heard about this post-exercise
induced increase in oxidative metabolism.
I’m probably not using the right language in here.
So if I were to go out, for instance, in sprint,
do some sprints, run hard for a minute,
jog for a minute, run hard for a minute,
and do that 10 times over,
let’s assume I burn 400 calories during that exercise bout.
But my understanding is that in the hours that follow,
my basal metabolic rate will have increased.
Is that true?
And is it significant enough to care about?
So answer both those questions.
Yes, there does seem to be a small increase
in metabolic rate.
And no, it does not appear to be enough
to actually make a difference.
So when they look at, and again, this is where
I tell people, I think I have a good perspective on this
because my undergraduate degree was a biochemistry degree.
So I was very into mechanisms, you know what I mean?
It was like, oh, if we just do this and this,
we’ll get this, right?
And then I did nutrition as a graduate degree.
And then my advisor was so great
because you could do something over here
and he could tell you how it would affect
vitamin D metabolism over here.
This is Don Lehman.
Yeah, Don Lehman.
So he would always kind of say,
yeah, but what’s the outcome gonna be, right?
So this is actually one of the things I changed my mind on
was I used to be very much, well, I think,
high intensity interval training is probably better
because you get this post-exercise energy burn,
which they do see in some of these studies.
But in the kind of meta-analyses
and more tightly controlled studies
where they equate work between high intensity intervals
and moderate or low intensity cardio.
So equating work,
they don’t see differences in the loss of body fat.
And so to me, if I’m looking at,
that’s the example of a mechanism, which is,
okay, we’re seeing this small increase
in basal metabolic rate
that should lead to increased loss of body fat.
But again, remember,
you’re capturing a snapshot in time, right?
But we don’t see a difference in the loss of body fat.
So what may be happening, and again, I’m just speculating,
but a way to explain it could be,
you might have an increase
and then you might actually have a decrease
that tends to just kind of wash it out, right?
And I have to imagine some forms of exercise,
this will be highly individual,
but will spike appetite more than others.
So for instance, if I go out for a 45 minute jog,
which I do a 45 to 60 minute hike or jog once a week,
I just make it a point to do that
or rock or something like that,
throw on a weight vest and hike.
After that, I find I’m very thirsty, I want to hydrate,
but I’m not that hungry.
And that’s true of most all cardiovascular exercise for me.
But after I weight train, about 60 to 90 minutes later,
I wanna eat the refrigerator.
And so obviously calories in, calories out dictates
that that will play an important role
as to whether or not I gain or lose weight, et cetera.
So is it safe to say that the specific form of exercise
that people choose needs to be taken
in consideration of calories in, calories out?
So how much is burned during the exercise?
Also, how much of that exercise
tends to stimulate appetite?
I don’t know whether or not people explore this
in the rigorous studies.
And whether or not that form of exercise
actually increases lean muscle mass or not.
So now we’ve taken exercise
and split it into a number of different dimensions,
but this is what you are so masterful at
is really parsing how the different components
work individually and together.
So if you would just expand on that,
I’d love to know what you’re thinking.
Yeah, so this is actually a really fascinating thing.
So first thing, I wanna just go back to talking about,
like for example, Bert and Tom and Joe,
we’re gonna do 500 calories a day on whatever.
So those apparatuses don’t measure those things
effectively either, right?
Just like these watches.
But the one thing I will say is if you are,
like for example, if I do two hours of resistance training,
typically this will say I burned about 1,000 calories.
That’s a lot of resistance training.
My weight workouts are like warm up for 10 minutes
and then one hour of work done.
I love to train.
And you can recover from,
my recovery quotient is pretty low.
So I’ve been training for 30 plus years
and I found that if I do more than an hour of hard work
in the gym, meaning resistance training,
if 75 minutes, maybe I’m okay, but past that,
I have to take two, maybe even three days off
before I can train.
My nervous system just doesn’t tolerate it well.
So I limit it to an hour, you know.
And part of that to remember is like,
I’ve kind of built up to that
over a long period of time, right?
You know, so you couldn’t just throw somebody in
and start having them do two hours a day.
It’s not gonna go well for them.
I’d like to take a quick break
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But I will say about the calorie trackers is,
so if I’m used to, okay,
usually burn about a thousand calories according to this,
it’s not accurate.
But if I go in tomorrow and I do 1300,
it may not be accurate.
I don’t know what the exact number is,
but I can be relatively confident
that it’s more than the previous session, right?
And so in terms of comparison, it might be okay.
Kind of within subject.
And then the other thing I was kind of circling around on
was if you’re worried about NEAT,
tracking your steps can be helpful
because people’s step counts can spontaneously decrease
when they’re on a fat loss diet.
They don’t even realize it.
So, and that, again, not a complete measure of NEAT,
but what we’ve had some clients do
with our team biling coaches is they’ll say,
okay, you’re at 8,000 steps right now.
We’re not gonna add any purposeful cardio,
but whatever you need to do
to maintain that 8,000 steps, do that.
And sometimes they have to add, you know,
15, 20, 30 minutes of cardio
because their spontaneous activity
that they’re not even aware of goes down.
That’s a really excellent point.
I’ve heard, you know, the 10,000 steps per day number was,
we all heard that.
And then I learned that 10,000 was just kind of thrown out
as an arbitrary number.
So we’re like the eight hour intermittent fasting thing.
There’s a story behind that.
Cause I actually spoke to Sao Chin
and it turns out that the graduate student in his lab
that did that initial study, which was on mice, by the way,
was limited to being in lab for about eight hours
by their significant other.
So the eight hour feeding window is actually the consequence
of this person’s relationship.
That is a really great point that people don’t realize
when they, a lot of people will try to copy
like scientific studies.
And I’ll tell people like, listen,
scientific studies are so confined.
You need to be very careful
with how broadly you apply what’s in there, right?
Like they’re a very big hammer
is kind of the way I look at it, okay?
They’re not a scalpel, they’re a big hammer.
And I think a lot of times in terms of coaching,
scientific studies will tell you what not to do
rather than what to do, right?
But getting back to your question
about like exercise appetite.
So first off, I’m not really aware
if there’s evidence showing like differential effects
of different forms of exercise on appetite.
But again, it also could be like a placebo effect, right?
Because we, like for example,
you and I grew up in an era where the muscle magazines,
it was like, well, as soon as you finish your workout,
you can have your biggest meal of the day, right?
And when I say placebo effect,
I think people have the wrong idea
of what the placebo effect is.
They think that’s just a feeling.
Placebo effect can actually change your physiology.
People don’t realize this.
There’s research showing that a placebo
or the power of suggestion is basically
as powerful as some pharmaceuticals.
And one of the great examples I like to use
is actually there was a study we just covered
in our research review on creatine
where they did four groups,
not supplemented with creatine,
told they weren’t supplemented with creatine,
not supplemented, told they were supplemented,
supplemented, told they weren’t,
supplemented, told they were.
Basically, it just matters what they told them.
This is incredible.
I have to get this study so we can link to it.
A colleague of mine at Stanford,
she’s been on the podcast.
I’d love to introduce you to her
because I think you guys would really riff.
First of all, she was a former D1 athlete
and then runs a lab at Stanford in psychology.
This is Leah Crum.
And she grew up in this,
very athletic, obviously, and very, very smart.
And her laboratory focuses
on these belief-slash-placebo effects
where if you tell people
all the horrible things that stress do to you
in terms of your memory and cognitive functioning,
and then you give them a memory test,
they perform well below baseline.
If you tell them that stress sharpens them
in the short term,
and that adrenaline is this powerful molecule
that can really tune up a number of memory systems,
And it’s remarkable.
And it’s consistent.
And they’ve done this for any number of different things,
including food allergies, for instance.
In any case, I’m so glad you’re bringing this up.
I take creatine monohydrate
and I have for years, five grams a day.
I don’t look.
And it’s great.
And it’s great.
And I believe it’s great.
So is there a compound effect of believing it’s great
and it actually being great?
Not in this study.
But so I think the thing to point out,
people will misinterpret that as creatine doesn’t work.
And that’s not what that says.
What it says is your beliefs about what it does
are probably just as powerful as what it does, right?
So they actually did a study,
and I don’t have the citation,
but it was I think within the last 10 years,
where they told people
they were putting them on anabolic steroids.
And wouldn’t you know it,
they had better gains,
even though they weren’t actually on anabolic steroids,
they had better gains than people
that they didn’t tell were anabolic steroids.
And that’s like hard outcomes, strength, lean body mass,
you know, those sorts of things.
So when people say,
well, I wouldn’t fall for the placebo effect.
It’s like, eh, you don’t have to fall for it.
If you believe it to be true,
the power of belief is very, very powerful.
And as a scientist,
I wish sometimes I was ignorant
so that I could subject myself
to the placebo effect more often.
So kind of getting back to,
that’s just a possible explanation of maybe why,
you know, and I’m the same way,
like I get done with a workout,
like a resistance training session,
I’m like, I’m ready to eat, right?
Now, if you look at the literature overall
on exercise and appetite,
it’s not always what you’d expect.
Consistently, it seems to show that exercise
actually has an appetite suppressant effect.
So people don’t tend to compensate at least fully
for the amount of movement they do.
And there is some evidence that,
you’ve probably heard people say,
well, exercise is a really poor weight loss tool, right?
Like if you figure out how many calories
you should be burning from it and you do that,
you end up getting less weight loss
than you would predict.
I have a family member who is perfectly happy to eat less,
but doesn’t loathe exercise, but dislikes exercise.
And they’re of healthy weight,
but I’m always encouraging them to exercise more.
And so this is an ongoing battle
in our sibling relationship.
Well, one thing I would say is that
exercise independent of anything
that happens with your body weight,
you will be healthier.
So exercise is one of the only things
that will actually improve your biomarkers of health
without even losing weight.
So there’s like it’ll improve your insulin sensitivity,
inflammation, all that stuff.
So everybody out there looking for a hack to be healthier,
exercise is the hack, right?
And our mutual friend, Dr. Peter Atiyah,
I think has gone on record several times now saying that
of all the things that one could take,
et cetera, metformin of all,
regardless of whether or not one takes those
or doesn’t take those,
that the positive effects on the longevity
by way of biomarkers from regular exercise
is far outweighs all of those things combined.
Not that those things don’t necessarily work,
but we’re not going through them in detail now,
but that exercise is by far the best thing we can do
for our healthspan and lifespan.
I 100% agree.
And when you’re talking about weight loss,
people miss the point of exercise, I think.
There’s some work that came out from Herman Ponser as well
that basically showed like,
well, if you do 100 calories from exercise,
you have a like 28 calorie reduction
in your basal metabolic rate in response to that.
So it’s kind of like this constrained energy expenditure
But what I would say is, okay,
well, there’s still a net of 72, right?
So it’s still okay.
And the other thing is,
I think the effects of exercise on weight loss
are actually more due to what it does to appetite.
So if you look at people who lose weight
and keep it off for a number of years,
kind of outliers because most people
don’t keep it off for years,
over 70% of them engage in regular exercise.
Of people who do not keep weight loss,
like maintain weight loss,
less than 30% exercise regularly.
So now that’s just a correlation
that doesn’t necessarily prove causation,
but there are some pretty compelling studies
showing that exercise increases your sensitivity
to satiety signals.
So basically you can have the same satiety signals,
but you’re more sensitive to them when you exercise.
And there’s actually a really classic study
from the 1950s in Bengali workers,
where they looked at basically
four different quadrants of activity.
So you had sedentary, lightly active,
moderately active, heavily active.
Basically based on their job choice.
And they didn’t have an intervention.
They just wanted to track them and see how much,
you know, how many calories did they actually eat?
So it was like a J-shaped curve.
So the sedentary actually ate more food
than the lightly active or moderately active,
but from lightly active to heavily active,
they almost perfectly compensated
how many calories they should be eating.
So to me, that suggests when you become active,
you can actually regulate your appetite appropriately
or much more appropriately than if you’re sedentary.
And do you think this has to do with changes in the brain,
brain centers that respond to satiety signals
from the periphery?
And, or do you think it has to do with
changes in blood sugar regulation?
What I was taught,
and I don’t know if this is still considered true,
is that, you know, spikes in blood sugar
will trigger a desire to eat more,
even though it’s kind of exactly the opposite
of what you need when you have a spike in blood sugar.
And there’s this kind of,
and we’ll get into this
when we talk about artificial sweeteners,
there’s this idea in mind,
I think I adopted perhaps falsely,
that, you know, you eat something that’s sweet
or that tastes really good
and you are suddenly on the train of wanting to eat more.
And I could imagine how exercise,
if it is increasing the satiety signals,
could be working in a number of different ways.
Yeah, I think the effect
is probably mostly at the brain level.
You know, the effects on blood sugar
and the research out there is not very compelling
for blood sugar driving appetite.
Now, if you become hypoglycemic,
yes, you’ll get hungry,
but it’s a different kind of hunger than like your normal,
like I feel kind of empty and my stomach’s growling.
Like those are, they can go together,
but usually like the hypoglycemia is like,
I am hot, I feel like I’m gonna pass out.
Like you wanna eat something,
not because your stomach’s growling,
but because you know that you just need some fuel.
It’s like you’re getting pulled under.
Oh yeah, absolutely.
I’ve been there when I’ve done longer fasts,
something I don’t do anymore,
and drank a lot of black coffee.
There was probably an electrolyte effect there
because coffee has you excrete sodium
and other electrolytes.
And then just feeling like I needed something,
this whole thing, like I need something,
this kind of desperation.
I never wanna be back here again.
Hypoglycemia is very uncomfortable.
That’s not fun.
So, you know, again, when they,
and then when they look at, you know,
actual randomized control trials
of implementing some exercise
where they’re, you know, pretty controlled environment,
they typically see people, if anything,
they eat less as opposed to eating more.
Now, some people, again, that’s, you know,
studies report averages, right?
And there’s individual data points.
So there are some people who at least anecdotally report
that exercise makes them more hungry.
That’s completely valid.
It’s now, it could be their beliefs around it.
It could be a number of different things,
but it’s important to understand
that there is individual variability.
And I think one of the things
that I’ve learned to appreciate more
is not trying to separate psychology and physiology.
We do this a lot.
And so, well, I wanna know the physiology.
I don’t care about the psychology of it.
And now I’m kind of appreciating more
psychology is physiology.
You know, that like with most things now
we have kind of the biopsychosocial model.
And I’ll give you an example of this.
A lot of people get really caught up with appetite.
And if we could just suppress people’s appetite,
that’s part of it.
But people don’t just eat because they’re hungry.
They eat for a lot of different reasons,
social reasons, especially.
So can you remember the last social event
you ever went to that didn’t have food?
If you look at dinner plates from the 1800s,
they’re about this big.
Now, how big are dinner plates?
The whole buffet.
If you, there’s situational cues, right?
You’re sitting down to watch TV.
Oh, grab some popcorn.
Grab some, you know, snack, whatever.
I even see this with, you know,
how one person will pick up their phone
and then everyone picks up their phone.
I think there’s a similar effect with food.
Yeah, and same thing, right?
Like how many times have we either done it ourselves
or been experienced people saying,
oh, you should have some, you should have like,
you know, alcohol especially, right?
Like people will,
I was hanging out with somebody last night
and I had a beer and they just had, you know, a water.
And I’m like, I feel no need to try and convince them
to do that with me.
You know what I mean?
But as humans, you know, we’re kind of herd animals.
Like we don’t want to be doing something out
in isolation on our own.
This is a very tenuous, I guess, belief of mine.
But, you know, doing things alone in isolation,
you know, during kind of, you know, ancestral times,
that’s gonna set off your alarm system, you know?
Because if you don’t have other people,
you can’t protect yourself, right?
So typically things were done together in groups.
And I think that’s a lot of the reason
why we tend to be just tribal in nature
about a lot of things, right?
So the whole point to that is, you know,
on the list of reasons why people eat,
I mean, I’ve gotten to the point where I think
that hunger is actually not even the main reason people eat.
You know, stress, lack of sleep.
So unless, you know, we can do something
that addresses all those things,
there’s a line from a review paper.
This review paper came out in 2011
by a researcher named McLean.
And it’s the best review paper I’ve ever read.
It was called,
Biology’s Response to Dieting,
The Impetus for Weight Regain.
And basically went through all the mechanisms
of these adaptations that happen during fat loss diets
and how biology’s response is to try to drive you back
to your previous.
And I’m gonna butcher the quote,
but at the end of the study,
he said, basically,
the body’s systems are comprehensive,
redundant, and well-focused
on restoring depleted energy reserves.
And any attempt or any kind of strategy for weight loss
that doesn’t attempt to address a broad spectrum
of these things is going to fail.
And so that’s why when people say,
well, just do low carb, you won’t be hungry.
I’m like, yeah, but people don’t just eat
because they’re hungry.
So I think really like trying to get outside the box
and think about these things.
And especially when you read some of the literature,
I recently read a systematic review
of successful weight loss maintainers,
which I thought was really interesting.
So they took people who had lost a significant amount
of body weight and kept it off for,
I think it was three years.
And they basically asked them questions
and tried to identify commonalities.
And there were some things that I expected
like cognitive restraint, self-monitoring,
And then one of the things they said
that I found really fascinating
was pretty ubiquitous between people.
They said, I had to develop a new identity.
So are you familiar with Ethan Supley?
So Ethan is a actor.
He’s been in like, remember the Titans
and American History X.
I certainly saw American History X.
Yeah, so he was very large.
Like he was like 550 pounds
and now he’s like 230 and jacked.
Wait, he was how much?
And whenever he puts a post on his Instagram
of him training, it’ll say, I killed my clone today.
And I asked him, like, is this what you’re talking about?
Like creating a new identity.
And he said, this is exactly what I’m talking about
because I had to kill who I was
because there was no way I was gonna be able
to make long-term changes
if I just didn’t become a new person.
Because there’s, I mean, and addicts talk about this, right?
Like people who are alcoholics,
they had to get new friends.
They had to hang out at different places
because their entire life had been set up
around this lifestyle for alcohol.
And I would actually argue that eating disorders
or disordered eating patterns is much harder to break
than other forms of addiction.
And think about food addiction.
Well, in some ways, bulimia and anorexia
are still addictions.
You can’t stop eating.
Like if you’re an alcoholic, you can abstain from alcohol.
If you become addicted to, say, cocaine,
you can abstain from that.
You can never abstain from food.
And so now imagine telling a gambling addict,
well, you’ve gotta play this slot a couple times a day,
but no more.
Like that’s really challenging.
So yeah, I just like all this stuff,
it’s so important to be comprehensive
with how we treat these things.
These are incredibly important points.
And to my knowledge, I don’t think anyone
has really described it in a cohesive way
the way that you’re doing here.
So important for people to understand this
because obviously as a neuroscientist,
I think the nervous system is creating our thoughts.
Our thoughts and feelings are related to psychology.
And therefore, of course, our physiology
and our psychology are one in the same.
Nowadays, there’s a lot of interest in brain body,
in particular gut-brain access.
And we can talk about that.
But I really appreciate that you’re spelling out
how there are these different variables.
Each one can account for a number of different things.
Exercise clearly has a remarkably potent effect,
both during the exercise in terms of caloric burn,
overall health and biomarkers.
And then this is wonderful to learn
that it can increase the sensitivity to satiety signals.
I think that makes, at least in my mind,
places very high on the list of things
that people should absolutely do.
But that there are other factors too.
And the identity piece is fascinating.
It reminds me also, your story reminds me also
of David Goggins, who is, you know,
he talks about his former very overweight self
almost as if it was a different person.
And he uses language that I’m not gonna use here.
I met David, know David a bit,
and he’s every bit as intense and driven
and a remarkable human being as he appears to be online.
He is that guy.
But it does seem like he had to more or less kill off
a former version of himself
and continues to do that every day.
And I think what your point about this other fellow
who does it through a similar process,
the word today seems to really matter.
It’s not like you defeat this former version of yourself
and then that person is buried and gone.
You said, you know, I killed my clone today.
And that’s the way that David talks about it also.
So this is a daily process.
And I think this is not just a small detail
in tying together all these things.
I think that what you are describing is fundamental
because we can pull on each one of these variables
and talk about each one of them.
But at the end of the day,
we’re a cohesive whole as an individual.
Sorry, you were about to say.
That’s actually one of my favorite topics,
which is, you know, why do we have such a hard time
with losing weight, but more so keeping it off?
Because of obese people,
six out of every seven obese people
will lose a significant amount of body weight in their life.
So why do we still have an obesity problem?
They don’t keep it off.
Why don’t they keep it off?
When you look at the research,
basically what it suggests is,
because people think about I’m going to do a diet
and I’m going to lose this weight,
and they do not give any thought
to what happens afterwards, right?
It’s like, think about if you have
some kind of chronic disease or a diabetic, right?
You can’t just take insulin once and that’s it, right?
You got to take it continuously,
otherwise you’re going to have problems.
If you do a diet and you lose, you know, 30 pounds, fantastic.
But if you then just go back to all your old habits,
you’re going to go back to where you were, if not more.
You can’t create a new version of yourself
while dragging your old habits and behaviors behind you.
So what I’ll tell people is,
because people say, well, I’m doing a carnivore diet
or I’m doing this diet or that diet.
And I’ll say, that’s fine.
Do you see yourself doing that for the rest of your life?
And if the answer is yes,
if you really believe that that’s going to be sustainable for you
and plenty of people, low carb, intermittent fasting,
whatever they say, felt easy.
You know, I could do this forever, great.
If you’re going to lose weight,
you have to invoke some form of restriction,
whether it is a nutrient restriction,
like low carb, low fat, a time restriction,
intermittent fasting, any form of time restricted eating,
or calorie restriction, tracking macros, whatever.
So you get to pick the form of restriction.
So pick the form of restriction
that feels the least restrictive to you as an individual.
And also do not assume
that it will feel the same for everybody else.
Because I made this mistake,
where it’s like, I track things.
And so I allow myself to eat a variety of foods.
I allow myself to eat some fun foods.
But I track everything.
And I’m able to modify my body composition
and be in good health doing that.
Now, it doesn’t feel hard for me.
Part of it is I’ve just been doing it for so long.
But to other people, that’s very stressful.
They said, well, I’d rather just not eat for 16 hours.
If that feels easy for them, do that.
Because the one thing that…
There was a couple of meta-analyses on popular diets.
And basically what they showed
was they were all equally terrible for long-term weight loss.
But when they stratified them by adherence,
and none of them were better for adherence overall,
but when they stratified people
just according from lowest adherence to best adherence,
it was a linear effect on weight loss.
So really what it says is,
what is the diet that’s going to be easiest for you to adhere to
in the long term?
And you should probably do that.
Again, this is where I step back and take the 10,000-foot view.
Somebody will say, well, I’m going to do ketogenic
because I want to increase my fat oxidation
and I want to do this.
And they’re talking about all these mechanisms and everything.
And that’s great.
Can you do it for the rest of your life?
Is this going to be something sustainable for you?
And if the answer is no,
you probably need to rethink what your approach is going to be.
It’s an incredibly important message.
If I could highlight…
If there was a version of highlighter, boldface, and underline
in the podcast space,
I would highlight boldface and underline what you just said.
And for those of you that heard it,
listen to it twice and then go forward because it’s absolutely key.
I think it also explains a lot of the so-called controversy
that exists out there.
I think it also crosses over with the placebo effect.
I almost want to say,
pick the nutrition plan that you think you can stick to
for a long period of time, ideally forever.
And pick your placebo too
because there is a lot of placebo woven into each and every one of these things.
Intermittent fasting, keto,
probably even vegan versus omnivore versus carnivore.
Well, they even talk about the diet honeymoon period, right?
Where you go into a diet and you’re all fired up about it.
You’re very adherent.
And then what happens with every single diet,
without exception in research studies,
is once you get past a few months,
adherence just starts waning and going off.
Here we are really talking about a form of relationship.
I’m not saying that to be tongue-in-cheek.
Actually, we had a guest early on in the podcast, Dr. Karl Deisseroth.
He’s a psychiatrist and bioengineer at Stanford.
Tremendously successful Lasker Award winner, etc.
And he talked about love as an interesting aspect of our psychology
where it’s a story that you co-create with somebody,
but that you live into the future of that story.
When you pair up with somebody,
he was referring to romantic love,
that there’s this sort of mutual agreement
to create this idea that you’re going to live into.
So it’s not just about how you feel in the moment.
It’s also that you project into the future quite a lot.
I’m seeing a lot of parallels with a highly functional and effective diet.
And I love it.
I’m not setting this parallel up artificially.
I’m setting it up because I think that ultimately
it boils down to what you said earlier,
which is that the brain and our decisions
about what we are going to stick to are tremendously powerful.
I think one thing I will say is keep in mind
when you look at the research data,
the meta-analyses on, say, time-restricted eating versus non,
when calories are equated,
it doesn’t seem to be a difference in weight loss, fat loss,
in most biomarkers of health.
Same thing for low-carb versus low-fat.
If you equate calories and protein,
there was a meta-analysis done by Kevin Hall back in 2017
where they looked at the, and again, actual loss of body fat.
And another important point was,
I think there was 22 studies in this,
but all of them provided food to the participants, right?
That’s important because that ensures
that adherence can be much higher in those studies,
whereas various free-living studies,
sometimes you can see funky results.
People are sneaking food or they’re just not really eating
the way that the study would ideally have them eat.
Unless the person is getting continuous support,
like studies where they have a dietician talk to people every week
tend to actually have pretty good adherence.
But I mean, that’s expensive to have done the study.
And again, like what limits studies?
Money, money, and money, right?
But the low-carb versus low-fat,
when protein and calories are equated,
basically no difference in fat loss.
Now, some people get upset about this,
but it’s like, well, to me, that’s like, this is great
because you get to pick the tool you want.
The one tool, it doesn’t seem to be that much better than another,
so pick the one that works for you, right?
Whatever lever you’ve got to pull, you’ve got a bunch of different options.
You mentioned picking something you can stick to for a period of time.
Is there ever a case for someone saying,
look, I like to eat low-carb or even keto for six months
and then switch to a more standard omnivore,
caloric maintenance type diet, and then switch back?
Is there any downside to doing that for sake of health
or weight loss over time or weight maintenance over time?
Because I realize not everyone is trying to lose weight.
And I definitely want to talk about, at some point,
how to eat to maintain weight
because I think there are a significant fraction of people out there
who are trying to do that.
But is there any downside to being a dabbler,
keto for a few months and then omnivore for a few months, et cetera?
I think that’s actually a great thing,
especially to maybe find what you feel is easiest for you, right?
But in terms of like as a strategy,
I mean I guess some people, this might get into dopamine,
but like, oh, change and get something new
and you feel a little bit more positive about it.
A new partner model.
Yeah, yeah, yeah, exactly.
So I don’t think it’s how I would usually set things up initially for somebody.
But if somebody said, hey, I just like to have some variety and change it up,
as long as they’re still like their behaviors
and they’re doing portion control or whatever it is
and they’re able to sustain a calorie deficit
or depending on whatever their goal is,
I don’t think there’s really any downside to it.
I do think the one thing to keep in mind is
when you look at like going between extremes,
so like low fat to low carb or vice versa,
there can be in that transition period a little bit of weirdness,
for lack of a better term.
Like for example, if you’ve been on a ketogenic diet
and all of a sudden you move to like a higher carb diet,
you’ll be like basically insulin resistant
for just a short period of time.
Now, is that going to cause any health problems?
Probably not in the long term,
especially if you’re still controlling calories.
But just because your body has kind of like upregulated these systems,
dealing mostly with fat and glucose production
rather than glucose metabolism,
so now if you start taking glucose or carbohydrate back in,
like for example, you get somebody on a glucose tolerance test
after they’ve been on keto,
they’ll do pretty terribly at it.
But that doesn’t last that long.
About how long?
A few weeks.
I think that’s important for people to know
because I have a feeling during those first few weeks
are the period of time when a lot of people go running back
to what they were doing previously,
which is not to say that they shouldn’t,
but I’ve certainly done that.
I’ve tried a very low carbohydrate diet
and I would have assumed, and now I know I’m completely wrong,
but I assumed that I was so carbohydrate starved for so long
that my insulin sensitivity,
which is a good thing by the way, folks,
would have gone through the roof
and I would be able to just sponge up every bit of glucose
that I would have ingested through carbohydrate.
So I did indeed switch over
and I felt like I had pretty terrible brain fog.
I even got some jitters and I thought, wait, what is this?
My blood sugar was low before.
Now my blood sugar should be in more moderate territory.
But based on what you just said,
I had upregulated the enzymes and systems in the body
for fat metabolism on the keto diet
and then switching over.
There was basically a ramping up of the molecules involved in,
presumably in glycolysis.
I mean, think about like if you haven’t weight trained before
and you start weight training,
you’re going to feel pretty terrible, right?
Like you’re going to be sore and stiff and all that kind of stuff.
But I will say you aren’t necessarily wrong
in what you said about being more insulin sensitive
because it depends on how you measure insulin sensitivity.
So if you measure with something like fasting blood glucose
or fasting insulin or even HOMA-IR,
those tend to be pretty good on low carb.
But then if you do an oral glucose tolerance test,
it tends to be pretty bad.
And so it depends on your specific measure, right?
So I think that the idea that keto makes you glucose intolerant
or insulin resistant, I think, again,
it’s just a transition period and I’m not too worried about it.
But there is something important to keep in mind
and one of the reasons like if somebody was to transition out of keto,
typically if like I’m working with them
or one of our coaches are working with them,
we’ll kind of instruct them to do it like slowly
and kind of systematically over like a four to eight week period.
That way hopefully they’re not having that period of two weeks
where they’re like, oh man, why do I feel so terrible?
Very important point.
I want to go to the other end literally and figuratively
and talk about gut health.
Because up until now-
I see what you did with that pun.
And certainly in the last few minutes,
we’ve been talking a lot about sort of top-down processes,
the brain, the psychology, placebo effects,
but the very real aspects of those.
Not that I can imagine 2,000 calories is 1,000 calories
and somehow change the law of thermodynamics.
Can’t do that.
But we’ve been sort of top-down
and integrating a lot of different ideas
into weight loss maintenance and weight gain.
But gut health,
at least the more popular studies on gut health,
have kind of blown a lot of things out of the water.
For instance, this idea that you could take obese mice
and literally give them fecal transplants from lean mice.
And yes, that sounds like what it sounds like.
Fecal transplants definitely inserted
through the same end in which it comes out.
And I point that out because a lot of people have asked me.
It was kind of scary to me.
I thought, yes, this is not about ingesting feces.
They literally do a transplant of feces from lean mice
into obese mice, and the obese mice get lean.
And yes, this has been done in humans.
Limited number of studies and observed
some pretty impressive effects on weight loss
that I have to assume could be related to placebo effect.
They might have told these obese people,
hey, look, you’re going to get lean
through this fecal transplant from lean people.
But more likely, it had some effect
on their core physiology.
I don’t know which aspects, although I
can speculate which ones.
And they became leaner.
They lost weight.
And that is, in some sense, miraculous,
especially given the important role of psychology and exercise
and satiety signals, because I’m going
to assume that they controlled for a number
of those other variables, although no study is perfect.
What are your thoughts about gut health
as it relates to metabolism, energy utilization, and balance?
Yeah, so the first thing I’ll say
is I’m not a gut health expert, but I
feel relatively comfortable talking about it
based on conversations I’ve had with people who are experts,
one being Suzanne Devcota, who’s, are you familiar with her?
Well, she’s sort of a phenom in this area,
from what I understand.
So she was actually doing her master’s when
I was doing my PhD in Lehman’s Lab.
So she was one of my lab mates.
And the other thing to say is even gut health experts,
and Suzanne will tell you this, they’re like,
talk to me in 20 years.
We just know so little.
I think that’s an overall thing that people don’t understand
is the scientific consensus moves very, very slow.
And probably for good reason, because if we just
flipped our scientific consensus based on one study,
I mean, it would be a mess, right?
So it’s going to take time before you really
understand the implications of the gut and what it means.
So when it comes to weight loss, there probably
is a role in there.
I mean, we’ve seen that there’s something going on.
Now, whether that’s, is it something
where a gut microbiome makeup that’s more obese resistant,
perhaps it extracts less calories out
of the food you eat, right?
Or perhaps it’s elevating BMR.
Although I think that that’s probably somewhat unlikely.
Do you think it could impact the way satiety signals are?
I mean, back to the brain again is the question.
So we know that there’s a link in the gut-brain axis.
And so my suspicion is that it probably
is working via appetite regulation.
So I mean, if we look at the most effective obesity
treatments out there, which is like semaglutide,
I mean, you consistently see a 15% on average
loss of body weight, which is massive.
And people keep it off.
That is a GLP-1 memetic, which is a gut hormone.
And it basically just is a very, very powerful appetite
Well, I guess I’m interrupting, but hopefully with a purpose.
There’s this really interesting study.
And it’s in mice, admittedly, but published
in a neuroscience journal recently.
And basically the takeaway is that like so many things
in neuroscience, the GLP-1 works in two parallel pathways.
In the brain, it seems to impact neurons
in the hypothalamus that control satiety.
So exactly what you’re saying.
And in the gut, it seems to create an activation
of the mechanosensors in the gut.
So the perception is that the gut is full or fuller.
I should say not full, because I think people
who take semaglutide don’t feel bloated.
I don’t know.
But that one feels as if their gut is actually fuller
because these mechanosensors that stretch
are sending signals to the brain.
Oh, I actually have some food.
I’m not empty down there.
Anyway, I’m tickled by this result, mostly
because every time I hear about a drug or a molecule having
an effect, we think it has an effect at one location.
But it’s kind of interesting that, especially
for something like appetite regulation,
that it would be impacting body and brain in parallel.
Anyway, forgive me.
You can tell I’m really excited about this.
And here, you are telling a neuroscientist, me,
that a lot perhaps circles back to these brain
mechanisms of satiety.
I mean, I think that, and especially looking
at the research on leptin, we used to think, OK,
metabolism is mostly like liver-based.
And then there’s metabolism in the adipocyte
and skeletal muscle.
But none of this stuff exists in isolation.
There’s so much crosstalk between these pathways.
And that’s, when we get into mechanisms,
the one of the things, I love mechanisms.
But one of the things I tell people
is keep in mind that when you’re dealing with an outcome,
so like when I say outcome-based,
we’re talking about physical outcomes like weight loss,
fat loss, changes in blood markers, whatever.
That is the summation of thousands
of different mechanisms.
So sure, sometimes you can affect a mechanistic pathway,
and you get kind of straight down the line outcome.
But not always.
Whenever you make a treatment or kind of anything
into the system, it’s like throwing a pebble in a lake.
It creates ripples.
And we don’t always know what those are going to be, right?
And that’s why, I mean, we’ve seen certain drugs.
Well, it works on this pathway.
And then they list off all the side effects.
And you go, well, how would it create that many side effects?
Because nothing, for the most part,
they don’t just work in one place.
There’s a multitude of places it works.
And to your point about semi-glutide
and the effects on mechanosensors,
that’s probably why a lot of people
report actually kind of like low-grade nausea
when they’re using semi-glutide.
Because of that.
Because that feeling is usually not
like a real comfortable feeling.
But I mean, it will get you to not eat.
So I think there’s absolutely likely a connection.
But we haven’t fully elucidated how that works.
And when you think about how complicated the gut is,
I think I heard something like there’s
more cells in our microbiome by far
than there are in our body.
So we’re actually more, in terms of a cell-per-cell level,
we’re actually more bacteria than we are eukaryote, right?
There’s Justin Sonnenberg,
who’s one of the world experts on microbiome.
He’s in the lab upstairs from mine at Stanford.
And he has this idea, it’s just an idea,
that because we are indeed more bacteria than we are cells,
the question is who’s the host and who’s the passenger?
You know, like maybe we are just,
maybe they’re exploiting us to take them around and interact
because they interact and grow on one another.
And so this idea, this freaks people out.
Lex Friedman will love this,
that maybe human beings are just actually the vehicles
for the microbiome and not the other way around.
Anyway, kind of a scary thought.
Do you do anything specifically to support your gut microbiome?
Are you a probiotic guy or a fermented foods guy
or a fiber guy?
So again, I’m going to kind of go straight down the line
from what I’ve heard from Suzanne and other experts.
So if you want to improve gut health,
one of the biggest levers,
the three biggest levers you can pull
is not eating too many calories, exercising.
There is a connection between exercise in the gut and fiber.
So we, it is, of the things we know,
dietary fiber seems to positively impact the gut
because it is a, what’s called a prebiotic.
So your gut microbiota can take, especially soluble fiber,
although there’s actually some evidence, at least in mice,
that it might be able to use some insoluble fiber as well.
I think Suzanne was doing a study looking at hemicellulose
and actually seeing that some specific forms of microbiota
flourish with hemicellulose,
suggesting that they may actually be getting
some kind of fuel out of it, which is really interesting.
But again, in mice, so just huge caveat.
So your gut microbiome can produce these short-chain fatty acids
from, by fermenting this soluble fiber,
and there’s quite a bit of evidence
that these volatile fatty acids,
which can be then actually reabsorbed into the liver,
that they have some positive effects.
Like, for example, butyrate,
when they’ve done butyrate supplementation,
they’ve actually seen positive effects on insulin sensitivity.
So what we seem to understand
is that more diversity seems to be better,
fiber seems to be positive,
prebiotics seem to work much better than probiotics.
So the problem with most of the probiotics
is they’re typically not concentrated enough
to actually colonize.
And even if you do colonize,
what happens is, like, let’s say you colonize some microbiota
that you didn’t really have much of.
If you’re not fueling it with the appropriate fiber,
it’s not going to stay anyway
because it’s essentially going to starve.
So the research seems to really clearly suggest
that eating enough fiber, which is, again, a prebiotic,
that that is a better way to get a healthier gut per se
What fiber sources do you use?
And I realize there’s a huge array of choices out there,
but people will want to have some ideas
as to how they could perhaps mimic what you’re doing.
And I would just say diversity, right?
So, you know, there’s various evidence
from various different fiber sources.
Fruits and vegetables, obviously.
You know, grains, some whole grains,
some cereals, and then various other sources.
So this is one of the things
where we don’t really have a good idea
if, you know, this one source of fiber
is better than another source of fiber.
We just know that fiber overall is pretty good.
And one thing I’ll tell people is, like,
if you want a longevity hack,
I mean, fiber is kind of the longevity hack.
If you look at some of these cohort studies,
there was actually a recent really large meta-analysis
of over a million subjects.
And basically what it showed was
that for every 10-gram increase in fiber,
there was a 10% reduction in the risk of mortality.
And that extended specifically also
to cardiovascular disease and cancer.
So one of the things I’ll tell people
when they get, like, really into, you know,
whether it’s intermittent fasting
or, you know, all these other things,
say, that’s great, that’s great.
Are you eating, like, over 50, 60 grams of fiber a day?
And I just conceptualize 50 to 60 grams.
So if I were to eat, like, a bowl,
like a, let’s just say a quarter plate of broccoli,
and the broccoli isn’t stacked to the ceiling.
The broccoli is just reasonably stacked on there.
Approximately how many grams of fiber is that?
If it’s, like, two cups of broccoli.
Yeah, so if you, like, 200 grams of broccoli per se
would probably be, like, five, six grams of fiber.
And I need to get how much per day, ideally?
Well, I would say, I would,
typically what the recommended dose is
is 15 grams per 1,000 calories intake.
Because if you’re eating, you know, low calories,
it’s difficult to get enough fiber in.
But based on, and again, these are cohort studies, so,
but you can’t do 20-year-long
randomized human control trials, unfortunately.
There doesn’t really appear to be a top end,
at least for the benefits of fiber.
It probably boils down to, like,
how much you can tolerate without feeling uncomfortable, right?
Because if you’re eating, like, a ton of fiber,
I mean, at some point,
it’s not going to be very comfortable.
Yeah, exercise becomes uncomfortable or hazardous, yeah.
And actually, kind of touching on that,
because I think it is important.
You know, a lot of people have kind of,
in the carnivore community, said,
well, you don’t need fiber.
You poop just fine without it.
And I always say, well,
pooping is the last reason to have fiber.
Like, yes, it does help.
It does seem to make elimination easier.
You can, you know, do it more frequently,
adds bulk to stool.
But that’s not why you should eat fiber.
Why you should eat fiber
is because of the effects of mortality.
And, you know, some of the pushback will be,
well, this is healthy user bias.
And what I’ll say is.
Meaning healthy people do this,
and therefore it’s working.
Healthy people eat more fiber, and therefore.
And, I mean, yeah, there’s something to that.
But if it was just healthy user bias,
typically you would see some disagreement
between the studies.
And a great example of that is, like, red meat.
So, not every study shows red meat
has an association with cancer and mortality.
There’s differences depending on the population used,
depending on, like, what they define as high red meat,
low red meat, whether it’s processed, unprocessed.
But I have not found a study on fiber
and cardiovascular disease and cancer and mortality
where it did not show improvements from higher fiber.
So, to me, that suggests that that effect is real.
And so, again, you know,
as much fiber as you can get in comfortably,
I would try to do it.
Because it seems to have some really powerful effects
and is good for the gut microbiome.
The other thing that may be a consideration
for the microbiome is there’s some evidence
that saturated fat may not be great for the microbiome,
that it reduces the prevalence
of some of the more positive strains of bacteria.
And that appears to be not so much
from the saturated fat itself,
but from the bile end products
that combine with saturated fat.
Seems to have a negative effect
on some of these more healthier forms of gut microbiota.
But, again, this is really difficult
because we don’t even know necessarily yet
which species of gut microbiota are positive or negative.
And that’s, I mean, this gets into some of these studies
where they may call it dysbiosis.
Sounds scary, but dysbiosis just means that the gut changed.
It doesn’t necessarily, I mean,
it doesn’t tell you anything qualitative
about whether the change was bad or good.
And so these are just things I think we need to keep in mind
when we talk about this stuff,
but this stuff is still very much in its infancy.
But in terms of the big levers,
I mean, it pretty much fits
with what we know about a healthy lifestyle.
Exercise, don’t eat too much,
consume a good amount of fiber from diverse sources.
Fantastic because it fits with what I like to think of
as kind of the center of mass of evidence, right?
And I’m starting to get some window
into what your process is around selection of studies
and no one study being holy.
But when you look at, as you mentioned,
all the studies on fiber having a positive effect
to some degree or another,
it’s pretty hard to refute that
there isn’t something really interesting there.
And one thing I’ll tell people is like, you know, one study,
I mean, sometimes I’ll change my opinion
based on a single study
when it’s really well done and very powerful.
But usually like one study is just going to move me
just a little bit, right?
And then maybe if another one comes up,
move me a little bit more, right?
And then like very slowly, I’m going to get some,
I mean, my experience with LDL cholesterol,
this is something I changed my mind on a while back
when I was younger, like circa 2005,
getting into grad school,
kind of the prevailing thought was,
well, it’s not so much the LDL,
it’s the ratio of LDL to HDL that’s what matters.
And probably about five years ago,
and I was pretty strong about that opinion.
And then five years ago,
looking at these Mendelian randomization studies,
I kind of went, I can’t hold this position anymore.
What’s your new, what is your revised position on LDL?
So, if you look at the research,
HDL is important because it’s a marker of metabolic health.
If you have high HDL,
it suggests that you are metabolically quite healthy.
You very rarely will you have high HDL
and like high CRP, which is an inflammatory marker,
or dysregulated blood glucose,
almost exclusively people who have high HDL
will have good biomarkers of metabolic health.
But if you take drugs that raise HDL,
it doesn’t reduce your risk of cardiovascular disease.
In Mendelian randomization studies,
which Mendelian randomization basically uses natural randomization.
So, some people are, in the case of HDL,
naturally higher secretors or naturally lower secretors of HDL.
And, you know, we talked about how you can’t really do
a 20-year human randomized control trial.
And when you’re trying to examine something like heart disease,
I mean, that is a lifetime exposure issue.
It’s very unlikely that you’re going to pick out differences
between treatments in two years or even five years.
I mean, people don’t develop,
typically don’t develop heart disease
until they’re in their, you know, 50s, 60s, and 70s.
What Mendelian randomization allows is to say,
okay, we have these people who naturally secrete more or less,
so we can stratify those and look at what is their risk.
So, if you look at people who are low secretors of HDL
versus high secretors of HDL
with holding some of the other key variables consistent, like LDL,
you don’t see an effect on heart disease, really.
Got it. Okay.
But when you look at LDL
and you look at the lifetime exposure to LDL,
it is like a linear effect on heart disease.
And we know that it’s actually not so much LDL,
but it’s more apolipoprotein B,
but that tends to track with LDL just in general.
And if you look at the mechanism,
I mean, we know that LDL can penetrate the endothelium,
so there’s the mechanism is present.
If we look at the epidemiology,
it supports that it’s an independent risk factor.
And then, again, these Mendelian randomization studies
where we can kind of look at people’s exposure over a lifetime
and then we see that linear kind of dose-dependent effect,
to me, that was convincing enough
to change my mind on that particular topic.
And then if you look at, like, some of the Framingham data,
look at high, if you, like, stratify,
like high HDL versus low HDL,
both groups looking at high LDL and low LDL.
So if you have high HDL, low LDL,
you will still be lower risk factor
than somebody who has high HDL and high LDL, right?
So the ratio does matter.
So the ratio does matter.
Same thing with inflammation.
If you look at people who are low inflammation, low LDL,
they’ll have a lower risk
than people who are low inflammation, high LDL.
So, again, that was kind of sufficient for me to change my mind.
But it took, it was like not just one study came out.
It was, okay, then there was another study
and then another study and then another study.
And at a certain point, I go, okay, well,
now I either have to change my mind
or I’m basically just going to be cognitively dissonant
and say, nope, I don’t believe all that, you know.
And so I think that’s one of the things to keep in mind.
People will say, oh, you’re saying this is a bad study.
Very rarely will I call something a bad study
because data is just data.
But the issue becomes how it is presented
and how broadly it’s applied in the mainstream media
or by people on fitness influencers.
And what I’ll do is try to step in and say,
okay, let’s consider X, Y, and Z as well.
And then it’s not a bad study,
but let’s just be careful about how broadly
we imply the interpretation.
Yeah, well, and I think you are in a very unique
and important position to be able to place things
into their proper context because of this,
for lack of a better word, holistic view
of how the psychology, placebo effects,
also core physiology relate to one another and so on.
In fact, I think that your training as a biochemist
and then training in nutrition with somebody who,
Don Lehman, who was pushing you to focus on outcomes,
I think that’s a beautiful capture of the continuum
at which one can look at something.
Because for those of you who don’t know out there,
you know a lot of laboratory studies on mice and humans,
for instance, in the realm of biochemistry
or in vitro studies, you’ll see a change
in some molecule can be quite traumatic.
And then the assumption is, oh, you just take the drug
that will change that molecule in a particular direction
and then you’ll get the effect you want
at the whole organism level.
The person will lose weight.
The person will gain muscle.
The animal will not have Alzheimer’s, et cetera.
But it just doesn’t work that way
because of the redundancy and this interplay.
Well, a great example of that is,
so my research was actually in rodents,
all my studies on protein metabolism,
and leucine in particular is what we were studying.
Well, we know if you give leucine,
it increases muscle protein synthesis.
But we also know if you supplement with leucine,
people don’t get more muscular.
I was about to say,
all you have to do is supplement with leucine?
Right, right, right.
And so how is that possible?
Muscle building is not just protein synthesis.
It’s also the balance between synthesis and degradation.
And degradation just happens to be
very, very difficult to measure.
But a great example, and again,
one of the cool things about my PhD
was it actually changed the way I ate,
which I think is interesting.
So before, I had been like,
I eat eight meals a day, eat every two hours.
Eight meals a day?
Yeah, when I got to grad school.
In order to get that 30 grams of protein per meal.
Get that amino drip going in was the idea, right?
Like just have an IV hooked up with amino acids.
Not really, folks.
Not really, yeah.
But that was kind of the concept.
But the first study I did,
we basically looked at, okay,
a lot of people had measured the amplitude
of protein synthesis in response to a meal.
We wanted to see how long does this last
and where does it peak, right?
And so my thought was, okay,
well, it’ll probably track with plasma leucine.
You give, for those that are not familiar,
leucine is the amino acid that is
almost exclusively responsible
for increasing muscle protein synthesis
when you eat protein.
So it’s one of the branched amino acids.
So we wanted to see, okay,
how long does this effect last?
So we fed these animals whey protein.
And again, I thought, okay,
well, however long plasma leucine stays up,
that will be how long protein synthesis stays up.
And so we got the protein synthesis data back
and it was peaked at 90 minutes,
or sorry, peaked from 45 to 90 minutes
and then was back down to baseline by 180 minutes.
And so when I went to do the plasma leucine analysis,
my shock was at three hours,
plasma leucine was still plateaued out.
And I said, okay, well,
when I look at the initiation factors,
that will show me something.
So for those not familiar,
this is part of the mTOR signaling pathway.
So one of the, two of the targets of mTOR,
when it’s stimulated, leucine stimulates mTOR,
two of the targets of mTOR are a protein compound
And then another one is called ribosomal protein S6K.
So I don’t want to get into the specifics about it
because it’s kind of beyond the scope,
but basically when these things are phosphorylated by mTOR,
it increases the rate of translation initiation,
which translation initiation is basically
the process of the ribosome hooking onto the mRNA
and then starting protein synthesis.
So I was looking at the phosphorylation of 4-EBP1
I was like, okay, well,
I’ll probably see these things come down at three hours,
And so then it was like, what is,
what’s going on here?
So I kept,
I actually kept rerunning the data and rerunning the data
and rerunning the data.
And I’ll never forget, I went into the layman’s office
and this is like, you know,
six months after we’ve done this study
because this analysis takes time.
I was like, so where are we with this duration study?
I said, well, I just got to run the plasma data again
because it’s not right.
And he’s like, well, why is it not right?
And I said, well, it just doesn’t make any sense.
And I kind of went through, he’s like, well,
like describe to me your technique.
Like, how are you doing this?
And I described it.
And he said, well, what, how’s your standard error?
I told him what the numbers were.
He said, it sounds like it’s good data.
He said, it sounds like you are trying to get the data
to fit your conclusion
and you need to change your conclusion to fit the data.
And that statement.
This is why we do PhDs.
This is why, yeah.
You need an advisor.
This is why I’m so skeptical of everything
because I have had so many of my ideas crushed
by my own data, right?
So we actually ended up, this kind of effect,
this phenomenon is called muscle protein
synthetic refractory period.
So basically like once you trigger the system,
kind of runs for a defined period of time
and then it takes time to essentially like reset
for lack of a better term.
It’s also been referred to as the muscle full effect.
But so I looked at that and said,
why am I eating every two hours then?
You know, and there was even a study out of Wolf’s lab,
like back in 99, I think,
where they infused essential amino acids for six hours.
Protein synthesis went up, peaked at 60 minutes,
came back down to 120 and never went back up again.
Maybe I’m being naive,
but I would have thought that if protein synthesis goes up
and then comes back down,
that eating more often would be exactly the thing
you would want to do
if your goal was to get increased protein synthesis
because you’d be pinging the system periodically.
But the problem is the plasma amino acids
are still elevated.
So it’s essentially like eating the whole way through.
From the perspective of leucine.
From the cells, yeah.
So that was one of those things where I said,
you know what, I’m actually going to eat less often
because like if I’m eating and three hours later
I’ve still got, you know, capped out plasma amino acids,
you know, and we looked at all kinds of stuff.
Like we looked at intracellular leucine
just to make sure that, you know,
that wasn’t falling off.
We looked at all the plasma essential amino acids
because we were thinking, well,
maybe protein synthesis is, you know,
sucking some of these amino acids out of the plasma
and they’re dropping and that’s causing it
to kind of short circuit the system.
That wasn’t the case.
It just essentially what the evidence suggests,
I think we’re the only ones to show this so far.
So I’m not ready to say that this is a real effect
because I hold out the idea that data artifacts do exist
and you can’t be totally sure.
But we saw an increase in AMP kinase
kind of around this mark where protein synthesis
started falling off.
And we also saw a decrease in intracellular ATP.
And protein synthesis is an ATP dependent process.
And so what we think might be happening is
you’re, you know, consuming protein
and you’re increasing muscle protein synthesis.
And then at a certain point it has enough effect
on your, you know, energy metabolism in your cells
that it kind of short, not short circuits it,
but it kind of cuts it off, right?
So again, we’re the only ones to show that,
that I’m aware of.
And that was, again, in rats.
I always talk about data.
Like there’s data I’m willing to bet my toe on,
my foot on, my leg on, and my life on.
I’d probably barely bet the end of my little toe on that one.
I’m not quite sure, but it’s interesting nonetheless.
So that’s a great example of, okay,
we’re looking at this mechanism of mTOR signaling.
And if we just looked at that, we’d say,
oh, well, protein synthesis is going to stay elevated
for, you know, past three hours.
But that’s not what we saw.
So yeah, I think it’s, again,
that’s why I really try to get people to say, well,
mechanisms are important.
And especially if you’re seeing an outcome,
it’s important to identify mechanisms that may explain that.
But let’s step back from the mechanisms,
from trying to chase mechanisms,
and let’s look at like chasing outcomes
in terms of what we recommend to people.
In terms of chasing outcomes,
a number of people I know are interested in weight loss
or weight maintenance.
And several times throughout today’s conversation,
we’ve come back to this issue of satiety signals,
whether or not they’re brain-based, body-based, or both.
You know, not wanting to eat more
is a great way to maintain or lose weight
because you simply don’t want to.
I heard you mention earlier that protein
and maybe specific types of protein or sources of protein
may provide better satiety signals
than other macronutrients.
Could you briefly talk about how macronutrients,
including protein, but also carbohydrates and fats,
And from the standpoint of somebody who, for instance,
would like to, quote-unquote, lose a few pounds, right,
probably would be happy to gain a little bit of lean body mass,
provided it was in a particular location on their body.
That seems to be a thing now,
directed hypertrophy, if you will.
And how much they should focus on protein
as a core component of creating this diet, you know,
assuming everything else is being done correctly.
They’re going to hit the right number of calories
relative to their output, meat, etc.
How should we think about protein and satiety signals?
And are animal sources of protein indeed more bioavailable?
That’s a tricky word.
For sake of muscle building,
but also for sake of somebody who just would like to lose body fat.
They don’t want to lose muscle,
they want to bring their weight down a few pounds.
Yeah, a lot of things to unpack there.
Of the macronutrients,
protein is definitely the biggest lever that you can pull.
Because even if, you know,
it doesn’t take a ton of protein to get a lot of the muscle building benefits.
I mean, I think the benefits really start to plateau out
around 1.6 grams per kilogram of body weight.
There’s some evidence that maybe even up to like 2.4 or 2.8 grams per kilo
may give like a little bit more benefit.
I think it probably looks something like an asymptote in terms of a curve
where as you put more into the system,
you always get a little bit more,
but it just gets to the point where it’s so infinitesimally small benefit
that it’s for all intents and purposes, no benefit.
But you mentioned 1.6 grams of protein per kilogram of body weight.
Would you consider that a threshold that most people should try and achieve daily?
I see very few downsides to hitting that.
I mean, I know some people,
and this is going to get into a separate conversation,
but I know some people will say,
well, I don’t want to stimulate mTOR because that’s going to make me die early.
I think one of the things to keep in mind is if you look at –
there’s kind of this thought process out there that if you’re stimulating mTOR,
the protein is going to make you die early.
First off, we have very little human outcome data to support that claim.
The second thing is if you look at any macronutrient isolation,
I can make a mechanistic argument that it’s going to kill you.
So fat, if you take in fat, it decreases flow-mediated dilation.
Flow-mediated dilation is important for heart health in the short term.
Carbohydrates stimulate insulin.
Insulin, pro-inflammatory and all these other things.
And so I can make an argument for any single macronutrient to be negative for longevity.
I really want people – this is something that even scientists get wrong.
They look at an acute response of something and assume that that is going to relate to long-term outcomes and signaling.
So let’s just take exercise, for example.
If I – if you didn’t know anything about exercise and I said to you,
Andrew, I’m going to do something that’s going to make you – your heart rate go up,
your blood pressure go up, your inflammatory markers go up,
your reactive oxygen species increase.
You’re going to say – and it’s going to damage your muscles.
You’re going to say, I’m not doing that.
That sounds horrible.
But it does all those things in the short term.
But what is the long-term effect of exercise?
You actually get healthier.
All those things improve.
Now, I’m not saying that protein is a longevity hack or anything like that.
But what I’m saying is I think some of the arguments out there based on mechanistic –
this increases mTOR, therefore we don’t want to do it.
I think it is a much more complicated argument than just that.
So there’s that.
So protein is the biggest lever.
I would shoot for 1.6 grams per kilogram.
If you can do more, great.
There doesn’t seem to be really downsides to it.
Even like up to very high levels of protein.
Jose Antonio did a study that was a year-long randomized control trial.
Again, it’s just one year.
But they were looking at all sorts of different biomarkers.
Basically, even up to like four grams per kilogram of protein,
they couldn’t really find any negative health outcomes from it.
Other than people were just so satiated, they ended up eating less calories.
So protein is a big lever because, one, it has a higher thermic effect to food.
So you’re getting a little bit more calorie burn per day even though it’s not a ton
because TEF is a pretty small percentage of your overall energy expenditure.
But still a benefit.
You’re getting the effects on lean body mass.
If you’re in a diet, it’s going to help preserve lean body mass.
If you’re at maintenance, it’s going to help build or preserve lean body mass.
And if you’re in a surplus, it’s going to help build or preserve lean body mass.
Then you get the effects on appetite.
So now I want to be careful because appetite effects
tend to be very specific to individual foods.
So you can take a high-protein food and make it not very satiating.
So take, for example, like a really tasty protein bar,
which back when we were getting into this, no such thing existed.
Now you have protein bars that actually taste pretty darn good.
But if you eat one of them, I mean, are you really satiated?
I don’t really feel satiated after a protein bar.
That’s my pre-meal snack.
Because, I mean, it’s processed, refined, and made to be very palatable.
Take something like a 200-gram chicken breast.
Very satiating, right?
And that’s why when people say, well, carbohydrates aren’t very satiating.
It depends on the carbohydrate.
I mean, when you look at the satiety index,
a plain baked potato is about as satiating as it gets.
If I eat a bowl of oatmeal, I feel pretty good afterward for a while.
I mean, usually I’ll eat that along with some other things.
But I completely agree.
You’re saying that the form that it comes in,
maybe even how much chewing is required, how good it smells,
that your psychological associations.
Because to me, a steak is an incredible meal.
I mean, if I had to pick one food that I could eat,
even though I’m not pure carnivore, for the rest of my life,
it would be that because I think it would get me where I need to go,
and then I’d probably have to sneak some fiber.
But it’s an excellent point.
I have a question that I don’t want to take us off track,
but I’m hoping it relates enough that you could answer it now.
In the context of this, if I’m going to eat, let’s say,
two grams per kilogram of body weight protein,
and I’m not eating multiple meals,
maybe I’m eating two or three meals per day,
I’m certainly going to be eating more than the 30-gram threshold
that was thrown around for a long time,
that we can only assimilate 30 grams of protein per meal.
Should I just not worry about that?
Some of it is going to go towards the thermic effect of food.
Some of that might be converted into glucose, of all things,
into a neogenesis.
So should I worry about this 30-gram cutoff?
Because I think balancing the 1.6 gram per kilogram body weight threshold
with number of meals, with the need to exercise and work and live my life
and sleep, et cetera, pretty soon you run into bottlenecks
where you just can’t do it all,
or you’re spending so much time trying to focus on it all.
You can’t optimize all the things at the same time.
You’d lose your mind and your body.
So what is necessary in terms of frequency
if one is getting enough protein?
And then tied into that question,
is there any reality to this idea that if you eat one meal per day
or you’re fasting and then you eat, let’s say, 200 grams of protein
in a single feeding,
that you can assimilate more because you were protein-starved?
Is that a real thing?
So most of the studies with protein are after a fast.
Because to assess it with stable isotope, you have to be in a steady state.
So we haven’t observed that.
It doesn’t appear that fasting really kind of allows you
to assimilate more protein after a fast.
So this gets into a core of one of the things I looked at in my PhD,
which is does protein distribution matter?
Because most Americans get about 65% to 70% of their protein at dinner.
Breakfast tends to be pretty minimal protein foods.
Do any cultures actually eat a big breakfast and not a big lunch and dinner?
We all heard that that was ideal.
We’ll get into circadian timing in a little bit.
But does anyone actually do that?
Steak and eggs for breakfast and then taper off the rest of the day?
I know German culture tends to have a big breakfast,
but it also tends to be like sugary foods and whatnot.
As far as teleologically, I’m actually not sure about that.
So if you look at that,
and then you consider that protein doesn’t really have a storage mechanism.
People will say, well, lean tissue is a storage mechanism.
That’s like saying a house is a storage facility for wood.
Yeah, if the house is made out of wood, you could get wood out of it,
but that’s not why you build the house.
You’re building the house out of a demand.
Same thing for muscle tissue.
There is a free pool of amino acids, but it’s very, very small.
So when you consider things like fat, which basically has unlimited storage capacity,
carbohydrate, a relatively large storage capacity,
you can store 400 or 500 grams of carbohydrate between your liver and muscles,
and then protein, which almost has no storage capacity.
The idea that, okay, you could make up for a low protein at one meal
by overconsuming another meal didn’t make sense to me.
So one of the studies we did, and again, in rats,
we took both groups were getting whey protein,
so high-quality protein.
They were getting the exact same amount of calories,
exact same amount of nitrogen, exact same macros.
Everything was the same.
The only difference was one group basically got kind of three meals
of similar amounts of protein, like dinner was a little bit bigger
because we wanted to keep it somewhat similar to how people eat,
but each meal was going to be over the threshold to stimulate muscle protein synthesis.
Whereas the other group, I constructed it so the first two meals of the day
should not stimulate muscle protein synthesis.
It should be under that threshold.
And then the last meal was about 70% of their total daily protein.
And so we had them eat those for 11 weeks, and I’ll never forget this.
This is how, like, obsessive I became about it,
is there was 110 animals in this study, and I made all the diets,
and I weighed out exactly every single meal for every single animal for 11 weeks.
So I was in there at 6 a.m., I was in there at noon,
and I was in there at 6 p.m., you know?
I love it.
That’s the kind of Ph.D. student that professors dream of.
You guys have been a dream student.
So at the end of 11 weeks, we looked at, like, lean body mass,
we looked at body fat, we looked at hind limb weights.
We didn’t really see differences in lean body mass,
but what we did see was a difference in hind limb weights.
It wasn’t massive, but there was a significant difference
in the size of the muscles of the hind limbs of these animals.
And so it was interesting that there wasn’t a difference in lean body mass,
and what we found, at least with the liver,
the animals that were eating, like, one meal with really high protein
actually had bigger livers, not, like, a huge amount
and not something that I would consider unsafe,
but it was a statistically significant difference.
And so to me, at least, like, if I’m trying to explain, like,
no difference in lean body mass but a difference in these hind limb weights,
maybe there’s some, like, sequestering of, you know,
like that’s fueling a little bit more protein synthesis of the splint neck tissues
rather than, you know, because you’re capping out skeletal muscle protein synthesis.
And we do know that the splint neck tissues are more sensitive
or have a greater rate of protein synthesis per day.
Like, the rate of skeletal muscle protein synthesis in humans is about, like, 1% per day.
So it takes, like, 100 days to turn over, you know, skeletal muscle,
whereas, like, your entire gut, your entire GI will turn itself over in, like,
two to three days, right?
So really, and the liver also has a very high amount of protein synthesis,
which is one of the reasons it’s actually one of the most metabolically active organs.
So all that to say, it has not—
there’s been one human study that showed something similar,
and then there’s been a couple others that didn’t.
And then in the intermittent fasting studies,
which is maybe a good tool to look at compared to continuous feeding,
one thing I will say is it looks like the 16-8 intermittent fasting style.
There’s been a couple studies with Grant Tinsley,
and this is something I’ve changed my mind on as well.
Grant Tinsley has done a couple studies where they did use the 16-8 protocol.
They had them train during their feeding window,
and they had them eat, I think it was at least three protein-containing meals during those eight hours.
These are humans?
These are humans.
And they saw no difference in lean body mass at the end of the study
compared to people who were eating, like, you know,
as many times as they wanted throughout the day.
Now, if you look at some of the more extreme forms of fasting,
like alternate-day fasting or, like, 22-2 or 24,
there are some studies where you do start to see differences in lean body mass.
So my suspicion is—and I’m just guessing, so this is tenuous—
my suspicion is probably if you’re getting, like,
two to three, like, high-quality protein meals in a day,
you’re getting the vast majority of the benefits of protein.
The most important thing is getting enough total.
And then secondarily, trying to get, you know,
at least two or three meals with high-quality protein in.
But if you’re going, like, pretty extreme with, like, alternate-day fasting
or, you know, maybe only one meal a day,
then I think there may be some effects on lean body mass.
But again, these can be mitigated as well if you’re doing, you know, hard resistance training.
Typically, that is the biggest lever in terms of lean body mass.
Yes, you know, protein distribution may make a difference,
but I’m trying to put it in context so people don’t feel like
they need to go out and eat, you know, four meals a day.
But again, so what I would say is, like, some of the more milder forms of,
you know, time-restricted eating appear to be fine for lean body mass.
Now, the caveat is the following.
One of the nice things about animal studies is when you consider
if you want to have a high subject number, high level of control,
and a long duration, it’s pretty much your only option, right?
So I’ve, in our research review reps, I created a Venn diagram,
which basically is, like, three, you know, circles crossing over.
One is study duration, one is level of control,
and the other one is subject number.
And to get all three of those circles to cross over,
it almost has to be in animals.
And reps, it’s a newsletter or a book?
So it’s our monthly research review.
So every month we review, like, five studies that come out
in fitness and nutrition.
Like, we’ll usually do at least one nutrition, one training,
and one supplement per month.
We will put a link to where people can sign up.
This is a sign-up format? Great.
Yeah, so it’s a subscription-based service.
So basically, when people might look at, like, my study,
well, why did you see a difference in muscle weights,
whereas some of these other studies don’t see a difference?
I weighed out every single meal for 11 weeks.
And keep in mind that 11 weeks in a rodent’s lifespan
is a really long time.
That’s about an eighth of their total lifespan.
So is it that there’s no effect,
or is it that the effect is relatively small
and would take a really long time
and very high level of control to see in humans?
I don’t know.
But I think what I would say, relatively confidently,
is if you’re going to do, like, a 16-8 intermittent fasting,
you’re probably fine.
Especially, and again, what is the goal, right?
Like, if you’re a bodybuilder looking to be
the most massive person you possibly can,
or you’re a football player,
in some field that having as much lean body mass as possible
is really important for you,
then I would say, well, you’re not really gaining a whole lot
by doing some form of time-restricted eating.
I think most of the people listening to this
do not fall into that category.
I think most people want to maintain or lose weight.
They’d like to perhaps add a bit of, quote-unquote,
shape or muscle to specific areas of their body
and lose body fat.
And I think your normal forms of time-restricted eating,
you’re probably perfectly fine for that, right?
And again, I don’t want somebody to think,
well, I do alternate-day fasting.
There’s no point to me resistance training
because I’m going to lose muscle mass.
No, no, no, no, no, no.
You can still build muscle doing that.
You just might not build as much muscle as you would
if you were eating in a more traditional format.
But if that’s something that works for you and your goals,
and especially if it’s fat loss or controlling your calories,
then again, it’s about the hierarchy of what’s important, right?
So, to answer your question,
I do think that timing and frequency matters a little.
Not so much frequency, but distribution more so.
So I think the distribution matters,
but it’s a much smaller lever
than just getting enough total protein in.
And then as far as animal versus plant,
I used to be in the camp of
there’s no way somebody can build as much muscle
on a plant-based diet.
And now I think I’ve come back to,
you can, it just requires a little bit more planning.
And I don’t want to say always,
but it’s very difficult to do
without an isolated source of protein.
So unless you’re going to supplement
with an isolated plant source of protein,
it’s very difficult to get enough
without going over on total calories
because you can figure that,
especially like take somebody who may be calorically restricted,
trying to get enough protein from whole intact plant sources.
So you’ve got a few different things working against you.
One, the sources of protein you’re consuming
also have carbohydrate and or fat.
Two, it’s a less bioavailable form of protein.
And three, it’s a lower quality of protein
in terms of it has typically less leucine,
less branched amino acids,
and less essential amino acids.
You answered the question
that I almost interrupted you to ask,
which was, does it boil down to the leucine content?
And it sounds like that is one of the components
and that a lot of the vegan and vegetarian sources
of excellent protein,
that excellent protein vegetarian or vegan source
is co-packaged with calories from carbohydrates and or fat
that make it hard to stay under the caloric threshold.
Whereas a steak is,
and obviously people might want to avoid that
for ethical reasons,
but that’s a different matter entirely.
But a steak or a piece of chicken or an egg is,
well an egg has a yolk, which is there’s fat there,
but is almost a pure protein fat source.
There’s no carbohydrate along for the ride.
So I think what I would say is,
you can do it,
but it takes a little more planning.
And you’re almost always,
if you’re a vegan,
especially you’re going to be better off
like something with some isolated form of protein
or vegan form of protein.
Now this is where it gets into people say,
well what about the limiting amino acids
and those sorts of things?
It’s a consideration.
Some of the better forms of vegan protein
in terms of amino acid content are like soy.
Now I can hear everybody screaming online
about their testosterone levels.
In terms of actual outcomes and looking at testosterone,
there was a recent meta-analysis looking at soy.
And I think if it’s your only source of protein,
then maybe the dosage is high enough
to cause some weird effects.
But if you’re just using it like once or twice a day,
it doesn’t seem to have an effect on testosterone or estrogen.
So that can be a decent source of protein
because it is a complete protein source.
It does have a PD cause of one,
which PD cause is basically a measure of protein quality
based on does it provide enough of all the amino acids
so that none are limiting.
And so soy is one of the only vegan sources that does that.
Interestingly, potato protein isolate
actually has a similar essential amino acid content to whey.
So isolated potato protein.
It’s just really hard to find.
I’ve been trying to source it.
Vegetarians take note because,
or vegans rather because whey is vegetarian.
And whey is a very high-quality protein source.
Very high-quality protein source.
And actually, they’re actually creating whey now out of,
I think it’s, I may mischaracterize this,
but I believe they’re able to produce it now
out of yeast or something like that.
So for vegans, now this is a great option
because you can have whey that’s not animal-based
that is going to be every bit as good as an animal-based whey.
So I think that’s great.
Getting to the leucine, let me go back, sorry.
So another reason that using an isolated protein can be helpful
is because it’s more bioavailable as well
when it’s been isolated out.
When it’s the protein bound up in the actual plant material,
it tends to be less bioavailable.
Now cooking can help increase the bioavailability
because it breaks some of those bonds and whatnot.
But it still seems to be lower.
And you don’t, it’s really interesting.
There was a recent study where they did a corn, wheat,
and pea blend of protein versus whey.
And basically the outcome was 30 grams of each
stimulated protein synthesis to a similar degree.
But the plasma amino acids in the plant-based protein
still did not get as high as with whey.
Now it may be that that’s just, it doesn’t matter
because once you get to a certain level,
you get all the benefits.
But I still found it interesting nonetheless
that they didn’t quite get as high.
The other thing to consider with the vegan sources of protein
is the leucine content.
So one of the studies we did was we looked at wheat, soy, egg, and whey.
Isonitrogenous, meaning we equated protein between the groups.
Isocaloric, we equated calories.
And we looked at muscle protein synthesis.
And I think this was the meals were 15% of total energy from protein.
So like your food guide pyramid level of protein.
And we saw that in the wheat and soy group,
they did not increase muscle protein synthesis.
But the egg and whey group increased muscle protein synthesis.
Now what’s really interesting is we went back
and we took wheat and added free leucine to it
to match the leucine content of whey.
And the protein synthetic response was identical.
So again, I don’t like to simplify things too much,
but leucine appears to really be driving this ship.
And I’ll never forget, Lehman called me into his office one day.
And he would always do these thought experiments.
He liked to think about why something occurs the way it does.
So he would say, one day, I’ll never forget.
He said, Lane, why do you think the body evolved
to just sense leucine for muscle protein synthesis?
And of course, I’m like, I don’t know, man.
I just work here.
I’m just trying to get my PhD.
And he said, well, think about it.
You would want something that really wasn’t extensively metabolized
by the gut and liver because you would want it to show up in the blood
in values that reflect what you just ate.
And you would want it to have passive diffusion across the muscle cell
because you’d want to be concentration dependent, which it is.
Get into the tissues and cells that need it most.
So not having active transport, but rather passive transport.
So yeah, I thought that that was really interesting,
the way he broke that down.
So a few different options for the vegan folks out there.
You can use an isolated source of protein.
And again, there’s going to be good options coming
because this plant-based way is going to be a great option for folks.
You can add free leucine to it, to whatever your source of protein is.
Just buy supplemented leucine powder.
Just buy leucine.
Now, it tastes horrible.
Yeah, I think I’ve heard that.
Maybe I’ve even tried it.
It’s completely nonpolar.
It does not dissolve in anything.
Can it be put into capsules?
It is gross.
It can be put into capsules, yeah.
So you could take a capsule.
Like, for example, if you’re eating your normal meal,
you could just take a capsule of like one gram of leucine.
It’s probably going to bump you up enough that you’re going to be good to go.
And then there’s options like blends, especially with corn.
Corn is actually very high in leucine as a percentage of its protein.
Now, you’ve got to remember, like, you go eat corn on a cob
and you’re getting like two grams of total protein,
so it’s not that much leucine.
But if you isolate out the protein, put it into a powder,
well, now, you know, when you’re getting like 80%, 90% of the weight is now protein,
corn is actually about 12% leucine in terms of the protein.
So a great source of leucine.
It is like almost frank deficient in some other amino acids,
but you can blend it with a few other sources of protein.
Like you could blend it with a soy, a pea,
and you can create these complementary blends
that would actually have quite a bit of leucine
but also some of the other essential amino acids.
So there are options out there for plant-based folks.
And, I mean, we have seen people who are plant-based, you know,
build impressive amounts of muscle.
There’s quite a few bodybuilders that are plant-based.
And a lot of the endurance athletes like it.
And even though when we talk about muscle,
we think about muscle building often, performance in endurance sports,
and also just performance for the typical person
who’s doing some cardiovascular training,
hopefully some resistance training also, and just living life.
I mean, many more people now, it seems, are vegan
or at least avoiding meat, in particular red meat.
I’m not one of those people.
I limit the amount and I certainly focus on the quality of what I eat,
but I do eat red meat.
Which brings me to a question about, you know,
just generally in terms of food choice.
Can we come up with a relatively short summary of the following?
Tell me if this is correct or not.
I think that most of us should be focused on, for sake of health,
healthspan and lifespan,
should be focused on ingesting minimally non-processed
and minimally processed foods.
You know, maybe even cooking our own food.
You know, I realize that’s heresy now, but ideally we would do some of that.
And really trying to avoid foods that are highly processed
and have lots of sugar.
And I’m using this as a segue to get into a question
that I really want your answer to.
I’ve been dying to ask you this,
which is if sugar intake is not actually going up
as much as people think it is,
why are people getting so much fatter?
So what do you think about just a general statement
that we should try and eat foods that are low to no,
minimally to not processed for about 80% of our foods?
Is that a reasonable number?
It’s hard to actually get, you know, completely unprocessed food
because almost everything goes through some form of processing.
So I’m thinking like anything that wouldn’t survive long on,
without refrigeration, yeah, on a shelf,
like an apple or a banana or something.
Oatmeal, like ground oats to me,
as long as there isn’t a bunch of other stuff in there,
would be minimally processed.
A steak is not really processed,
although it’s cut off the animal, et cetera.
So there’s a few steps in there.
But that’s sort of, that’s what I mean.
And I think everybody kind of gets the gist.
I’m probably a little bit pedantic when it comes to this stuff.
No, this is good.
Actually, one of the things I appreciate about you
is something that I get teased a lot by people close to me,
which is the caveats and the insistence on precision is really important
because especially with online communications these days,
it’s like a runaway train.
You know, people will…
It’s too easy to misinterpret what you’re saying.
Very easy to misinterpret.
And the misinterpretations are often used to leverage whole new ideas
about what is and isn’t true, mostly about what is true.
So I really appreciate the nuance.
And this is what a long-form podcast really allows us to do
is catch every curve.
So I would 100% agree with what you said
that if you were going to make a broad stroke
that trying to focus on minimally processed foods is very important.
The one caveat I would say is I think it’s important to understand why
because otherwise people can make this weird association
that like if I eat any processed food, it’s going to kill me
or like every time I eat it, it’s like I’m smoking a cigarette
and my health, you know, my longevity is declining.
Based on the studies we have, it’s mostly about the energy
that processed food just gets people to spontaneously eat more.
And Kevin Hull showed this in his study that was very…
I mean, he designed some of the most elegant studies in nutrition.
And they basically took people from a minimally processed food diet
and then gave them access to ultra-processed foods,
very few instructions, just eat till you feel satisfied
and they spontaneously increased their calorie intake by 500 calories a day.
I mean, that’s massive.
So there’s… and we haven’t quite figured it out.
You know, people said, well, it’s sugar.
It doesn’t appear to be sugar in terms of just an isolation.
Well, it’s fats.
It doesn’t appear to be fats in isolation.
Well, it’s the combination of sugar and fat.
Partly, well, it’s the combination of sugar, fat, and salt.
Partly, but there’s some kind of like overall magic to the texture
and the mouthfeel and just the overall palatability of stuff,
which is always why I say there’s like right and wrong ways
to do these different diets.
Like for example, there’s a right way to do plant-based
and then there’s, you know, like what’s in some of these documentaries
where they’re eating like plant-based mac and cheese.
And again, I love a good mac and cheese, but like that should not form…
like that should not be pitched as a healthy diet
just because it’s plant-based, right?
Because, I mean, you’re eating a highly processed food
that’s very palatable and easy to overeat.
Same thing for keto.
You’ve now got like keto ice creams and you’ve got, you know,
keto cookies and all these sorts of things.
And I’m like, yeah.
And if you look at them,
they actually have more calories than the normal stuff.
And I’m like, yeah, this is completely missing the point here.
Like you’re actually just taking yourself…
like the whole point of those diets is the reason you tend to lose weight
is originally like good luck, you know, 10 years ago
doing a keto diet eating processed food, right?
Like you just couldn’t do it really.
Now you can.
But the problem is it’s not going to work
because you’re going to be still consuming too many calories
because even though it’s keto, what are they doing?
Well, they’re trying to make it more palatable.
They’re trying to make it better mouthfeel,
which I guess if you’re being keto for the sake of being keto, great.
But if you have hopes of body composition modification,
it’s going to really negatively impact.
So yes, I think minimizing the amount of processed food you consume
can be important.
Now that being said, it depends on the individual and their goals.
If your goal is to, for example, build muscle
or maintain a high body weight for a sport, for example,
like an NFL offensive lineman or something of that nature,
or if you’re, you know, I worked with an NBA team.
They were kind of, I can’t disclose anything,
but they were looking at drafting a certain player.
And, you know, like for them, processed foods may actually be a tool.
You know, we all want young people to eat more healthily, I think,
develop great habits.
But some of them, their caloric needs are so high.
That if they were eating what I eat,
they’re going to dissolve into, you know, they’re just waste away.
So I describe this again with a financial example.
It’s like a budget, right?
So if I make a million dollars a year, for example,
is it okay for me to buy like a hundred thousand dollars sports car?
Let’s assume that loans don’t exist, right?
Is it okay for me to buy a hundred thousand dollars sports car
if I still am able to pay my mortgage and pay my utilities
and like take care of my responsibilities,
the things I should do?
Is it okay if I do that?
If it like makes me feel good and it’s fun?
Yeah, it’s fine, right?
Like it fits in your budget.
If I make, you know, 50 grand a year,
should I be going out and buying a sports car?
Probably not because I’m not going to be able to pay my mortgage
and all these other responsibilities.
So your protein, your fiber, your micronutrients,
these are your responsibilities.
But those become much easier to hit when you have higher calories.
So if you’re, you know, eating 4,000 calories a day
for whatever goal you have,
you’re probably going to have some left over
and like good luck eating 4,000 calories from minimally processed foods.
Quite frankly, you’ll be miserable
because you’re going to have such gut fill
that you’re going to feel like you can’t even move.
And so again, now it becomes,
okay, well, is there something inherent to that food processing?
Is there something, you know, that we can pick out that we know,
okay, well, this is going to be a negative effect on health,
even like body composition stuff aside.
And I would say there’s not really great evidence of that so far.
And a great example of that is sugar.
I mean, I actually just wrote a really long article on my website
about why I think sugar was not the root cause of the obesity epidemic.
And you kind of mentioned like sugar intake in the last 20 years
has actually gone down a little bit.
Well, if you look on the whole, it might have gone up a little bit,
but certainly in the male sector, it’s gone way down.
Drinking used to be, there was a five o’clock.
People were drinking all day.
People were smoking a lot less.
I think it’s a real puzzle.
I’d love to know what your hypotheses are.
Smoking can actually be an opposition
because nicotine is actually an appetite suppressant.
Appetite suppressant also increases focus.
The problem is it often arrives in a delivery device that can kill you.
But nicotine itself is a powerful agent.
It also can offset age-related cognitive decline.
Not entirely, but it makes the brain work better.
I’ve got a buddy who doesn’t like caffeine,
and he just takes those nicotine pouches
and basically has one in almost all day
because he has a very stressful job and is a high performer.
You have to be careful how you deliver it.
But there’s a Nobel Prize winning neuroscientist
that will chew five or six pieces of Nicorette an hour,
which I do not recommend.
But when he quit smoking, he just simply couldn’t function as well.
He was the one who pointed me to the literature
on offsetting age-related cognitive decline,
even neuron maintenance.
It’s pretty interesting.
It’s a pretty impressive nootropic, to be honest.
The first thing to realize is when we’re talking about consumption data,
this is based on actual production, basically.
They’re assuming that, okay, we’re producing this amount of these foods
so we can assume the consumption is going to follow that.
So it’s not a direct measurement.
But it has been validated in a few different studies.
We know that oil consumption has gone up.
That’s one of the big ones.
This kind of forms the crux of the seed oils or the root of-
It’s definitely a question that I’m going to ping you on.
They’re going to come into your house and kick your dog
and punch your mom and all kinds of stuff,
and I’m happy to address those.
So calories have still gone up.
There’s some people who claim that they’ve plateaued.
I think the data seems to suggest that calorie intake is still increasing.
And the other thing to keep in mind is even if it’s plateaued,
it’s still at a high enough level that obesity is probably going to continue
to increase up to a point where it will probably plateau if calories are plateaued.
What about energy output?
Leaving aside meat, because that sounds highly individual.
I mean, the people we know are focusing on exercise,
but there are a lot of folks out there that don’t exercise.
And energy output has gone down over the years.
I mean, it’s very obvious when you look at how people work now
compared to even 30, 40 years ago.
It’s much different.
Also, I learned recently that kids in high school
don’t take PE class in many schools.
We had to suit up and run and suit up,
and if you didn’t bring your change of clothes
or you didn’t wash them, in which case you’d be better off just not wearing them.
Nothing like the smell of a boy’s locker room after a weekend.
He’s going to still remember it, and it’s not pleasant.
But you had to run and do your push-ups with everybody else
or play volleyball in your regular school day clothes.
So my understanding is that physical education
is not part of the basic education any longer.
It probably depends on the state,
but I know many states have done away with it just because of budget cuts.
Caloric intake is going up, maybe plateauing.
Is that sufficient to explain the obesity epidemic?
Based on what I’ve seen, I think it’s pretty sufficient.
So it might not be that big of a mystery after all.
No, I don’t think it’s a big mystery.
I think that people don’t like the concept of energy balance,
and I think because they insert judgment into it,
which is, okay, if you’re gaining weight over time,
on a fundamental level, it means you are eating,
you’re consuming more energy than you’re expending.
People insert the judgment, which is, you’re lazy.
You’re a sloth. You’re whatever it is.
And I think there’s a lot of people out there who actually think that.
I actually remember talking to somebody who was like,
well, I would never hire an obese person for a job
because it’s just obvious that they’re lazy.
And I just remember going, are you serious?
There are plenty of very, very smart, high-achieving people who are obese.
This is what happens when you just put people in buckets.
People are much more complicated than this.
Yes, there is some personal responsibility,
but then when you look through the data and you take –
there was a study done in obese women
where they found that women who were obese were 50% more likely
to have had some form of sexual assault trauma in their past.
We know that people from lower income areas are more prone to be obese.
There are several people who have a higher ACE score, I believe,
which is kind of measures like traumatic childhood events.
I believe there was a study showing they’re more likely to be obese.
So there’s – yes, it is an energy imbalance problem.
But just saying eat less, move more, that’s like telling broke people,
well, just earn more money than you spend.
It’s technically right, but it’s very unhelpful, right?
What is more helpful is to describe and implement the habits and behaviors
that will allow them to achieve that, right?
So kind of – I realize we kind of got off track a little bit,
but circling back to like sugar, circa 2005,
I believe that sugar was fattening and bad for your health
independent of any other variable.
So independent risk factor.
And again, I want to be very clear about what independent means.
Independent means independent of all of the variables.
This thing is bad for your health and body composition.
So on its own, independent of whether or not, for instance,
it increases hunger and appetite.
Right, or caloric intake, right?
I was at a graduate school mixer, and one of the professors there
was somebody who had done research on high fructose corn syrup
and fructose specifically as well.
And he was talking to another professor,
and he had done this study in rodents where he had fed like –
I think it was like 60% or 70% of their calories from fructose.
And they saw some really weird things happen in the liver
with the NOVA lipogenesis and all this kind of stuff.
The other professor is saying to him,
yeah, it’s pretty obvious that high fructose corn syrup is fattening.
And this professor who had done this research said,
yeah, because it’s – people overeat.
And he’s like, don’t you think there’s something inherent to it?
And he said, no, I think it’s just calories.
People are eating too many calories.
He’s like, we did a proof of concept looking at could we –
like try eating 70% of your daily calories from fructose.
You actually can’t do it.
Like high fructose corn syrup is only 55% fructose.
So if you ate nothing but high fructose corn syrup,
you would still not get to this level that they fed in this study.
So that got me kind of like questioning my beliefs about it.
So then I went through and I said, okay, like let’s take out the epidemiology.
Not that epidemiology is useless,
but people who eat more sugar are also likely to eat more calories.
So then I looked for the randomized control trials
where they match calories and vary the amount of sugar.
And it doesn’t seem to make a difference,
at least from fat loss or fat gain.
But what about health?
So for instance, if somebody – and I know somebody like this who loves sweets,
is thin, gets some exercise, not a ton.
But my concern is that a significant fraction of their calories
are coming from these sugary foods
and therefore they’re not getting enough fiber, maybe protein, et cetera.
So let’s look at epidemiology for a second.
Then I’ll address this more directly.
When we look at epidemiology,
people who eat higher amounts of sugar tend to be more obese.
They tend to have worse biomarkers of health.
But people who eat fruit, a lot of fruit sugar,
don’t have those same associations.
So why is that?
Well, because fruit has fiber with it, right?
So I started to kind of believe, based on the data I was looking at,
that high sugar intake was not the problem per se.
The problem was that high sugary foods typically are very low in fiber.
But if you’re getting enough fiber, is sugar a problem?
So there was a classic study by Surwit in 1997.
I think it’s still the best study to this day looking at this.
I know those people say, well, it was done in 1997.
It has no relevance.
You know, I know.
If it’s a good study, it’s a good study.
Some studies are timeless.
In fact, they have greater relevance.
I’m not going to go back and undo the discovery of DNA
because it was 60 years ago or whatever it is.
So they looked at an 1100 calorie diet, so low calorie diet.
One group was eating over 110 grams of sugar a day, like sucrose.
The other group was eating about 10 grams of sugar per day.
Calories, protein, carbs, fats all matched, right?
And they provided all the meals to these participants.
So very tightly controlled.
And it was over six weeks.
Both groups lost the exact same amount of body fat.
So it doesn’t seem to matter for body composition
in terms of like sugar per se.
Then they also looked at some biomarkers of health
like blood lipids and blood sugar and some other things.
Again, there was no real differences.
The only difference was – so all their biomarkers improved in both groups.
The only real difference was a small difference in LDL.
So the group eating low sugar had a better improvement slightly in LDL.
But that’s probably because they were eating more fiber.
And we know fiber can bind to cholesterol and lower LDL cholesterol.
So is – now I want to caveat this.
Sugar probably doesn’t have any like positive health effects.
So there’s that, right?
And nutrition is an exchange.
If you’re eating one thing, you’re not eating another thing, right?
So I – but what I would tell people is focus probably less on sugar.
Focus more on fiber.
If you’re eating 30, 40, 50, 60 grams of fiber a day,
but your sugar is 80, 90 grams, I would not be that worried about it,
especially if you’re controlling calories as well.
What I would be worried about is if you’re eating just a decent amount of calories
and not getting enough fiber in general, right?
And even in studies, there’s a few meta-analyses out now
looking at isoenergetic exchange of different carbohydrates with sugar carbohydrates,
so fructose and glucose and sucrose.
Now why is this important?
Well, again, if you’re not – when I say isoenergetic,
that means equal in energy, equal in calories.
So basically when they exchange either sucrose or glucose or fructose
for other forms of carbohydrate,
do they see differences in these markers of health like HbA1c,
fasting blood glucose, blood lipids, and with rare exceptions,
and I can’t remember all the data points exactly,
but the take home is it doesn’t really seem to make a difference.
Now before anybody out there strawmans my argument,
I am not advocating for sugar consumption,
but I think it’s important for people to not create weird associations in their minds
because one of the things I’ve observed, especially in the fitness industry,
is when people feel like they can’t eat something,
like it’s one thing if you say I am choosing not to eat this just because I’m choosing to,
but it’s a very different thing when you’re purposely restricting
because you feel like something is bad.
And this – I mean you know the human brain is in many ways amazing,
in many ways really dumb.
So when you purposely try to restrict something,
what tends to happen is you’re more prone to binge on it.
So people who will try to – well, I’m never going to eat sugar again,
or I’m going to try and limit sugar.
This isn’t the case for everybody,
but they have actually shown now in studies people who are purposely restricting a specific nutrient,
they tend to crave more of that nutrient.
And if they do get exposed to it,
they’re more likely to have what’s called a disinhibition reflex,
which is basically a binge response.
Because the thinking goes, well, this is bad,
and there’s no context on dosage making the poison.
This is just bad in general.
So if I have it, I’ve already screwed up.
I might as well just have as much as I want.
And I like Spencer Nadolsky’s comparison to this.
That’s like getting a flat and then going out and slashing your other three tires
because you might as well.
So I really – I try to come from that perspective of I’ve seen so many people struggle with –
maybe not an eating disorder,
but disordered eating patterns because of these kind of associations they’ve made in their mind.
And so that’s why I’m so pedantic and a stickler about saying,
okay, yes, it’s a good idea to eat minimally processed food and try to avoid processed foods,
but not because processed foods are bad per se,
but what the outcome tends to be from a lot of processed food consumption,
which is overconsuming calories and then therefore energy toxicity negatively contributing to your health.
Yeah, it seems like it again returns this –
the potential for a positive, negative, or neutral behavioral change
and perceptual change of like craving a food all the time that you can’t have is terrible.
It’s a terrible state to be in.
And this I think is a perfect segue for something that first brought us together.
Which was this thing about artificial sweeteners.
And let me just for the record be very clear.
I have long ingested foods with artificial sweeteners.
So I – throughout graduate school, I didn’t have the best habits.
They’re healthier now than they were back then.
But I would drink a Diet Coke or two per day.
I still have the occasional Diet Coke.
I’m not completely averse to drink something that has artificial sweetener.
Although I do avoid sucralose for reasons that maybe I can get into a little bit later.
But a lot of the things I consume contain stevia, which is not artificial,
but it is a plant-based non-caloric sweetener or low-caloric sweetener.
And I don’t have a problem with that.
I became very interested in artificial sweeteners because of the animal data
pointing to the idea that they may disrupt the gut microbiome.
And then disrupt the gut microbiome, as you pointed out, is a very broad statement.
We don’t really know the percentage of lactobacillus, exobacillus, or whatever,
whatever, cillus, illus in there.
They all seem to end in illus, is ideal.
And in fact, a lot of these companies that are having people send in their stool samples
for analysis of the microbiome, I mean, take note.
We don’t really know what a healthy microbiome looks like.
But we know what an unhealthy microbiome might look like.
And it’s one that doesn’t have a lot of diversity in there.
So I was interested in that.
Then there’s the recent human study, which we should definitely get into.
But I was mostly interested in artificial sweeteners for the reason that
there is this food conditioning effect.
And you see it in animals and you see it in humans that if you ingest –
well, coffee is a really good example.
Coffee doesn’t actually taste good, folks, even though I like it.
But when you taste coffee for the first time, most people think it’s bitter and disgusting.
Most everybody, like 95% of people, will say this doesn’t taste good.
Wine, beer, same thing.
Yep, but people learn to associate the state of being caffeinated,
which most people like in order to just feel normal.
Caffeine is one of the few drugs we ingest just to feel ourselves enough that soon
myself included, really look forward to and enjoy a cup of coffee.
So it’s a powerful example, in my opinion, of the food conditioning effect.
So it’s like a Pavlovian thing.
Instead of salivating, you crave.
And it did seem that this study from Dana Small’s lab,
which admittedly was a small, no-pun-intended study itself,
not very many subjects, showed that if you ingested artificial sweeteners
along with food that contained glucose, that you could maybe even get a heightened
glucose response just from the artificial sweeteners after a while.
You and I connected over this study on social media.
You pointed out that the design of the study wasn’t superb.
There was co-consumption of glucose, which made it complicated.
We can go into that.
But the reason I’m spouting off all this context is artificial sweeteners are many things.
So I’d like to talk about their effects on blood sugar in the acute sense
and according to what we might ingest them with
and how they might be changing blood sugar regulation at the level of brain and or body.
And then the gut microbiome data I think are interesting enough to discuss.
And I have changed my view on artificial sweeteners based on what you’ve taught me.
So this is a case where I’ve completely changed my view,
which is that now I don’t have any problem with them whatsoever based on the current data,
which is not to say that I’m gulping down a cup full of super lows,
but I feel okay ingesting some stevia and some aspartame and I’m not too worried about it.
So I think kind of stepping back from a broad view,
we have to think about, again, the hierarchy of importance, right?
And what are you replacing with, right?
So there is no situation where it is not a net positive to take somebody who drinks sugar sweetened beverages
and have them drink an artificially sweetened beverage.
Like in the meta-analysis, there was actually a recent network meta-analysis
looking at markers of adiposity, HbA1c, a bunch of different health markers.
And when you substitute, we’ll call it non-nutritive sweeteners since stevia is not artificial.
But so when you substitute NNS for the sugar sweetened beverages,
you see improvements in a lot of different things, okay?
What was really interesting about this network meta-analysis was
they also looked at water substitution in place of sugar sweetened beverages.
And the effect wasn’t as powerful.
And these are randomized control trials.
So artificial sweetener containing beverages are more beneficial?
Were better for adiposity, for improving adiposity.
And then in the health markers, it was kind of a wash.
Water and non-nutritive sweetener beverages performed similar.
But they were better than sugar sweetened beverages, obviously.
So they then based on a network meta-analysis is kind of where you can compare two things
that didn’t get compared directly.
So there’s not many studies comparing NNS versus water directly.
But if you have a common comparator, so if you compare A to B and B gets compared to C,
you compare A to C based on how they interacted with B.
Butchering it a little bit, but that’s kind of the crux of a network meta-analysis.
So they looked at NNS versus water and found that actually NNS was slightly better
for improving adiposity.
NNS, of course, being non-nutritive sweeteners.
So now again, if you like drinking water and you don’t want to –
I’m not trying to convince anybody to do that.
What that seems to suggest is there is a little bit of an appetite suppressant effect
from these artificial sweeteners or non-nutritive sweeteners.
Now, this gets a little more complicated because if these were people drinking
sugar sweetened beverages, maybe they’ve already developed a sweet taste
and trying to go to water is too much of a jump for them.
And so going to having something like intermediate is a little bit better.
Like there’s a lot wrapped up in this.
But these are the randomized control trials, which are a little bit more tightly controlled,
which I tend to default to a little bit more than I do the epidemiology,
which epidemiology is just so messy because, sure,
non-nutritive sweetener consumption may be associated with different things,
but there’s also a whole other set of lifestyle and habits that are tied up in that.
So I tend to hang my hat a little bit more on the randomized control trials.
So understanding that, okay, now all things being equal,
understanding that this is a tool that may help some people,
and whenever I post about non-nutritive sweeteners in the comments,
there’s always one or two or three people who say,
all I did was cut out soda and I drank diet soda instead and I lost 50 pounds
or I lost 75 pounds. I even have 1%. I lost 100 pounds.
That’s the only thing I did. I mean, that’s a pretty massive lever to pull.
If you consider somebody who might be having like, I mean, five or six cokes a day.
I mean, that’s, you know, we’re talking a serious amount of calories.
And that also means that by replacing with artificial sweetener containing beverages,
they did not replace the soda with food.
Correct. So like, let’s now let’s talk about, right,
this is where we can get into the micro analysis,
but is that obese person who lost a hundred pounds by doing that?
Do I really care about maybe a small alteration to their gut microbiome?
No, because their gut microbiome is actually much more healthy now by them,
having lost all that excess adipose tissue.
So again, the ranking of what I’m worried about, you know,
can change depending on the specific situation.
Now let’s take somebody like me who’s lean and doesn’t really have, you know,
any health problems that I’m aware of.
What about artificial sweeteners for me?
Well, for me, I kind of got using them because of bodybuilding contest prep,
because it was about the only appetite suppressant that worked for me.
But do I think that they are healthful? Probably not.
Do I think they’re unhealthy?
I would say based on the current data, I don’t think that they’re unhealthy.
Now, the information on blood glucose.
So there’s some of the problems with some of these meta-analyses or these reviews
is they kind of lump all the non-nutritive sweeteners together,
and then they may say, well, there’s no effect on this,
or there’s an effect on this.
Well, the problem is these are different molecules,
and they can interact differently.
Aspartame very clearly seems to have no effect on blood sugar or insulin.
That has been repeatedly shown.
Stevia doesn’t appear to have much effect.
Saccharin and sucralose, the jury is kind of mixed.
Now, there was the study that we first connected on,
which I think their primary outcome measure was actually
they were looking at like kind of the sweet taste,
like how it affected sweet taste.
So what they did was the group that was getting the sucralose
was also paired with maltodextrin.
The control group was getting sucrose,
which is an appropriate way to compare the sweet taste
because maltodextrin is not as sweet as sucrose.
So when you’re trying to combine sucralose, which is already sweet,
with another form of carbohydrate,
you’d want something less sweet compared to your control.
But for the outcome measure of insulin and blood glucose,
probably not as appropriate because we know maltodextrin
has a much higher glycemic index than sucrose.
So they appropriately controlled for taste
and not for the effect of the sweeteners.
And I think that that was a key component.
And I think, yeah, the part of that study that intrigued me
actually was in a talk version of that
because that study drove me to watch a talk that,
and we’ll get Dana Small on the podcast at some point, hopefully,
was that they had kids do this study
and they actually had to cease the study
because a couple of the kids became pre-diabetic.
I mean, it seemed like there was something hazardous about,
this was at Yale School of Medicine, it’s a good place.
There’s a range everywhere,
but it just seemed like there’s something about sweet tastes
that if taken to the extreme might be able to impact blood sugar.
This has impacted my sort of behavior.
I try to avoid really sweet things
unless they’re exceptionally delicious or the occasion calls for them
because I do think that it increases my craving for sweet things.
Well, it might not be necessarily a craving,
but it just programs you.
So your taste buds are extremely adaptable.
So take, for example, Indian food.
If you bring Indian people over to America
and have them eat some of our food, they think it tastes extremely bland
because they are used to such spicy food
that unless they have a certain level of spice,
they hardly even taste it.
If you’ve ever done a high-sodium diet
and then gone to a low-sodium diet, it feels very bland.
That’s a styrofoam.
But over time, your taste buds adjust.
So sweet is the same thing.
If you’re used to eating a lot of sweet,
you get kind of desensitized to it,
and then if you go to something less sweet,
it can kind of taste bland at first.
Over time, it’ll get better.
So I think it’s one of those things that, again,
it depends on the situation, right?
If somebody’s obese and they said,
well, this is going to help me eliminate sugar, sweet, and beverage,
why would you want to take that tool away from them?
That’s a great lever to pull.
I mean, if somebody can lose literally 100 pounds
from just one change in lifestyle
that’s not even really that inconvenient of a change,
that is powerful.
But, again, is it the most healthy thing they could do?
And I think that’s kind of what tends to get asked.
We don’t know.
Is it healthier than water?
Maybe as healthy as it?
But I really make all those caveats
because you don’t want to have people
who could use this as a tool think,
well, no, I can’t do this because it’s actually bad for me.
If it helps you lose 50 pounds or 75 pounds or whatever it is,
trust me, it’s not bad for you, right?
Well, it does seem to increase these satiety signals.
What do you think about the microbiome effects in this recent study?
Because the recent study, I think, had some nice features to it.
And you’ve done a detailed description of the study.
So for those that want that.
Is this a two-week study?
Yeah, and we will provide a link.
You did an excellent video on this on your YouTube channel
that really parses each piece.
But they compared the various artificial sweeteners
and looked at the glucose response,
looked at microbiome, a number of different measures.
What was your general takeaway?
And this was in humans for, I think,
the first time looking at microbiome in humans
due to artificial sweetener.
There are a few studies on the microbiome in humans
with artificial sweeteners.
The first two that came out showed pretty much no effect.
But they were a little bit shorter in duration.
They were like two to four weeks.
And again, it depends on what bacteria are getting measured, right?
Like there’s many different kinds of bacteria.
So they could just be measuring one that didn’t change.
And then there was a 10-week study that came out
that got a lot of press.
And they showed, I think it was sucralose, I think.
They showed an effect of change on the gut microbiome.
Now, what was interesting is when I went into the species that changed,
the species that changed the most compared to control
was a species called, I’m going to butcher the name,
but it’s like Blaudia coccoidus, I think it’s called.
I must say for those that work on the microbiome,
it’s so difficult to pronounce.
You need a nomenclature committee and you need acronyms.
I’m sorry. Just do it. Enough already.
You’re killing us.
We’ll call it BC.
We’re going to start the nomenclature committee without you
if you don’t do it soon.
So they noticed that this went up by like three to fourfold.
So I kind of went down the rabbit hole on this.
So interestingly, that particular species of bacteria
is actually associated with lower adiposity,
better insulin sensitivity,
and people who are obese and children who are obese
tend to have less of it.
So I said, well, based on that study,
you could actually argue that maybe sucralose
actually improved the gut microbiome.
Now, again, I’m not making that claim
because we have a hard time understanding
what a healthy microbiome looks like already.
This last study that came out,
my biggest take-home was I think it’s safe to say
that some of these non-nutritive sweeteners
are not metabolically inert.
There are some effects.
Now, are those effects good, bad, or neutral?
I think has yet to be fully elucidated.
Now, I focused more on the blood glucose responses in my analysis.
So in that 10-week study,
they did oral glucose tolerance tests.
And their conclusion, I didn’t really feel like fit their data.
So their conclusion was that, and again, I think it was sucralose,
that it elevated blood glucose.
And this is where statistics can get kind of tricky.
So my take-home was the area under the curve,
the incremental area under the curve,
which is looking at basically the entire glucose response,
was not different between the control and the sucralose group.
To me, that’s the biggest take-home.
There was one time point at the end of the study in the sucralose group,
the 30-minute time point,
that was statistically significantly higher blood glucose
than the control group.
It’s kind of one of those things where I go,
okay, it was one time point.
It’s statistically significant,
but even then we’ve seen things be statistically significant
that end up being data artifacts because they’re not reproduced.
So I’m not saying that’s what’s happening here,
but again, the overall area under the curve was not different.
So to me, that was the biggest take-home.
And papers, we should probably mention,
are published because of effects, generally.
Lack of effect, harder to publish.
Null hypothesis doesn’t, it’s actually really unfortunate
because a null hypothesis is just as useful data
as the non-null hypothesis.
But you’re right, there is a very strong publication bias
towards showing an effect versus not.
Unless you can flip a field on its head entirely
by showing something did not happen,
typically the positive result out does the negative result in.
Positive meaning you see a result.
And then, of course, it’s one study.
And I think that, as you talked about earlier,
the center of mass of data in a given field
are probably the best basis for what we should do.
And so I’m not changing my behavior
around the intake of artificial sweeteners.
I personally am still going to consume stevia and aspartame
in relatively small amounts.
But now I’m thinking, well, okay,
if something contains sucralose,
I don’t have to perhaps actively avoid it.
Whereas before I was, I was actively avoiding it.
The new study I thought was very elegantly, very involved.
I mean, to be quite frank,
some of the animal stuff they did was extremely impressive.
So there was actually two arms to this study.
One was a human arm, one was the animal arm.
I focused much more on the human side of it.
So basically this was a two-week study.
And the really unique aspect of this,
which I think is both a strength and a weakness,
they had almost 1,400 people apply for this study.
And they only had 120, I think, that actually went into it
because they did a very detailed food analysis of these folks.
All these people said that they avoided artificial sweeteners
or didn’t consume them.
And I think people don’t realize how ubiquitous sweeteners are.
Prior to the study, these people were like,
it was like jury selection.
It’s like not ever hearing of the plaintiff and the defendant.
These are these mutant people
who have never had an artificial sweetener.
So the strength is now you don’t have a lot of preexisting effects
that may be clouding what would actually happen when you add it in.
Like, for example,
if you have people who are already consuming artificial sweeteners
and then you have them consume artificial sweeteners,
the likelihood things are going to change is pretty low, right?
So I think that that’s a strength.
It’s also a weakness.
And I want to be really careful
because I think people took my words a little bit too far,
which means I probably didn’t do a good job of being nuanced enough.
There is the possibility for a placebo effect here.
So to me, if somebody has gone through that much painstaking care
to avoid artificial sweeteners,
it’s likely they have a preconceived notion that those are bad for you
because they’re difficult to avoid.
Yes, it’s possible if they’re eating a very minimally processed diet
that they’re just not exposed to them.
And that’s very true as well.
But the other thing that the researchers acknowledged
was they weren’t able to blind the study
because if you’ve never had an artificial sweetener before,
you’re only used to, like, regular sugar,
and you have an artificial sweetener, you know.
You taste it.
It’s still sweet, but it’s not the same sweet.
Yeah, and there’s an interesting effect there
where a lot of people don’t like the taste of aspartame the first time.
I actually quit drinking diet soda for a while thinking I should
and then had one.
It tasted really, I can only describe it as kind of artificial, chemical.
And then pretty soon, it tasted great again.
And so there is some attenuation there.
And whether or not that’s central, meaning within the brain,
or peripheral, I don’t know, but very interesting.
Well, I see you as playing a critical role
in defining what is and what isn’t,
what still needs to be determined in terms of this landscape
and the entire landscape, really, of nutrition.
And that study did change my opinion in terms of,
okay, I think we can clearly say now that these aren’t neutral,
or sorry, that they’re not inert, right?
That was the thought process before.
It was, well, they’re not digested or whatnot,
so they must be inert.
That doesn’t appear to be the case.
But again, when we look at the blood glucose data,
and I’m not saying this is what happened.
I want to be very clear.
I’m not saying this is what happened.
I’m saying it’s possible this happened.
And so this is why we need more studies to verify.
If these people had a preconceived notion
that artificial sweeteners were bad for them,
it’s possible, knowing they’re ingesting artificial sweeteners,
that they could have had a blood glucose response.
Now, my pushback on my own point there would be,
then we should have expected to see it
in all the non-nutritive sweeteners, which they didn’t.
It was just in sucralose and saccharin.
It was kind of a graded effect,
where sucralose and saccharin showed the most dramatic change,
and stevia and a few of the others did not.
And the other issue I took with it,
maybe it’s a ticky-tack thing,
was their primary outcome measure was blood glucose,
the oral glucose tolerance test.
But they had people administer their own oral glucose tolerance test,
which basically they said, okay, drink this drink,
and they were wearing continuous glucose monitors,
which should have been fine.
But again, to me, and I’m being ticky-tacky,
and again, I know all studies are limited by funding,
so I think overall this was a great study,
but I would have liked to have seen them monitor
the oral glucose tolerance test to administer it.
Yeah, and what they did before or after.
You want to know that they didn’t ingest this or didn’t ingest that.
Right. Those two things.
But one of the caveat is it was a two-week study.
So we’ve got to be really careful how much we interpret in this,
because it’s also possible that this is a transient effect.
And maybe it goes away over time. We don’t know.
But again, I think we can clearly say it’s not inert.
Now, how much emphasis we put on that on a two-week study,
I still will say, okay, maybe if you’re worried,
don’t consume Sucralose.
But if you’re 100 pounds overweight
and you want to use some Sucralose as a replacement to help you lose weight,
I would say don’t let this study deter you from doing that,
because the net effect is still going to be more positive
than you not losing the weight.
So if it’s a tool that helps you, fine.
But I do hold open the idea that, well,
there could be negative effects from it as well.
But again, we’re looking at what is the overall outcome, right?
And then when I looked at – they examined some of the different things
that were increased with these different sweeteners.
And again, this word gets messy,
because one of the things they saw was a big increase in butyrate production
from the change in the gut microbiome, presumably.
Well, as we discussed earlier,
butyrate is actually associated with positive outcomes
in terms of insulin sensitivity, inflammation, and some other things.
So I just – I want to be real cautious before people say,
well, there’s a change in the microbiome. It must be a bad change.
We don’t know. It’s possible.
And again, if we have 10 more studies come out and start to show this,
then I will start to shift my personal opinion of artificial sweeteners.
So in anticipation of sitting down today,
I did solicit for questions on social media.
And one of the questions that got a lot of upvotes, likes, if you will,
was one that I think raises interesting questions
about short-term and long-term health, and it’s the following.
I think it’s a common scenario.
A number of people want to know,
what is the healthiest way to approach a kind of rapid weight loss?
And here what I think is happening is somebody has an event coming up
or they’re just tired of being the weight they are
or carrying the amount of adipose tissue they are,
and they wanted to know whether or not it is safe to, for instance,
lose three pounds a week for a few weeks in anticipation of a wedding
or some other event, and whether or not straight caloric restriction
and increasing activity is the best way to approach that.
With the understanding that they may gain back a little afterwards,
I think ideally they’d like to maintain it afterwards,
but what do you think of that sort of approach,
cutting caloric intake in half, for instance,
and then doubling and also doubling your physical output?
So it’s interesting because you might be surprised by what I’m going to say,
which is the research data actually tends to suggest
that people who are obese, who lose a lot more weight early,
are more likely to keep it off,
which seems a little bit kind of contradictory, right?
Like, well, that doesn’t seem very sustainable,
but again, you’re weighing competing things,
so there’s sustainability aspect,
but then there’s also like buy-in is huge for sustainability, right?
So for a lot of overweight or obese people,
if they start a diet and they don’t see something quickly,
they kind of bail on it because it’s not working,
whereas if they see some rapid results pretty quickly,
they buy in even harder, right?
And so I think the conversation,
especially for if there’s any coaches or trainers out there,
is just presenting that as the –
one of my favorite lines is there are no solutions,
there’s only tradeoffs.
I think Thomas Sowell said that.
So you’re having a tradeoff here.
It is – yes, you’re going to lose fat faster.
You might lose lean mass a little bit faster too,
which can be a problem.
But I will say the more adipose tissue you have,
the more aggressively you can diet without negative consequences.
Somebody like me doing a really aggressive diet
is not going to be good for my lean mass.
One, I have a higher lean mass than normal.
Two, I have a lower body fat than normal.
As your body fat goes down,
the percentage of weight loss from lean mass goes up.
So people who are very obese,
because they have so much adipose tissue to pull from,
there’s very little reason for the body to catabolize lean tissue.
Now, that being said,
if you go on a – people misinterpret like –
they’re like, well, I got an in-body done and –
or a dexed done and I’ve lost two pounds of lean mass
and they’ve lost 20 pounds overall.
Well, keep in mind adipose tissue itself is 13% lean mass.
So there’s actually like protein component to –
like the structural component of the adipose tissue
and it does have some water.
So it’s about 87% lipid but the other part is lean.
So at minimum, you should expect a 13% reduction in lean mass when you diet
and then when you consider like you lose body water overall,
which is – registers as lean mass and you lose –
your spleen tissues can shrink a little bit.
So it’s normal to lose –
for the average person to lose like 25% or 30% of the weight
that they lose from lean mass but that doesn’t mean skeletal muscle tissue.
And again, the more adipose you have,
the more aggressively you can approach the diet
without really negative long-term consequences to lean mass or your overall health.
But balance that with, okay, if I’m going to do this,
I need to understand that I’m not going to be dieting this way forever.
I’m doing this to give myself a boost at the beginning
and I have to be okay at some point with transitioning to something
that’s a little bit more sustainable.
Based on what you just said, it reminds me of the satiety signal effect
of exercise you mentioned earlier,
that exercising can improve our sense of when we’ve had enough to eat.
I just want to briefly mention that when Allie Crum was on the podcast,
she mentioned that they’ve been doing a study that –
I have to pair you two and hear the conversation as a fly on the wall
because what she was telling me was that if people believe
that a food is nutritious for them,
then eating less of it registers as more satiating.
Whereas if people view dieting as a deprivation system,
like, oh, dieting is hard and the food sucks and it’s terrible,
well, then they crave all sorts of other things.
Whereas they actually observe in their studies where people report reduced craving
if they are told, for instance, a chicken breast and broccoli
and some olive oil and rice is actually quite nourishing.
It’s actually really good for you.
Then people eat that and they feel like they’ve actually eaten more.
The satiety signaling goes up.
So it’s just a point that Allie made.
Those aren’t my data.
Satiety is so impressive because even the rate at which you eat
and right down to the size of the plate and the color of the plate,
like the contrast in color.
They see – I can’t remember exactly.
I think it’s if the plate is a similar color to the food,
I think people eat more.
Whereas if it’s a bigger contrast, they eat less.
So even like plate color can make a difference on how much you eat.
So again, human brain, very amazing but also very dumb in some ways, right?
Not an optimized algorithm.
I always joke with people.
I’m like, just look at how stupid humans are.
You put some water in front of them like the ocean.
They’re like, oh, yeah, I’ll pay ten times more for this.
But it’s just we’re kind of wired that way.
The reward signaling pathways in the brain run one chemical mainly, dopamine.
There are others, of course, and very few algorithms.
It’s sort of like an intermittent reinforcement is one random reinforcement.
But in the end, there aren’t many algorithms,
and we are probably not optimized, certainly not optimized for our own health
because people will eat themselves to death, drug themselves to death, et cetera,
simply because something felt good at one point.
It proves your point.
One of the things I tell people,
I said this on Andy Frisella’s podcast was interestingly,
the dichotomy of life is if you do what’s easy in the short term,
your life will be hard.
If you do what’s hard in the short term, your life will get easier.
It’s very strange, and actually, Ethan Suplee had a great example of this.
When he was over 500 pounds, he said,
the amount of work I had to do to construct my life that I could just live
was so much more work than just going to the gym for a couple hours a day.
He’s like, the gym work is hard.
He’s like, but when I look back at how much work I had to do to sustain that lifestyle
versus just going to the gym and restricting calories,
he’s like, to maintain the lifestyle of being 500 pounds
was infinitely more difficult than what I do now.
And so, again, a great example.
Short term, hard, going to the gym, calorie restriction.
Long term, life’s easier.
Just really interesting dichotomy, I think, about a lot.
And it probably can’t be restated often enough.
People want to ask about seed oils.
And for those of you that are listening who are wondering why we’re sort of chuckling already,
I should mention that both in the Twitter sphere and Instagram and online,
there are these very polarized views that probably aren’t worth focusing on for too long.
But there are a number of folks out there who are arguing that seed oils
are the source of all the obesity epidemic, inflammation, et cetera.
And then there are those that would argue just the opposite,
that meat is the source of all problems, et cetera.
And I think we’ve, thanks to your nuance and expertise,
we’ve hopefully appropriately framed things that it’s never that black and white.
It’s simply not.
I love olive oil.
I realize that doesn’t fit exactly into the seed oil category.
I love olive oil.
I use it in moderation.
I do also consume some butter in moderation, et cetera.
But are there any data on seed oils?
And here a good example I think would be like canola oil,
which comes from the rape seed that literally was renamed canola oil
because rape seed oil is not good marketing.
So the first thing I’ll say is seed oils have negatively contributed
to our overall health because people in the last 20, 30 years,
what they have tended to add into their diet that has increased
the overall calorie load is oil, like these various,
mostly from seed oils.
But when we look at like one-to-one replacement with other fats,
and so if you look at the epidemiology, yeah,
you can find some epidemiology showing people who consume more seed oil
have more negative health outcomes.
Problem is, again, tied up with a multitude of other behaviors.
And then you can find mechanisms and the idea is, well, these have,
they’re polyunsaturated, which means in the fatty acid chain,
there’s multiple double bonds,
which those double bonds can be oxidized when they’re exposed to heat
and some other things.
And so the idea is, well, when you cook with these things and they get,
they may get oxidized and that’s going to cause inflammation in your body.
So that’s a plausible mechanism.
So as always, I defer to the human randomized control trials.
And so what you tend to find is when you substitute polyunsaturated fats,
or sorry, when you substitute saturated fats for polyunsaturated fats,
it’s either neutral or positive in terms of the effects on,
like inflammation is basically neutral.
There’s some studies that show a positive effect of doing polyunsaturated fats,
but it probably depends on the individual polyunsaturated fat.
And that’s the other thing I don’t really,
is difficult because you’re categorizing like everything in this one bucket
and there are some differences between individual fatty acids.
Even with saturated fat, like for example,
stearic acid doesn’t tend to raise LDL cholesterol,
whereas saturated fat as a whole tends to raise LDL cholesterol,
but there are some saturated fats that don’t.
So again, it’s like we’re putting things in buckets
and it’s a little more nuanced than that.
Then if you look at like the effects of polyunsaturated fats
on markers of cardiovascular disease,
again tends to either be a neutral or positive effect
when you substitute saturated fat for polyunsaturated fat.
Now if you want to get into like monounsaturated versus polyunsaturated,
there’s quite a bit of disagreement between the studies.
What I would say based on the human randomized control trials
is that you’re probably better off consuming monounsaturated
and polyunsaturated in place of saturated fat.
But again, if the idea is,
well, that means polyunsaturated are good for me,
so I’m just going to dump a bunch of oil on everything
and now you’re upping your calories.
Well, that’s a negative now because you have to deal
with the bigger problem of overall energy toxicity.
So I’m not somebody who likes to demonize individual nutrients.
I just haven’t seen really compelling evidence
that seed oils are the root cause of the problems that are being suggested.
And I think this is a good example of kind of like
whenever there’s something that pops up in the fitness industry,
there’s always like the opposite thing that pops up
and it’s like the reactionary extreme reaction
to whatever this thing was over here.
I think that’s what we’re seeing with some of the seed oil stuff
is it’s mostly people who are trying to kind of expose
the virtues of saturated fat.
And listen, I think it’s fine to consume some saturated fat.
But again, I think limiting it to 7% to 10% of your daily calorie intake
is probably wise, again, based on all the consensus of the evidence I’ve seen.
And so once again, like we’re struggling with this.
Okay, we’ve got this epidemiology and these mechanisms that sound good,
but then what actually happens when we do some human randomized control trials
and so far I just haven’t seen the evidence to suggest that
seed oils are independently bad for you independent of the calories they contain.
You said the words overall energy toxicity
and I just want to highlight that I think that’s a fabulous term.
I don’t think enough people think about that
because they are primed or we are all primed to think,
okay, seed oils might be bad or artificial sweeteners might be bad
or this particular component of blood work might represent something good or bad
without taking into account overall energy toxicity,
the toxicity of over-consuming calories, energy.
And thank you for pointing out that most of the data point to the fact
that saturated fat should make up about no more than 7% to 10% of total daily caloric intake.
There’s a lower end threshold that can be problematic.
For instance, I’ve noticed that my blood profiles,
especially in terms of hormones, improve when I’m getting sufficient saturated fat.
Maybe I’m a mutant, but years ago because I’m a product of growing up in the 90s,
I tried a low-fat diet.
It certainly crushed my androgen levels.
I started adding some butter back in and I was right back in the sweet zone where I wanted to be.
So 7% to 10% of total daily caloric intake, I’m guessing, is probably about what I do now.
I’ll have to check.
But is there a danger to going too low in saturated fats?
So again, no solutions, only trade-offs, right?
What maximizes out testosterone might not be the best thing for longevity and vice versa.
I’m not making that claim specifically, but I think it’s important to understand this,
that I think we all have this idea that there’s this one iconic diet out there
that is going to be the best diet for building muscle and burning fat and preventing cancer and heart disease.
And the reality is there’s overall healthy dietary patterns that we see that are good for those things.
But when we get down into the weeds, there’s probably some push and pull here as well, right?
So when it comes to saturated fat, there is some evidence that if you’re too low on it,
that yes, you can have a reduction in testosterone.
Now, is that reduction in testosterone, let’s say 15%, 20%, whatever it may be,
is that sufficient to actually cause loss of lean mass?
That we don’t know.
That’s never been shown.
Interestingly, I just remembered this.
There was one study that was comparing polyunsaturated fat versus saturated fat,
and they equated total fat.
And one of the really interesting things was the group getting the polyunsaturated fat
had more lean mass at the end of the study compared to the group getting saturated fat.
Now, it’s only one study.
I’ve never seen this replicated.
So I’m very – this is a situation where I say I would like to find out what the mechanism of that is
because this could just be random.
But if that gets shown over and over, what I might say is,
okay, well, what are we – if polyunsaturateds are somehow increasing lean mass compared to saturated fat,
who cares what happens with testosterone,
unless that reduction in testosterone is causing some kind of impotence for your life, right?
So all that to say, I don’t really know.
And by the way, that’s something for those watching and listening, real experts,
every once in a while you should hear them say the following words, I don’t know.
My graduate advisor was exceptional at that and she was brilliant, right?
And then in terms of like cholesterol synthesis,
you really need a very, very small amount of saturated fat for LDL cholesterol synthesis.
Your liver can synthesize.
Like the amount of LDL cholesterol or cholesterol that your body requires is so small
in terms of like just living and being healthy.
So I don’t think you need to worry about that.
And from a cardiovascular disease standpoint,
there is some evidence that even taking people who have like quote unquote low LDL of like 80 or 90
and taking them down to like 30 or 40,
that there is still a benefit for the risk of cardiovascular disease.
So again, you’re weighing these two buckets, right?
So what I say, if you’re doing 7 to 10 percent from saturated fat, you’re probably fine.
I received a lot of questions about whether or not there are female specific diet
and exercise protocols.
And I realize this is a vast landscape,
but some of those questions related to menopause and premenopause
and some related to the menstrual cycle,
most related to variations across the menstrual cycle.
In terms of let’s just say diet maintenance or subcaloric diet,
are there any things that you’ve observed?
We’ll talk a little bit later about this wonderful app that you’ve produced,
this carbon app, which helps people manage their energy intake and a number of other things.
And so there you have a sort of a database or at least an experience base.
And then I’m guessing there are probably also studies exploring male versus female differences
in terms of adherence and what sorts of diets work.
Are there any general themes that one can extract from that?
This is going to be a really unpopular segment for the women.
It doesn’t seem to make a big difference.
Well, actually, they may be relieved to hear that
because it would make sorting through the information space
and certainly the information we’ve covered in this podcast up until now simpler.
It means that everything isn’t different for them.
So if you look at the male versus female studies in relation to diet,
they seem to respond to some similar way,
like similar calorie deficit seems to produce similar results.
If you do low carb, high carb, regardless, it seems to boil down to the same principles.
Now, training wise, we do know that female,
like the muscle fibers adapt a little bit differently to training,
but without getting too far into the weeds,
it doesn’t really change the way you should train
because for the most part, building muscle, there’s a lot of different ways to build muscle.
So we know that light loads up to maybe like 30 reps,
as long as it’s taken close to failure,
have basically the same effect on building muscle,
at least in the short term, as heavy loads for low reps.
It’s mostly about taking the muscle close to fatigue or failure.
You don’t have to go to failure, but getting close within a few reps.
If you’re between one rep and 30 reps,
if you’re getting close to failure, seem to produce similar results.
So again, great.
You can pick with whichever form of discomfort you prefer, right?
When it comes to female specific training,
again, females actually, this is one thing that a lot of people don’t know.
They actually put on a similar amount of lean mass
as a percentage of their starting lean mass as men.
In fact, there’s no statistically significant difference
in the amount of lean mass they put on.
Now, the absolute amount of lean mass that’s added will be greater for men
because they started with a greater amount of lean mass.
But the relative increase in lean mass is pretty much the same from similar training.
Now, females, there’s some differences in like fiber types.
Females tend to be a little bit less fatigable than men.
They can go a little bit harder, a little bit longer.
And there’s also some evidence that they recover a little bit better.
But that also could be simply due to the fact that they’re not able to use
as heavy of loads to induce hypertrophy.
So I kind of have this theory that while, you know,
as a percentage of your one rep max, you can program things,
I think absolute load matters.
When you look at like the most elite power lifters,
the super heavyweights aren’t squatting three or four times a week
because, you know, they’re squatting 800, 900 pounds.
I think that there’s an overall recovery effect there.
Again, I have no data to back this up.
This is just my observation.
But when you get into the lighter weight classes, and this goes for men too,
you do see quite a few people who do, you know, many training sessions at high RPEs
and seem to be able to recover from that.
So I do think the absolute load makes a difference.
Now, when it comes to like menstrual cycle,
this is one of those things where I kind of tell people,
you know, do what you prefer.
So there’s some people who have said you should program,
you should like kind of schedule your training around your menstrual cycle,
which is whenever you’re going through your menstrual cycle,
you know, reduce the intensity, reduce the volume,
because you’re, you know, you’re not going to feel as good,
you’re not going to train as well.
What I would say is just auto-regulate that.
If you go in and you’re on your period but you feel good
and you’re doing well that day,
then I don’t think you necessarily need to back it off.
And there was one study that kind of supported that notion.
But if you go in and you feel terrible and, you know,
you feel like you could use, you know, a reduction in intensity and volume,
then it’s totally fine to auto-regulate that.
And when I say auto-regulation,
auto-regulation means you are regulating the individual training session
based on your performance.
So I auto-regulate insofar as like I’m a super nerd,
so I have a velocity device so I can actually attach to the bar
and see how fast the load moves.
And I know at various different like warm-up weights
what velocities I should be hitting.
So if I hit my last warm-up and my velocity is about 10% higher than usual,
I can be pretty confident that that’s going to be a good day for me.
If it’s lower, then I can back it off a little bit.
In fact, at Worlds, when I hit my last deadlift,
it was 30% – my last deadlift warm-up,
it was 30% faster than I usually hit in the gym.
And I turned and looked at my coach and I said,
yeah, we’re going to get this today.
So there’s various forms of ways to auto-regulate.
But again, women, if you’re on your period but you feel good,
I don’t think there’s any reason you need to back off.
But if you’re not feeling good, then it’s totally appropriate to back off.
Raw versus cooked foods.
People wanted to know whether or not, for instance,
eating a raw apple versus – I don’t know.
Does anyone cook apples?
People used to bake.
They were baked apples was a dessert when I was a kid.
It was kind of the letdown dessert.
It was kind of like not awesome unless it had a scoop of ice cream in it.
Even then, maybe not awesome.
But anyway, raw versus cooked.
Obviously, if you burn a piece of meat to the point where it’s pure charcoal,
that’s too much.
There is a small movement surrounding eating raw meats.
That’s not something I particularly enjoy, frankly.
Sushi is the only raw food I personally ingest.
I am very careful about the sourcing, frankly.
Is there anything real about this in terms of being able to extract the amino acids,
vitamins, and minerals from the food raw versus cooked?
It just looks cool for Instagram.
When you cook foods, they actually tend to become – in terms of protein-containing foods,
they tend to become more digestible, not less.
Eggs are this way.
Meats are this way.
People say, well, when you heat protein, you denature it.
I think they hear that word denature and they think destroy.
That is not what denature means.
Proteins fold up into 3D dimensional structures.
You know this, of course, based on their amino acid sequence
and their specific energies of those amino acids.
When you heat protein or add acid, it starts to unfold that protein structure.
That happens during digestion anyway.
So I always chuckle when – like I’ve seen some companies come out with
way that you can cook with, right?
That’s not going to destroy the amino acids.
I’m like, so you mean like regular way, right?
So yeah, typically cooking actually makes amino acids more bioavailable, not less.
Now I would stay away from charring your meat because there is some evidence
that charring creates polyaromatic hydrocarbons, which at least in animals,
when they give those, they appear to be carcinogenic.
So if you do char your meat by accident, I would just cut off the charred portions
and then you should be fine.
Char is delicious.
Not if it’s charred too much, but there is something about a charred crust on a meat.
My dad’s Argentinean. I would like a good charred barbecue.
What about – people referred to them in their questions as carb blockers,
but I think what they’re referring to are things like berberine
and some of the glucose scavengers.
One glucose scavenger I’d love for you to comment on is this assertion
that taking a brisk walk after a meal or maybe even a slow walk after a meal,
some movement can help downshift the amount of circulating glucose in some way.
I’ve heard that.
Not a lot of people, but some are starting to pay attention to this idea
of taking things like berberine or even metformin can scavenge glucose.
I personally can’t take berberine.
If I take it, I get massive headaches unless I’ve ingested tons of sugar
and carbohydrates, so I just don’t mess around with it.
But I know there are a number of people out there that want to know
whether or not these glucose scavengers can be useful.
I think that is really majoring in the minors, if I’m being honest.
As far as the carb blockers, there’s some white kidney bean extract
and those sorts of things.
They do block the digestion of carbohydrates, some.
So when I say block, that’s those watching or listening.
Metabolism is typically not on and off switches.
When we say things like block or attenuate or inhibit,
typically we’re not talking about just a switch on the wall
that you press it and everything turns off.
We’re talking about a dimmer switch.
It just changes the emphasis.
But these carb blockers can reduce the absorption of carbohydrate.
Now, they don’t seem to cause weight loss when you just do it a normal diet.
Now, why is that?
Well, all it does is once those carbohydrates get to the large intestine
and your bacteria get a hold of them,
they start fermenting them to volatile fatty acids
which get reabsorbed into your liver.
So you don’t get the increase in blood glucose,
but you still get almost all the calories from it.
It’s just in a different form.
So if carb blockers, if they actually worked really well,
I mean, if you block something from being absorbed,
your GI typically does not just let undigested materials sit in there.
You get diarrhea.
I mean, that would be the outcome.
It’s also how I debunk the whole 30 grams of protein at a meal.
You can’t absorb any more than that.
If that was the case, when you ate a steak,
you would just start having diarrhea
every time you went over that 30-gram threshold, right?
I remember during college, so this would be early 90s,
there was the Olestra craze,
this idea of putting a non-digestible thing into things like potato chips
so that it would clear through the GI tract faster,
not absorb as many calories.
This went nowhere, obviously.
You don’t hear about this anymore.
But it does raise an interesting question related to energy balance,
which is gastric emptying time.
And obviously in the landscape of eating disorders,
in particular anorexia, abuse and abuse of laxatives
is a way in which people will, in an unhealthy way,
try and control their weight.
And there’s a lot of problems with that approach.
But what about gastric emptying time?
Is this one way that people could control their energy balance in a healthy way?
And where does fiber come into play?
Fiber tends to improve GI transit time because it adds bulk.
Your GI system is basically a tube,
and it has peristalsis, which is wave-like contractions
that moves the food down through the tube.
Well, if you have more bulk to the food, like with fiber,
you can move it through a little bit better.
Now, in the gastric, the stomach specifically,
fiber tends to delay gastric emptying and slow it a bit,
probably because it congeals a little bit.
Now, this kind of gets into the glycemic index argument.
If you do low GI foods, you’ll have a slower release of glucose.
It’s a slower gastric emptying time.
Does that affect energy balance?
And so there are quite a few studies looking at low GI versus high GI foods.
In the studies where they don’t control calories,
low GI tends to outperform high GI.
But when they control calories, there’s no difference.
And so what I think that suggests is low GI foods,
just by their nature, tend to be higher in fiber.
And so I think it just kind of comes back to the fiber issue.
I’d like to ask you about supplements for a moment.
It’s an enormous landscape,
but I believe there are a few things that you believe in,
meaning they exist and there are decent data to support their use,
maybe even some anecdotal data based on your own experience.
As long as we highlight it as such, it could be interesting.
I’ve heard you talk about two in particular,
one that I’m very familiar with, which is creatine monohydrate.
If you could share your thoughts on that,
not just for muscle building, but maybe any other purposes for it.
And then the other one is one that, frankly,
I’m learning more about all the time now thanks to your prompt,
which is Redolia Rosea.
I think I pronounced that correctly.
And why that might be interesting or of use to people.
Touching on creatine, it is the most tested,
safe and effective sports supplement we have.
I mean, it’s just,
there are thousands of studies on creatine monohydrate now.
And I would say very clearly too,
if you’re using any other form of creatine,
I think you’re wasting your money.
Creatine hydrochloride has some hype around it.
It’s apparently it’s a little more soluble.
The claim is that you need less,
but there’s only a couple of studies on it and it’s more expensive.
And creatine monohydrate is not particularly expensive.
I realize people have different budgets, but it’s not,
it doesn’t land in the, it’s not a budget breaker.
It’s gotten more expensive because of COVID and supply chain issues.
Even the there’s forms of creatine that appear to be as good like
hydrochloride, but it’s more expensive.
And then things like creatine ethyl ester has been shown to be worse than
Buffered creatine is as good or worse.
And it’s much more expensive.
So I tell people just take creatine monohydrate.
It is tried and true.
It’s been shown to saturate the muscle cells 100% with phosphocreatine.
And that’s what you want.
So creatine works through a few different methodologies.
One through increasing phosphocreatine content,
which helps improve exercise performance.
It also appears to improve in cover.
It appears to improve recovery and it increases lean mass.
A lot of which is through bringing water into the muscle cells,
but that is, I mean, muscle cells are mostly water.
So when people say, well, it’s just water,
that’s what muscle cells mostly are.
And it also increases strength and some other metrics.
Now it also has been shown in studies that people tend to get a decrease in
body fat percentage.
Now that’s probably because they’re getting an increase in lean mass.
And so the relative is a decrease in body fat percentage,
but there are a few studies that show a decrease in fat mass as well.
I don’t think that creatine is a fat burner.
I think that people are able to train harder, build more lean tissue.
And so that’s probably having an effect on fat mass.
Then they’ve actually shown more recently some cognitive benefits to creatine,
which I find really interesting as well,
but the only knock on creatine that anybody’s been able to come up with,
because they’ve debunked the kidney stuff, they’ve debunked the liver study.
There’s no evidence that it harms healthy kidney or liver.
Is hair loss.
So what about hair loss?
Because there was one study in 2009 that showed the creatine increased DHT,
but they didn’t really show an effect on any other sex hormone.
So it’s kind of strange.
Like you would think if there was an increase in DHT,
there would be like something else that changes as well.
And it’s only one study.
And again, didn’t directly measure hair loss, measured DHT,
which we know is involved in the loss of the follicle.
So what I would say is that I am not convinced.
It’s only one study, never been replicated to my knowledge,
and it was looking at a mechanism rather than an outcome.
So if you’re somebody who’s prone to hair loss
and you want to avoid creatine because of that, I understand.
But for most people, I don’t think it’s something to worry about.
Do you emphasize the classic loading of creatine,
taking it a bunch of times per day and then backing off
or just taking it consistently at the, I think, 5 grams per day
is kind of the typical dose that people take?
So again, no solutions, only trade-offs.
You can load it and you will saturate your phosphocreatine stores faster,
like usually within a week.
If you just take 5 grams per day, it’ll take 2, 3, 4 weeks.
But you will get to the same place,
and you’re probably going to have a much lower risk of GI issues.
Some people, creatine can be a gut irritant.
If it is for some folks, I would recommend splitting it into multiple doses,
so maybe like multiple to 1 or 2 gram doses per day.
And definitely don’t load it if you’re somebody who has GI issues from it.
As far as rhodiola rosea, the research is still in its infancy.
I was just reading a new systematic review
that kind of concluded that we need more high-quality research.
But the research that is out there seems to suggest
that not only does it reduce physical fatigue,
but it also reduces the perception of fatigue
and may also enhance memory and cognition as well.
And it’s referred to as an adaptogen.
So I really like it.
My anecdotal experience is when I combine that with caffeine,
it tends to kind of smooth out the effects of caffeine.
It’s a more pleasant experience.
And there’s also some evidence that if you’re like coming off caffeine,
that it can reduce the negative side effects to caffeine withdrawal,
which by the way, I didn’t really believe in that
until I actually did a cold turkey.
So before I meet, I will cut out caffeine for 7 days
because you can basically reset your caffeine tolerance in 7 days.
And like 2 days in, I mean, I’m groggy.
I’ve got the headaches.
I’ll get like body aches that come up because caffeine is actually a mild analgesic.
And yeah, so it’s very interesting.
But I slept like a baby, I’ll tell you that.
And then you took caffeine prior to your event.
To the meat, yeah.
So you really want the maximum punch from it.
That’s why you do that.
Yeah, and like I said, rhodiola tends to –
it doesn’t eliminate those negative effects,
but it tends to dampen them a little bit.
So I really like it.
Again, would like to see more research on it.
But there’s a lot more stuff coming out.
Like ashwagandha is another thing that looks pretty promising.
Seems to increase testosterone modestly.
I don’t think it’s – like they’ve shown increases in lean mass.
I don’t think the increase in testosterone explains the increase in lean mass.
It’s just not a big enough increase.
Could it be the decrease in cortisol?
People have talked about –
It does decrease stress, stress hormones.
It also has been shown to help with sleep.
But I would like to see more research looking at mechanistically
how it’s increasing lean mass before I kind of say conclusively
that this is the next creatine.
There’s more research that needs to come out.
Then there’s some other things that have an effect.
Citrulline malate, there was a new meta-analysis
that showed that citrulline malate can reduce fatigue
and increase I think time to fatigue.
It may actually have some small recovery benefits as well.
Different forms of carnitine can actually have recovery benefits
and actually interesting, I think it’s carnitine tartrate
actually has been shown.
Volick published a study that actually showed
that it increased androgen receptor density in muscle cells.
L-carnitine and its other forms are pretty –
I think there’s good evidence that they can improve sperm
and egg health for people who are looking to conceive.
There are surprising number of studies on this in humans.
But yeah, androgen receptor density.
That’s from oral L-carnitine.
People are taking capsules, not injecting directly into a muscle.
Then you’ve got things like –
obviously like the other most effective supplement out there
is probably caffeine.
I mean like if you look at the research studies,
caffeine produces very consistently improvements in performance.
So that’s another one.
Some people don’t like the effect of caffeine.
That’s OK but –
I wouldn’t know because I’ve never come off it.
Well, interestingly, they do show that the effect appears to be consistent,
that even if you’re a habitual caffeine user,
you do still get a benefit every time you take it.
But like you said, you’re just used to it.
So there’s those things.
Then you’ve got things like beta-alanine, which for –
it’s in our pre-workout.
Probably not super helpful for most people for resistance training.
It does seem to have some benefits for like high intensity.
Like if you get out more than like 45 seconds or 60 seconds
of like really hard training,
it does appear to help with delaying fatigue for that.
Then you’ve got things like betaine, also called trimethylglycine,
which there’s some evidence it can improve lean mass.
There’s some evidence that it can improve power output.
So there’s a few things out there.
But most of the stuff is not very good.
So I think that that’s – those kinds of supplements, very useful.
But again, I would never tell people they need supplements.
Again, even like something like creatine is going to be a very small effect
compared to like proper nutrition, recovery, and hard training.
One of the things I was – I was talking with Ben Bruno the other day
and I said, you know, like some people will ask me like,
how does this person make progress because their programming is not evidence-based
or this guy, how is he – like his exercises are dumb.
I’ll say, yeah, but they train really hard for 20 years.
Like one commonality you see between like really successful athletes
or bodybuilders is they train really hard.
One of the things I have observed is the more into the weeds people tend to get,
and again, this is just my own anecdote and observation.
The more in the weeds they tend to get, the less hard I see them train.
So one of the things I really like that Mike Israetel said,
who’s got a PhD and is a bodybuilder himself.
He said you can’t out-science hard training,
that if you’re looking to build muscle
and you’re looking to improve your body composition,
that the main thing is just doing the work over time.
And I would add to that, and this is true of academic endeavors too, of course.
I think – I hope you’ll agree.
Which is that, yeah, you know, the other thing is given the mental side.
Earlier we were talking about how satiety signals in the brain
and what you think about foods can be relevant.
Learning to really enjoy training hard in addition to learning to really enjoy eating well,
not just for the effects that it has on body composition,
excuse me, those two, of course,
but just learning to really enjoy the process of training hard
and a really hard workout or a really hard paper that you have to sort through
or really digging through a book that’s challenging.
Learning to really enjoy that I think is a –
if there is a power tool out there, it’s the psychological end.
And I think a lot of that is getting the confidence of doing something hard
that there’s a payoff at the end.
A lot of people – I get asked a lot in my Q&As, how do I get more confident?
How do I become more confident?
I’ll tell people you have to do.
There’s no hack.
You can’t read about it.
You got to get in the arena.
And I don’t mean like compete in sports necessarily,
but like doing a PhD or doing something, just something hard
where you’re putting yourself out there and you’re saying this is my goal
and I’m going to go for it.
You just learn so much by doing that about yourself.
And so just what you said, I will reframe things in my mind
when bad things happen from – it’s not to say I never get stressed out
because I do and it’s not to say that I never get down because I do
because I’m a human.
But when something bad happens – I should post about this in my story today.
When something bad happens, I very rarely anymore do I go,
woe is me, why did this happen to me?
Because you’re in the universe, random bad things are going to happen.
So instead I say – if I’m not dead.
Instead I say, well, what an exciting opportunity to overcome an obstacle
and I bet because in the experience of my life, the biggest lessons
and the best things in my life have actually come out of the most challenging,
worst things that have happened.
And so again, this is – I would never have been able to do these sorts of things
if I hadn’t taken up weightlifting because weightlifting taught me so much
about perseverance, delayed gratification, overcoming obstacles.
And that’s why I love it even to this day.
And I’ll still get butterflies when I go in for a squat session
even though I’ve been doing it for 23 years.
Well, it’s clear that you embrace hard things.
And for people listening to this, obviously it doesn’t have to be weightlifting,
picking hard things, learning an instrument, learning a language.
Challenge is an absolute builder.
And they’ve actually shown like those sorts of things,
like when you challenge yourself and also mentally that –
I think there was a new study that came out basically showing a reduction
in the risk of Alzheimer’s and other age-related cognitive decline.
I mean basically like use it or lose it, right?
Yeah, the will – the desire and the will to persevere no doubt
translates to this thing that we call the will to live, right?
It’s related to the will to live.
Well, I think that what you just said beautifully embodies
what most people are aspiring to, which is to –
I think most people actually want to do hard things.
They don’t just want to have the results.
I think that most people deep down have some understanding
that their reward system works that way.
I must say this conversation for me has been tremendously rewarding.
First of all, it allowed me to meet you in person for the first time,
which I’ve really enjoyed.
Again, this won’t be our last interaction on this podcast and elsewhere.
Also, the amount of knowledge that you contain inside you is astonishing.
There’s a lot of stuff rattling around out there.
We all benefit because your ability to pull from the mechanistic side,
again, I think not limited to but relate to your background in biochemistry
all the way through to the impact in humans, animal studies,
being able to understand where those sit relative to one another.
Then you’re obviously a practitioner.
You practice what you preach.
What you talk about pertains to men, to women, younger people, older people,
people who are vegan, keto, carnivore.
You really are able to net a tremendous number of ideas
while staying really nuanced and data-driven.
So I just want to say for myself and on behalf of the listeners,
really appreciate you coming in here today and sharing with us your knowledge.
We will absolutely point people in the direction
of where they can learn more about you.
One of the places that I definitely want to mention before we part, however,
is this Carbon app.
I should just mention this isn’t a paid promotion or anything of that sort.
Actually, one of our podcast team members has been using Carbon for a long time.
This is an app that you devised which allows people to navigate
the exercise, nutrition, energy balance space for weight loss,
muscle gain, fat loss, weight maintenance.
I would just like to briefly ask you about that before we conclude.
Without necessarily telling us everything that’s in the Carbon app,
I’d love to know what are the major things that it does and is good for,
and then what were some of the key things that you wanted to make sure
were in there when you built it?
What’s the sort of logical backbone behind it?
Because I think there are a lot of food counting, calorie counting,
exercise apps out there.
Everyone I’ve talked to that uses Carbon,
including our mutual friend Cigar and Getty,
this member of my podcast, etc., raves about it.
What is Carbon and what does it do,
and what was your mindset in building it?
What did you really want to see there that you didn’t see elsewhere?
Those listening may not know, but I started online coaching people
for nutrition back in 2005.
That was the vast majority of my business all the way up until 2017.
I had a lot of success with that,
whether it be just average folks looking to lose weight or build muscle,
and right up to elite-level competitors in physique sport.
I kind of had this idea.
I don’t want to say I had the idea.
A few people had the idea.
I wanted to take what I do in coaching
and try to automate as much of that as possible.
By the time I was becoming a really popular coach, I was expensive.
You were looking at me charging.
I got to the point where I was charging about $1,000 a month for coaching.
Most people cannot afford that.
I would like to not just coach rich people.
You know what I mean?
I would like to be able to help other people.
The idea was to create an app that could do some of this stuff.
Now, there’s always a place for human interaction,
but for people who can’t afford that, our app is basically $10 a month.
Basically, what we wanted to do was set up an app
where think about if you went to a nutrition coach.
What would they do?
They would probably ask you some questions about your goals,
take some anthropometrics,
and then they would use that information, maybe dietary preference.
They’d use that information to formulate a baseline plan.
That’s what Carbon does.
We ask you, I think there’s eight questions in the sign-up flow,
about your activity, your exercise, your lifestyle,
your body weight, your body fat percentage.
If you don’t know it, we help you calculate it.
It’s not perfect, but it’s better than nothing.
Then your dietary preferences.
We use that to come up with your baseline.
Your baseline will be your calories, your protein, your carbohydrates, and fats.
What’s different about our app,
because apps like MyFitnessPal or whatever will do that as well,
what’s different about ours is we encourage people to log their weight daily
for the reasons that we talked about earlier.
Then you can also track your food in the app.
Honestly, I think our food tracker is actually way easier to use
than most of them out there.
What we typically get great, rave reviews about
is how user-friendly our interface is, that it makes intuitive sense.
So you track your food, try to hit these macros that you’re prescribed,
and each week you will be prompted to check in with the coach
on your check-in day.
Then you put in some information, and then based on how you’re progressing,
the app will adjust or not adjust based on how you’re progressing.
For example, if you’re hitting a weight loss plateau,
it will sense that, and it will reduce your calories.
Or if you’re trying to gain weight and you hit a plateau,
it will increase your calories.
There’s a lot of back-end algorithm stuff that takes care of this,
but the fundamental crux of the app is we try to determine
your total daily energy expenditure,
because that’s going to tell us the first big thing we need to know,
which is how many calories do you need to be eating for your goal, right?
So on the front end, we basically do our best guess
based on your anthropometrics.
Not going to be perfect, but it will get us in the ballpark.
And if you do know, like some people already know,
well, I know what I maintain my body weight on,
there’s actually a spot where you can manually enter that
during the sign-up flow.
So that’s helpful for people who are super nerds like me.
But then if you’re just, people will ask,
well, do you take Apple Watch data?
Do you take this? Do you take that?
And no, for the reasons we talked about,
that it overestimates energy expenditure.
What our app does is it’s an algebra equation.
If you, because your body weight, your maintenance calories
is your total daily energy expenditure.
Your average calories that you eat to maintain your body weight
will be the same as your total daily energy expenditure.
So if we know how body weight is changing
and we know how many calories the person’s consuming,
we can actually solve for what energy expenditure is, right?
And you can see in the app that we’ll,
there’s a kind of a maintenance calorie tracker
or energy expenditure tracker.
And typically after about three to four weeks,
even if the app was off at first,
it will have you pretty darn close.
Because, like let’s say somebody comes on
and their goal is to lose, you know,
a pound and a half a week or something like that.
And the first week they lose three pounds.
Now the app actually accounts for the fact
that you can lose more water weight the first week,
so they probably wouldn’t get an adjustment.
But let’s say the next week they lose three pounds.
The app will sense that and adjust their calories up
because it will be estimating that their energy expenditures
are actually higher than what it had previously estimated
based on the amount of weight they’re losing.
And the same thing goes in reverse.
If they’re not losing the amount of weight
that they’re supposed to, it will lower them
based on the fact that it may have overestimated
their energy expenditure.
But that’s the first crux of it,
is tracking that energy expenditure.
And then the next thing is protein.
So when the backend algorithm stuff is happening,
calories are set first based on your energy expenditure
and your goal.
So for example, if you’re on an aggressive diet,
your calories are going to be lower
even if your energy expenditure might be a little bit high.
Just because if you’re trying to lose two pounds a week,
I mean, you’re going to be in a pretty aggressive calorie deficit.
So it’s going to set the calories first.
Then it will set protein based on your lean body mass.
Then the calories that are left over
will be allotted to carbohydrate and fat
depending on your dietary preference.
And we have a few different dietary preferences.
You have balanced, which is about 50-50 to 60-40
carbohydrate to fat of the remaining calories.
Then you have low fat,
which is obviously a higher ratio of carbohydrate.
You have low carb.
You have a ketogenic diet, which is very, very low carb.
And then there’s also a plant-based option.
And within each of those options,
still you can go in and actually shimmy the macros
a little bit within a certain range
to kind of dial in what your specific dietary preference is.
Because again, if we go back to
what is going to produce the best long-term results,
it’s whatever the person can adhere to.
So we really try to start with the concept of adherence
by allowing people to have the dietary preference that they want.
And there’s some other apps out there that are good apps.
Like, for example, we get asked a lot,
what’s the difference between our app and the Renaissance Periodization app?
And they have a great app.
But theirs is kind of more rigid, and it’ll say,
you’re going to eat this many meals,
and you’re going to have these foods at these times.
So we’re kind of the opposite.
We want to give you maximum flexibility.
Now, for some people, they would prefer the rigid structure at first.
But we find that for most people,
giving them more flexibility
typically improves adherence over the long run.
So that’s kind of how the app works.
And again, there’s multiple different goals.
It’s not just a weight loss app.
There’s a maintenance.
There’s a muscle building.
So you’ve got all kinds of different goals that can be accommodated,
different rates of each of those goals.
And, I mean, I’ve used the app for over three years now to do my body weight.
And, I mean, like when I say that it’s dialed me in
because I’m very regimented with logging and logging my weight.
So what I targeted to weigh in at Worlds,
I got down to the 0.1 kilogram.
So it’s pretty cool to be able to use a tool that I helped develop
to actually coach me.
So it’s a great tool.
We did some statistics.
We polled 2,500 members.
And one of the questions we asked is,
would you recommend this to a friend?
And 91% said yes.
So I think our average retention is like seven months,
which for an app that costs $10 a month is really great.
Yeah, as I mentioned, a number of people I know use it.
This is not a paid promotion.
But I think people need guidance and tools.
And what we know about the human brain is that winging it can work,
but that the brain will cheat itself often.
There’s a Feynman quote about this, and I’ll get it wrong.
And always bad to try and quote Feynman anyway because he said it so much better.
But that we are the easiest.
It’s easy to fool ourselves, basically, is what he was saying.
Easiest to fool ourselves.
We will put a link to it so that people can check it out.
Again, it sounds like a wonderful tool.
And a tool that nets a lot of the principles that sit as major themes for weight loss,
weight gain, I would assume directed lean muscle, lean tissue gain is what most people are after,
and weight maintenance because a number of people would like to just maintain.
Listen, I really appreciate your time and all that you’re doing.
Certainly your time and energy and knowledge today,
but also what you’re doing on the various social media channels.
And just the fact that somebody from the depths of academia is out there sharing so much knowledge across so many domains.
You’re a gem in this landscape of nutrition and one that people really need to hear from.
So thank you so much for your time.
I appreciate the opportunity.
I really enjoyed it.
We’ll do it again.
Thank you for joining me today for my discussion with Dr. Lane Norton.
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