Huberman Lab - Using Salt to Optimize Mental and Physical Performance

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, we are going to discuss salt,

also referred to as sodium.

Now, most of us think of salt

as something that we put on and in our food,

maybe something to avoid.

Maybe some of you are actually trying to get more salt.

Some of you are trying to get less salt.

We all seem to associate salt

with things like blood pressure, et cetera.

Today, we’re going to go down a different set of avenues

related to salt.

We will certainly cover how salt regulates blood pressure.

We are also going to talk about

how the brain regulates our appetite for salt

or our aversion for salt.

We are also going to talk about

how our sensing of salty tastes

actually mediates how much sugar we crave

and whether or not we ingest more or less sugar

than we actually need.

So what you’re going to learn today

is that the so-called salt system,

meaning the cells and connections in our brain and body

that mediate salt craving and avoidance

are regulating many, many aspects of our health

and our ability to perform in various contexts,

things like athletic performance,

things like cognitive performance.

We’re also going to talk about aging and dementia

and avoiding aging and dementia

and what role salt and salt avoidance might play in that.

We’re going to touch on some themes

that for some of you might seem controversial

and indeed, if they are controversial,

I’ll be sure to highlight them as such.

I’m going to cover a lot of new data

that point to the possibility,

I want to emphasize the possibility that for some people,

more salt might help them in terms of health,

cognitive and bodily functioning.

And for other people, less salt is going to be better.

I’m going to talk about what the various parameters are.

I’m going to give you some guidelines

that in concert with your physician,

who you should absolutely talk to

before adding or changing anything

to your diet or supplementation regime,

can help you arrive at a salt intake

that’s going to optimize your mental,

physical health and performance.

So we’re going to cover neurobiology,

we’re going to cover hormone biology,

we’re going to talk about liver function,

we’re going to talk about kidney function

and of course, brain function.

I’m excited to share this information with you today.

I’m certain you’re going to come away with it

a lot of information and actionable items.

Before we dive into the topic of today’s episode,

I want to highlight a really exciting new study.

This is a study from Diego Bohorta’s lab

at Duke University.

The Bohorta’s lab studies interactions

between the gut and the brain

and has made some incredible discoveries

of the so-called neuropod cells.

Neuropod cells are neurons, nerve cells

that reside in our gut and that detect things

like fatty acids, amino acids

and some neuropod cells sense sugar.

Previous work from this laboratory

has shown that when we ingest sugar,

these neuropod cells respond to that sugar

and send electrical signals up a little wire

that we call an axon through the vagus nerve,

for those of you that want to know and into the brain

and through subsequent stations of neural processing

evoke the release of dopamine.

Dopamine is a molecule known to promote craving

and motivation and indeed action.

And what these neuropod cells that send sugar

are thought to do is to promote seeking

and consumption eating of more sugary foods.

Now, the incredible thing is that it’s all subconscious.

This is a taste system in the gut

that is not available to your conscious awareness.

Now, of course, when you ingest sweet foods,

you taste them on your mouth too.

And so part of the reason that you crave sweet foods

perhaps is because they taste good to you.

And the other reason is that these neuropod cells

are driving a chemical craving

below your conscious detection.

So they’re really two systems.

Your gut is sensing at a subconscious level what’s in it

and sending signals to your brain that work in concert

in parallel with the signals coming from your mouth

and your experience of the taste of the food.

Now, that alone is incredible.

And it’s been the subject of many important landmark papers

over the last decade or so.

You can imagine how the system would be very important

for things like hidden sugars

when nowadays in a lot of processed foods,

they’re putting hidden sugars.

They’re putting a lot of things that cause your gut

to send signals to your brain

that make you crave more of those foods.

So for those of you that really love sugar,

just understand it’s not just about how that sugar tastes.

The new study from the Borges Lab

deserves attention, I believe.

This is a paper published just recently,

February 25th, this year, 2022,

in Nature Neuroscience, an excellent journal.

And the title of the paper is

The Preference for Sugar over Sweetener

Depends on a Gut Sensor Cell.

The Borges Lab has now discovered a neuropod cell,

meaning a category of neurons,

that can distinguish between sweet things in the gut

that contain calories, for instance, sugar,

and things in the gut that are sweet

but do not contain calories,

artificial sweeteners like aspartame, sucralose,

and so forth.

There are also, of course,

non-artificial, non-caloric sweeteners

like stevia, monk fruit, et cetera.

They did not explore the full gallery

of artificial sweeteners.

What they did find, however,

ought to pertain to all forms

of sweet, non-caloric substances.

What they discovered was

that there is a signature pattern of signals

sent from the gut to the brain

when we ingest artificial or non-caloric sweeteners.

This is important because what it says

is that at a subconscious level,

the gut can distinguish between sweet things

that contain calories and sweet things that do not.

Now, what the downstream consequences

of this sensing is or what they are isn’t yet clear.

Now, I believe everyone should be aware

of these kinds of studies for a couple of reasons.

First of all, it’s important to understand

that what you crave,

meaning the foods you crave and the drinks you crave,

is in part due to your conscious experience

of the taste of those things,

but also due to biochemical and neural events

that start in the body and impinge on your brain

and cause you to seek out certain things

even though you might not know

why you’re seeking out more sugar.

You find that you’re craving a lot of sugar

or you’re craving a lot of foods with artificial sweeteners

and you don’t necessarily know why.

Now, artificial sweeteners themselves

are a somewhat controversial topic.

I want to highlight that.

Some months back, I described a study from Yale University

about how one can condition the insulin system.

Insulin is involved in mobilizing a blood sugar

and so forth in the body, as many of you know,

and I described some studies

that were done from Yale University School of Medicine

looking at how artificial sweeteners

can actually evoke an insulin response

under certain conditions.

Now, a couple of key things.

I got a little bit of pushback after covering those studies

and I encourage pushback all the time.

Pushback is one of those things

that forces all of us to drill deeper into a topic.

I want to be clear.

First of all, I am not one to demonize artificial sweeteners.

There is evidence in animal models, in animal models,

that artificial sweeteners can disrupt the gut microbiome,

but those were fairly high doses of artificial sweeteners

and it’s unclear if the same thing pertains to humans.

Still unclear, I should say.

Has not been investigated thoroughly.

Some people don’t like the taste of artificial sweeteners.

Some people do.

Some people find that they really help them

avoid excessive caloric intake.

Some people believe, and yet I should emphasize,

there still isn’t evidence

that they can adjust the insulin response in all people.

I just want to repeat that three times

so that people are clear on that fact.

What these new data emphasize, however,

is that we need to understand how artificial sweeteners

are consumed at the level of the gut,

or I should say registered at the level of the gut

and how that changes brain function.

Because one thing that I’m familiar with

and that many people report

is that when they first taste artificial sweeteners,

they taste sort of not right to them.

They don’t like the taste, but over time,

they actually start to crave that taste.

I’ve experienced this.

I used to drink a lot of diet sodas

when I was in graduate school.

So this would be aspartame.

And I found that I actually needed them.

Now, maybe it was the caffeine.

Maybe I just liked the sweet taste or the carbonation.

We actually have a drive for carbonation,

which is a topic of a future episode.

But when I finally quit them

for reasons that were independent

of any fear of artificial sweeteners,

I found that I didn’t like the taste.

Nowadays, I only occasionally drink a diet soda.

I usually do that if I’m on a plane

and there’s nothing else available to me.

So I don’t demonize them.

I might drink one every once in a while.

No big deal.

I also want to be clear.

I consume Stevia on a number of different supplements

and foods that I consume.

Stevia, of course,

is a plant-based non-caloric sweetener.

So I myself consume artificial sweeteners.

Many people hate them.

Many people like them and find them useful

for their nutrition and in fact,

to keep their caloric intake in a range

that’s right for them.

And many people like myself are curious about them

and somewhat wary of them

and yet continue to consume them in small amounts.

I think most people probably fall into that category.

I should also mention that many food manufacturers

put artificial sweeteners,

such as sucralose, et cetera, into foods.

And it’s always been unclear

as to why they might want to do that.

And yet we know that the sweet taste consumption,

even if it doesn’t contain calories,

can drive more craving of sweet food.

So there may be a logic or a strategy to why they do that.

Again, a topic for exploration on today’s podcast

and in future podcasts,

because where we’re headed today

is a discussion about how salt and salt sensing,

both consciously and unconsciously,

can adjust our craving for other things

like sugar and water and so on.

So I want to highlight this beautiful work

from the Borges Lab.

We’ll put a link to the study.

I want to open this as a chapter for further exploration.

I like to think that the listeners of this podcast

are looking for answers where we have answers,

but are also, I would hope,

excited about some of the new and emerging themes

in what we call nutritional neurobiology.

And indeed, the Borges Lab really stands

as one of the premier laboratories out there

that’s looking at how foods, as consumed in the gut,

are modifying our nervous system,

the foods we crave, and how we utilize those foods.

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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what your cognitive and physical demands are.

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Okay, let’s talk about salt.

Salt has many, many important functions

in the brain and body.

For instance, it regulates fluid balance,

how much fluid you desire and how much fluid you excrete.

It also regulates your desire for salt itself,

meaning your salt appetite.

You have a homeostatically driven salt appetite.

I’ll talk about the mechanisms today

and make them all very clear.

What that means is that you crave salty things,

beverages and foods, when your salt stores are low,

and you tend to avoid salty beverages and foods

when your salt stores are high,

although that’s not always the case.

There are circumstances where you will continue

to crave salt, even though you don’t need salt,

or indeed, even if you need to eliminate salt

from your system.

Salt also regulates your appetite for other nutrients,

things like sugar, things like carbohydrates.

And today we’ll explore all of that.

Technically, salt is a mineral.

And I should mention that when I say salt,

I am indeed referring to sodium in most cases,

although I will be clear to distinguish salt from sodium,

meaning table salt from sodium.

Most people don’t realize this,

but one gram of table salt

contains about 388 milligrams of sodium.

So technically, we should be talking about sodium today

and not salt.

I will use them interchangeably,

unless I’m referring to some specific recommendations

or ideas about trying to define your ideal salt,

aka sodium intake.

Okay, so this is important.

I think right off the bat,

a lot of people get themselves into a place of confusion

and potentially even to a place of trouble

by thinking that table salt in grams

always equates to sodium in grams,

and that’s simply not the case.

Today, we’re going to explore the neural mechanisms

by which we regulate our salt appetite

and the way that the brain and body interact

in the context of salt seeking, salt avoidance,

how to determine when we need more salt,

when we need less salt.

We’ll talk about kidney function.

We’ll get into all of it,

and we’re going to do it very systematically.

So let’s start in the brain.

We all harbor small sets of neurons.

We call these sets of neurons nuclei,

meaning little clusters of neurons

that sense the levels of salt in our brain and body.

There are a couple of brain regions that do this,

and these brain regions are very, very special,

special because they lack biological fences around them

that other brain areas have,

and those fences, or I should say that fence,

goes by a particular name,

and that name is the blood-brain barrier, or BBB.

Most substances that are circulating around in your body

do not have access to the brain,

in particular, large molecules

can’t just pass into the brain.

The brain is a privileged organ in this sense.

There are a couple other organs that are privileged

and that have very strict barriers,

very particular fences, if you will,

and those other organs include things

like the ovaries and testes,

and that makes sense for the following reason.

First of all, the brain, at least most of the brain,

cannot regenerate after injury.

You just simply can’t replace brain cells after injury.

I know people get really excited about neurogenesis,

the birth of new neurons,

and indeed, neurogenesis has been demonstrated

in animal models, and to some extent,

it exists in humans in a few places,

for instance, the olfactory bulb,

where neurons are responsible for detecting odorants

in the environment, for smell, that is,

and in a little subregion of the hippocampus,

a memory area, there’s probably some neurogenesis,

but the bulk of really good data out there

point to the fact that in humans,

there’s not much turnover of neurons.

What that means is that the neurons you’re born with

are the ones that you’re going to be using

most, if not all, of your life.

In fact, you’re born with many more neurons

than you’ll have later,

and there’s a process of naturally occurring cell death

called apoptosis that occurs during development,

so you actually are born with many more neurons

than you have later in life,

and that’s the reflection of a normal, healthy process

of nerve cell elimination.

The estimates vary, but anywhere from a third

to maybe even a half or even two thirds of neurons,

depending on the brain area,

are just going to die across development.

That might sound terrible,

but that’s actually one of the ways in which you go

from being kind of like a little potato bug

flopping around helplessly in your crib

to being an organism that can walk and talk

and articulate and calculate math

or do whatever it is that you do for a living.

The brain has a set of elements,

these nerve cells and other cells,

and it needs to use those for the entire lifespan,

so having a BBB, a blood-brain barrier,

around the brain is absolutely critical.

The ovaries and testes have a barrier

for, we assume, the reason that they contain

the genetic material by which we can pass on our genes

to our offspring, progeny, meaning make children,

and those children will have our genes

or at least half of them.

The other half from the partner, of course.

If the cells within the ovaries and testes are mutated,

well, then you can get mutations in offspring,

so that’s very costly in the evolutionary sense,

so it makes sense that you would have

a barrier from the blood,

so if you ingest what’s called a mutagen,

if you ingest something that can mutate the genes of cells,

you can imagine why there would be a premium

on not allowing those mutagens to get into the brain,

the ovaries, or the testes, okay?

So the brain has this BBB,

this blood-brain barrier around it,

which makes it very, very hard for substances

to pass into the brain unless those substances

are very small or those substances and molecules

are critically required for brain function.

However, there are a couple of regions in the brain

that have a fence around them, but that fence is weaker,

okay, it’s sort of like going from a really big wall,

thick, electronic, 24-hour surveillance fence

where nothing can pass through

except only the exclusive cargo that’s allowed to go through

to having a little cyclone fence

with a couple of holes in it,

or it’s kind of a picket fence that’s falling over,

and substances can move freely from the blood

circulating in the body into the brain,

and it turns out that the areas of the brain

that monitor salt balance and other features

of what’s happening in the body

at the level of what we call osmolarity,

at the concentration of salt reside

in these little sets of neurons

that sit just on the other side of these weak fences,

and the most important and famous of these

for the sake of today’s conversation is one called OVLT.

OVLT stands for the organum vasculosum

of the lateral terminalis.

It is what’s called a circumventricular organ.

Why circumventricular?

Well, not to bog you down with neuroanatomy,

but your brain is a big squishy mass

of neurons and other cell types,

but it has to be nourished,

and through the middle of that brain,

there is a tube, there’s a hollow that creates spaces,

and those spaces are called ventricles.

The ventricles are spaces

in which cerebral spinal fluid circulates,

and it nourishes the brain.

It does a number of other things as well.

The circumventricular organs are areas of the brain

that are near that circulating fluid,

and that circulating fluid has access to the bloodstream,

and the bloodstream has access to it,

and this structure that I’m referring to,

OVLT, organum vasculosum of the lateral terminalis,

has neurons that can sense the contents of the blood

and to some extent, the cerebral spinal fluid.

There are a couple other brain areas

that can do this as well.

They go also by the name of circumventricular organs,

and I’ll talk about the names of some of those other areas,

but for today, and I think for sake

of most of the discussion,

understand that the OVLT is special.

Why?

Because it doesn’t have this thick barrier fence,

which sounds like a bad thing,

and yet it’s a terrific border detector.

The neurons in that region are able to pay attention

to what’s passing through in the bloodstream

and can detect, for instance,

if the levels of sodium in the bloodstream are too low,

if the level of blood pressure in the body

is too low or too high,

and then the OVLT can send signals to other brain areas,

and then those other brain areas

can do things like release hormones

that can go and act on tissues

in what we call the periphery in the body,

and for instance, have the kidneys secrete more urine

to get rid of salt, that’s excessive salt in the body,

or have the kidneys hold on to urine

to hold on to whatever water or fluid that one might need.

So before I go any deeper into this pathway,

just understand that the OVLT has a very limited barrier.

It can detect things in the bloodstream,

and this incredible area of the brain

almost single-handedly sets off the cascades of things

that allow you to regulate your salt balance,

which turns out to be absolutely critical,

not just for your ability to think

and for your neurons to work, but indeed for all of life.

If the OVLT doesn’t function correctly,

you’re effectively dead or dead soon.

So this is a very important brain region.

So let’s talk about the function of the OVLT

and flesh out some of the other aspects of its circuitry,

of its communication with other brain areas

and with the body in the context of something

that we are all familiar with, which is thirst.

Have you ever wondered just why you get thirsty?

Well, it’s because neurons in your OVLT

are detecting changes in your bloodstream,

which detect global changes within your body.

And in response to that,

your OVLT sets off certain events within your brain and body

that make you either want to drink more fluid

or to stop drinking fluid.

There are two main kinds of thirst.

The first one is called osmotic thirst,

and the second is called hypovolemic thirst.

Osmotic thirst has to do with the concentration of salt

in your bloodstream.

So let’s say you ingest something very, very salty.

Let’s say you ingest a big bag of,

I confess I don’t eat these very often,

but I really like those kettle potato chips

and they’re pretty salty.

I’ve never actually measured how much sodium is in them.

I’m sure the information is there.

Every once in a while,

I’m particularly interested in doing so,

I’ll just down a bag of those things.

And I really like them and they’re very salty,

but they almost always make me feel thirsty.

And the reason is that by eating those,

I’ve ingested a lot of sodium.

Again, not a frequent occurrence for me,

but happens every now and again.

And I don’t have too much shame about that

because I think I have a pretty healthy relationship to food

and I enjoy them.

And I understand that it will drive salt levels

up in my bloodstream and that will cause me to be thirsty.

But why?

Why?

Because neurons in the OVLT come in two main varieties.

One variety senses the osmolarity of the blood

that’s getting across that weak little fence

that we talked about before.

And when the osmolarity,

meaning the salt concentration in the blood is high,

it activates these specific neurons in the OVLT.

And by activates,

I mean it causes them to send electrical potentials,

literally send electrical signals to other brain areas.

And those other brain areas inspire a number

of different downstream events.

So what are those other brain areas?

Well, the OVLT signals to an area

called the supraoptic nucleus.

The name and why it’s called the supraoptic nucleus

is not necessarily important.

It also signals to the so-called paraventricular nucleus,

another nucleus that sits near the ventricles

and can monitor the qualities,

the chemical qualities of the cerebral spinal fluid,

as well as probably the bloodstream as well.

And the consequence of that communication

is that a particular hormone is eventually released

from the posterior pituitary.

Now, the pituitary is a gland

that sits near the roof of your mouth.

It releases all sorts of things like growth hormone

and luteinizing hormone.

Luteinizing hormone will stimulate things like estrogen

and testosterone production

and release from the ovaries and testes and so on.

The pituitary has a bunch of different compartments

and functions, but what’s really cool about the pituitary

is that certain regions of the pituitary

actually contain the axons, the wires of neurons,

and the neurons reside in the brain.

And so the supraoptic nucleus gets a signal from the OVLT.

The signal is purely in the form of electrical activity.

Remember, neurons aren’t talking to one another

about what’s happening out there.

They’re not saying, hey, there’s too much salt

in the bloodstream.

Let’s do something about it.

All they receive are our so-called action potential,

waves of electricity.

The neurons in the supraoptic nucleus

then release their own electrical signals

within the pituitary.

And some of those neurons and nearby neurons

are capable of releasing hormones

as well as electrical signals.

So from the pituitary, there’s a hormonal signal

that’s released called vasopressin.

Vasopressin also goes by the name antidiuretic hormone.

And antidiuretic hormone has the capacity

to either restrict the amount of urine that we secrete

or when that system is turned off

to increase the amount of urine that we secrete.

So there’s a complicated set of cascades

that’s evoked by having high salt concentration

in the blood.

There’s also a complicated set of cascades

that are evoked by having low concentrations

of sodium in the blood.

But the pathway is nonetheless the same.

It’s OVLT is detecting those osmolarity changes,

communicating to the supraoptic nucleus.

Supraoptic nucleus is either causing the release of

or is releasing vasopressin, antidiuretic hormone,

or that system is shut off

so that the antidiuretic hormone is not secreted,

which would allow urine to flow more freely, right?

Antidiuretic means anti-release of urine.

And by shutting that off,

you are going to cause the release of urine.

You’re sort of allowing a system to flow, so to speak.

The second category of thirst is hypovolemic thirst.

Hypovolemic thirst occurs

when there’s a drop in blood pressure, okay?

So the OVLT, as I mentioned before,

can sense osmolarity based on the fact

that it has these neurons that can detect

how much salt is in the bloodstream.

But the OVLT also harbors neurons

that are of the baroreceptor mechanoreceptor category.

Now, more on baroreceptors and mechanoreceptors later,

but baroreceptors are essentially a receptor,

meaning a protein that’s in a cell

that responds to changes in blood pressure.

So there are a number of things

that can cause decreases in blood pressure.

Some of those include, for instance,

if you lose a lot of blood, right?

If you’re bleeding quite a lot,

or in some cases, if you vomit quite a lot,

or if you have extensive diarrhea

or any combination of those.

And there are other things that can reduce blood volume,

and we will talk about some of those later.

But in the classic case of hypovolemic thirst,

one is simply losing blood,

and therefore blood pressure goes down.

So very simple to imagine in your mind,

you have these pipes,

which are the arteries, veins, and capillaries.

And when you lose some blood volume,

the pressure in those arteries, veins,

and capillaries goes down.

OVLT has neurons that can sense

that reduction in blood pressure

because of the presence of baroreceptors in OVLT.

There are other elements that also play into the response

to what we call hypovolemic thirst.

For instance, the kidney will secrete

something called renin.

Renin will activate something called angiotensin II

from the lungs of all things, amazing.

And angiotensin II itself can act on OVLT,

organobasculosomal lateral terminalis,

which in turn will create thirst, okay?

So in both cases, right,

the osmolarity sensing system,

meaning osmotic thirst,

and in hypovolemic thirst, where blood pressure has dropped,

the end result is a desire to drink more.

And that desire to drink more

comes through a variety of pathways

that are both direct and indirect,

include vasopressin and don’t include vasopressin.

But I think for just sake of general example,

and even for those of you that don’t have

any biology background or physiology background,

just understand that there are two main types of thirst.

Both types of thirst,

osmotic thirst and hypovolemic thirst,

are not just about seeking water,

but they also are about seeking salt.

In very general terms, salt, aka sodium,

can help retain water.

Now that doesn’t mean that salt always retains water.

If you have excessive amounts of salt,

will you retain excessive amounts of water?

Well, sort of, as we’ll soon learn, it’s all contextual.

But for most cases,

we can say that by having salt in our system,

our brain and our body can function normally,

provided the levels of salt are adequate

and not too high or too low.

And thirst, while we often think of it

as just a way to bring fluid into our body,

is designed as a kind of a interoceptive perception.

What I mean by that,

interoception as many of you know now

from listening to this podcast,

is a paying of attention or a recognition rather,

a conscious recognition of the events

going on within our body.

So when we are thirsty,

it’s a certain form of interoception.

We go, oh, I need something, or I crave something.

You may not know exactly what you need,

but when you are thirsty, you’re not just seeking water,

you’re also seeking to balance your osmolarity,

which means you may be seeking salty fluids or foods.

In some cases, you’ll try and accomplish this by eating,

or it may be that you’re trying to avoid,

or you will be inspired to avoid salty fluids and foods.

But if you want to understand sodium

and its roles in the body, you have to understand thirst.

And if you want to understand thirst,

you have to understand how fluid balance

is regulated in the body.

That’s not surprising at all.

But sodium and water work together

in order to generate what we call thirst.

Sodium water work together in order to either retain water

or inspire us to let go of water to urinate.

So before we can dive into the specifics around salt

and how to use salt for performance

and various recommendations and things to avoid,

we need to drill a little bit deeper

into this fluid balance mechanism in the body.

And for that reason, we have to pay

at least a little bit of attention to the kidney.

The kidney is an incredible organ.

And one of the reasons the kidney is so amazing

is that it’s responsible for both retaining, holding onto,

or allowing the release of various substances from the body,

substances like glucose or amino acids, urea, uric acid,

salt, potassium, magnesium.

It’s basically a filter,

but it’s a very, very intelligent filter.

I mean, intelligent, meaning it doesn’t have its own mind,

but the way it works is really beautiful.

Basically, blood enters the kidney

and it goes through a series of tubes,

which are arranged into loops.

If you want to look more into this,

there’s the beautiful loop of Henle

and other aspects of the kidney design

that allow certain substances to be retained

and other substances to be released,

depending on how concentrated

those substances are in the blood.

The kidney responds to a number of hormonal signals,

including vasopressin, in order to, for instance,

antidiuretic hormone, in order to hold onto more fluid,

if that’s what your brain and body need.

And it responds to other hormonal signals as well.

So it’s a pretty complex organ.

Nonetheless, there’s a key point,

which I already mentioned,

that I think most people don’t realize.

This is actually something that I like to tell kids

when I meet them, provided that they’re of appropriate age.

I’ll say, oftentimes when kids learn that I’m a scientist,

they’ll ask a question about something related to science

and hopefully, for my sake,

it’s something about neuroscience.

But one thing that I’ll tell kids, I’ll say,

do you know that your urine, your pee,

is actually filtered blood?

And occasionally, that will really terrify a kid,

but that also occasionally really terrifies an adult.

But indeed, your urine is filtered blood.

Basically, blood gets into the kidney.

The kidney is going to filter out certain things.

Certain things are going to be allowed to pass through

and others are not, okay?

So the way the kidney is designed

is that about 90% of the stuff that’s absorbed

from the blood is going to be absorbed early

in this series of tubes.

And only a small percentage is going to be regulated

or worked out as you get into

what’s called the distal kidney.

I mean, distal just means the furthest part away, okay?

The proximal is up close.

So like your shoulder is proximal

to your midline of your body and your hand is distal.

So in biological terms, you hear about proximal distal,

which just means near or far from.

So just to give a really simple example,

let’s say that you are very low on fluid.

You haven’t had much to drink in a while.

Maybe you’re walking around on a hot day.

Chances are that the neurons in your OVLT

will sense the increase in osmolarity, right?

The concentration of salt is going to be increased

relative to the fluid volume that’s circulating.

This of course assumes that you haven’t excreted

a lot of sodium for one reason or another,

but that increase in osmolarity is detected by the OVLT.

The OVLT is going to signal a bunch of different cascades

through the supraoptic nucleus, et cetera.

And then vasopressin is going to be released

into the bloodstream and vasopressin,

again, also called antidiuretic hormone,

is going to act on the kidney

and change the kidney’s function

in a couple of different ways,

some mechanical, some chemical, okay?

In order to make sure that your kidney

does not release much water,

doesn’t make you want to urinate.

And in fact, even if you would try to urinate,

your body’s going to tend to hold on to its fluid stores.

Okay, so very simple, straightforward example.

We can also give the other example

whereby if you are ingesting a lot, a lot, a lot of water,

and it’s not a particularly hot day

and you’re not sweating very much,

let’s assume your salt intake is constant

or is low for whatever reason.

Well, then the osmolarity,

the salt concentration in your blood is going to be lower.

Your OVLT will detect that

because of these osmosensing neurons in your OVLT.

Your OVLT will fail to signal to the supraoptic nucleus

and there will not be the release

of vasopressin antidiuretic hormone

and you can excrete all the water

that your body wants to excrete,

meaning you’ll be able to urinate.

There’s no holding on to water at the level of the kidney.

Okay, very simple examples,

but hopefully it illustrates how events within the blood,

meaning the concentration of salt

relative to the amount of fluid, right?

That’s what osmolarity is, is detected by the OVLT.

The brain then communicates to the pituitary.

The pituitary sends a hormone out into the blood

and the hormone acts on the kidney

to either hold onto or let go of fluid,

meaning to prevent you from wanting to urinate

or from stimulating you to want to urinate.

Very, very simple kind of yes, no type situation here.

There’s a lot of nuance to this in reality.

There are a lot of other hormones in this pathway,

but I think for at least this stage of the discussion,

this should be sufficient.

Some of you may have noticed

that a molecule we’ve been talking a lot about today,

vasopressin, was also mentioned on a previous episode

of the Huberman Lab Podcast,

but in a very different context.

Molecule I’m referring to is vasopressin

and as I mentioned, it’s a hormone involved in antidiuresis,

meaning preventing urination.

It’s an antidiuretic,

but we also talked about vasopressin

in the context of desire, love, and attachment.

We talked about it in the context of monogamy

and non-monogamy in a species of animal

called the prairie vole.

You can check out that episode.

I believe vasopressin and the non-monogamous prairie voles

are mentioned in the timestamp, so it should be easy to find.

Vasopressin is made at multiple locations

in the nervous system, mainly the superoptic nucleus,

and indeed, it’s also involved in aspects

of sexual behavior and mating.

Now, it does that through mechanisms

that are distinct from its antidiuretic effects.

In fact, there are people who take vasopressin

as an aphrodisiac.

Now, I’m certainly not suggesting people do that,

but I have all the confidence in the world

that the moment I talk about vasopressin,

someone in the comments is going to say,

what do you think about vasopressin nasal sprays

and this kind of thing?

Vasopressin and indeed oxytocin,

another hormone that’s involved in pair bonding

and various aspects of brain and body function,

are available as nasal sprays that can get up

into the deep recesses of the brain

and can impact some of these core,

what we call hypothalamic functions,

these primitive drives and hypothalamic functions.

I would encourage a lot of caution,

maybe even extreme caution in recreational use

of things like vasopressin and oxytocin,

unless you are working with an MD and they prescribe it

or they really know what they’re doing.

These are powerful hormones

that have a lot of different effects on the brain and body.

The way that vasopressin, meaning antidiuretic hormone,

prevents the release of fluid as urine from the body

is pretty interesting.

It acts directly on the kidney.

So as I mentioned before, blood flows into the kidney.

A number of things are retained

in the early part of the kidney.

Vasopressin acts at a fairly distal,

meaning kind of end game,

part of the loops of tubes through the kidney,

and it increases the permeability of those tubes.

In other words, it makes sure that the fluid

that would otherwise pass into a collecting duct

and then go out to the bladder,

never actually makes it to the bladder.

I point this out because what antidiuretic hormone does

is it prevents the bladder from filling at all.

It’s not as if it locks fluid in the bladder

and prevents you from urinating.

I think the way I’ve been describing things up until now

and the way you’ll hear about antidiuretic hormone,

it might sound like it kind of locks up the bladder

or prevents you from being able to urinate,

but you have a full bladder.

That would be very uncomfortable.

That’s not the way it works.

It actually causes the tubes headed towards the bladder

from the kidney to become permeable,

meaning to allow fluid to go back into the bloodstream

into the rest of the body

so that fluid never actually fills the bladder

and so you never feel the urge to urinate.

Now, this is an episode about salt.

A key thing to understand about the kidney

is that the kidney uses sodium in order to conserve water,

which has everything to do with the fact

that sodium can actually hold water.

Put differently, water tends to follow sodium.

So where we have sodium, we tend to have water

and sodium, when it’s concentrated, can hold onto water.

And that’s one of the main ways

that the kidney holds onto water in the body.

And as we’ll soon learn,

there is no simple and direct formula to say,

for instance, okay, if salt levels are high,

a lot of water is retained.

And if salt levels are low, a lot of water is released.

On the one hand, that can be true,

but it’s also the case

because these systems are homeostatic,

meaning they’re always seeking balance,

both within system, within the salt system,

and between systems, the salt and water system.

It’s also the case often that if we have enough sodium,

well, then we can secrete sodium and some water will follow.

Or if we don’t have enough sodium, then yes, indeed,

because we’re not holding onto water,

more fluid can be excreted.

But if that condition of low sodium lasts long enough,

then we start to retain water

because the body recognizes, ah, salt is low

and water is being excreted

and eventually a system will kick in to retain water.

So I’d love to give you a simple black and white,

yes or no answer for low sodium, high sodium,

moderate sodium, and water balance,

but it’s all contextual.

And when I say contextual,

I mean it will depend on blood pressure,

hypertension, pre-hypertension, if that’s there,

maybe normal tension, hormone levels,

exercise, et cetera, et cetera.

A pretty good example of how complicated this can all be

is one that some of you may be familiar with.

It’s pretty well known that during certain phases

of the menstrual cycle,

when estrogen and progesterone

and other hormones are fluctuating,

that water can be retained in the body.

There’s, it’s what’s called edema or a swelling sometimes.

So the common assumption, and indeed it can be true,

that when estrogen levels are high,

there’s water retention in the body.

Also in males, if estrogen levels are high,

there can be water retention in the body.

This is one of the reasons why athletes

and in particular bodybuilders who take anabolic steroids

like testosterone, which can be converted into estrogens,

sometimes they’ll look, they’ll walk around,

they look like they were partially inflated.

They look like they’re going to pop

and it looks like a swelling of the skin,

not just because they have large muscles.

And that’s not always, but often water retention

due to testosterone conversion into estrogen.

Now that all sounds consistent, right?

Estrogen levels fluctuate in the menstrual cycle.

In males where there’s an increase in estrogen,

there’s retention of water.

But actually estrogen acts as a diuretic.

So one would think, okay, when estrogen levels go up,

there should be a lot of fluid excreted.

But I bring up this example to point out

that it’s a very complicated and dynamic balance

between hormones and salt and fluid.

You can’t draw a one-to-one relationship there.

And that turns out to be a very important point.

And we can use that not as a way

to further complicate things,

but as a way to understand under which contexts

less sodium intake or more sodium intake can be beneficial.

So that’s where I’d like to turn our attention now.

So how much salt do we need?

And what can we trust in terms of trying to guide

our ingestion of salt?

First of all, I want to be very, very clear

that there are a number of people out there

that have prehypertension or hypertension.

You need to know if you have prehypertension

or hypertension.

You need to know if you have normal tension,

meaning normal blood pressure.

Everyone should know their blood pressure

is an absolutely crucial measurement

that has a lot of impact on your immediate

and long-term health outcomes.

It informs a lot about what you should do.

Should you be doing more cardiovascular exercise?

Should you be ingesting more or less salt?

Should you be adjusting any number

of different lifestyle factors?

So you need to know that.

And without knowing what your blood pressure is,

I can’t give a one-size-fits-all recommendation.

And indeed, I’m not going to give medical recommendations.

I’m simply going to spell out what I know about the research

which hopefully will point you in the direction

of figuring out what’s right for you

in terms of salt and indeed fluid intake.

There is a school of thought

that everybody is consuming too much salt.

And I do want to highlight the fact

that there are dozens, if not hundreds,

of quality papers that point to the fact

that a quote-unquote high-salt diet can be bad

for various organs and tissues in the body,

including the brain.

It just so happens that because fluid balance,

both inside and outside of cells, is crucial,

not just for your heart and for your lungs

and for your liver and for all the organs of your body,

but also for your brain,

that if the salt concentration inside of cells

in your brain becomes too high, neurons suffer, right?

They will draw fluid into those cells

because water tends to follow salt,

as I mentioned before, and those cells can swell.

You can literally get swelling of brain tissue.

Conversely, if salt levels are too low inside of cells

in any tissue of the body, but in the brain included,

then the cells of the body and brain can shrink

because water is pulled into the extracellular space

away from cells.

And indeed, under those conditions,

brain function can suffer,

and indeed, the overall health of the brain can suffer.

So there are many reports out there

indicating, both in experimental models

and to some extent in humans,

that overconsumption of salt is bad

for brain function and longevity,

and yet there is also decent evidence

in both animal models and humans

that if salt consumption is too low,

then brain health and longevity will suffer,

as will other organs and tissues of the body.

So like most things in biology,

you don’t want things too high or too low.

Now, I would say that the vast majority

of studies out there point to the fact

that a high salt diet is detrimental

to brain health and function.

Most of the studies have focused on that aspect

of salt balance and its consequences on brain function.

One critical issue with many of those studies, however,

is that the high salt diet is often coupled

to other elements of diet that are also unhealthy,

things like excessively high levels of carbohydrates

or fats or combinations of carbohydrates and fats.

And so while I know there are many burning questions

out there about how much salt one needs

if they are on a low carbohydrate diet,

or if they are fasting, or if they are on a vegan diet,

there have simply not been many studies

that have explored the low, moderate,

and high salt conditions

on a backdrop of very controlled nutrition.

And that’s probably reflective of the fact

that there are not a lot

of very well-controlled nutrition studies out there.

There are some, of course,

but it’s very hard to get people to adhere

to nutritional plans in a very strict way

and to do that for sufficient periods of time

that would allow the various health outcomes to occur.

Nonetheless, there’s some interesting reports

that indicate that the amount of salt intake

can indeed predict health outcomes

or what we call hazardous events,

things like cardiovascular events and stroke and so forth.

And what’s interesting is that indeed a lower,

I’m not saying low, right?

Because I don’t believe that you want your diet

to be truly low in anything except perhaps poison,

but a lower salt diet can reduce the number

of these so-called hazardous events,

but it’s a somewhat of a shallow U-shaped function

such that yes, indeed,

a high salt intake can be very detrimental for your health,

both in terms of cardiovascular events,

stroke, and other deleterious health events,

but somewhere in the middle

that actually sits quite to the right,

meaning higher than what is typically recommended

for salt intake,

can actually reduce the number of these hazardous events.

At least some reports point to that.

And so I want to emphasize

what one of those particular reports says,

and I also want to be sure to counter it

from the perspective of the context

that that study was set in,

because again, my goal here is not to give you

a strict set of recommendations at all,

it’s to point you to the literature,

try and make that literature as clear as possible

and allow you to evaluate for yourself.

And I don’t just say that to protect us,

I say that to protect you,

because indeed you are responsible

for your health and your health choices.

So the paper that I’m referring to

is a very interesting one.

We of course never want to put too much weight

on any one report,

but this is a paper that was published in 2011

in the Journal of the American Medical Association.

The title of the paper is

Urinary Sodium and Potassium Excretion

and a Risk of Cardiovascular Events.

We have not talked much about potassium yet,

but sodium and potassium tend to work in concert

in the brain and body

in order to regulate various physiological functions

and health.

And we’ll talk more about potassium as time goes on.

The key plot or set of data in this study,

for those of you that want to look it up,

we will link to it.

And there are a lot of data in here,

but is figure one,

which is basically evaluating the amount

of urinary excretion of sodium,

which is a somewhat indirect,

but nonetheless valuable measure

of how much sodium people were ingesting.

And plotted against that

is what they call the hazard ratio.

And the hazard ratio points to the composite

of cardiovascular death, stroke, myocardial infarction,

and an infarct is an injury,

and hospitalization for congestive heart failure.

And what it points to is the fact that the hazard ratio

is low-ish at sodium excretion of about two grams per day,

but then continues to go down

until about 4.5 to five grams per day.

Remember this is sodium excretion.

So it’s reflective of how much sodium was in the body,

which is reflective of how much sodium was ingested.

And then the hazard ratio increases fairly dramatically,

a very steep slope,

heading anywhere from seven to eight to 10

and out towards 12 grams of sodium excretion per day.

So the simplest way to interpret these data

are that at fairly low levels of sodium,

meaning at about two grams per day,

you run fewer health risks,

but the number of risk continues to decline

as you move towards four and five grams per day.

And then as you increase your salt intake further,

then the risk dramatically increases.

So no study is holy, nor is any figure in any study

or any collection of studies holy.

Rather, we always want to look at what the bulk of data

in a particular field reveal.

Nonetheless, I think that the plot that we described,

meaning the graph that we described is pretty interesting

in light of the 2020 to 2025 dietary recommendations

for Americans, which is that people consume

no more than 2.3 grams,

meaning 2,300 milligrams of sodium per day.

That’s about a half a teaspoon of salt per day.

Now, most people are probably consuming more than that

because of the fact that they are ingesting processed foods

and processed foods tend to have more salt in them

than non-processed foods.

Now, of course, that’s not always the case, right?

Sea salt is not a processed food in most cases.

And there are a lot of unprocessed foods

that can be high in sodium,

but processed foods in particular

tend to have a lot of sodium.

You can see this simply by looking at the packaging

of any number of different foods.

But if we were to take this number of 2.3 grams,

that’s the recommended cutoff for ingestion of sodium,

it actually falls in a portion of the curve

that we were talking about a moment ago

that indeed is associated with low incidence

of hazardous outcomes, cardiovascular events, stroke,

et cetera.

But according to that plot,

the ingestion of four or five grams of sodium,

almost double or more sodium than is currently recommended

is associated with even lower numbers of hazardous events.

So we need to think about this

and we need to explore it in the context

of other studies, of course.

And we need to evaluate it in terms of this thing

that we’ve been going back to again and again,

which is context, right?

These recommendations of 2.3 gram per day cutoff

is in the context of a landscape

where some people do indeed have hypertension

or prehypertension.

The incidence of hypertension has gone up dramatically

in the last hundred years

and seems to continue to go up.

Whether or not that’s because of increased salt intake

or whether or not it’s because of increased salt intake

and other things such as highly processed foods,

that isn’t clear.

Again, pointing to the challenge

in doing these epidemiological studies

and really parsing what aspects of a change

in some health metric is due to, for instance,

the ingestion of more sugars versus more salts

or simply because of the ingestion of more salts.

It’s a complicated, almost barbed wire topic by now,

but we can start to pull apart that barbed wire tangle

and start to evaluate some of the other people

in other conditions that exist out there, maybe for you,

that actually warrant more sodium intake

and where more sodium intake might actually be beneficial.

So again, I want to be very, very clear

that you need to know your blood pressure.

If you have high blood pressure or you’re prehypertensive,

you should be especially cautious

about doing anything that increases your blood pressure.

And as always, you want to, of course,

talk to your doctor about doing anything

that could adjust your health in any direction.

But nonetheless, there are some important papers

that have been published in recent years.

I want to point to one of them in particular.

This is a paper that was published

in the journal Autonomic Neuroscience, Basic and Clinical,

because this paper, like several other papers,

ask the question, and indeed they ask the question

in the title, it’s a review,

dietary sodium and health,

how much is too much for those with orthostatic disorders?

Now, orthostatic disorders

come in a bunch of different varieties,

and we’re going to talk about those in a moment,

but there are a number of people out there

that have low blood pressure, right?

People that get dizzy when they stand up,

people that are feeling chronically fatigued,

and in some cases, not all,

those groups can actually benefit

from increasing their sodium intake.

Several episodes ago on the Huberman Lab podcast,

I gave a, what, it’s just clearly what we call anecdata,

which is not even really data, it’s just anecdotal data

of an individual who was always feeling hungry

and craving sugar, and based on the fact

that they also had low blood pressure,

I had them talk to a physician,

and they got permission to try

a little mini experiment on themselves,

and so they did, and that mini experiment was

anytime they felt like they were craving sugar

or they were feeling a little lightheaded and dizzy,

rather than reaching for something with caloric intake,

they took a little bit of sea salt,

a little pinch of sea salt,

and put it into some water and drank it,

or in the case of this individual,

they would actually take a little sea salt packet,

and they would actually just down a sea salt packet,

and for them, that provided tremendous relief

for their dizziness, but that, of course,

was in the context of somewhat abnormally low blood pressure,

so I don’t think that they are alone in the fact

that many people out there suffer

from a low blood pressure condition.

Many people out there suffer

from a high blood pressure condition,

so know your blood pressure and understand

that blood pressure in part is regulated

by your sodium intake and your sodium balance.

Why?

Well, because of the osmolarity of blood

that we talked about before,

where if you have a certain concentration of sodium,

meaning sufficient sodium in your bloodstream,

that will tend to draw water into the bloodstream,

and essentially, the pipes that are your capillaries,

arteries, and veins will be full.

The blood pressure will get up to your head,

whereas some people, their blood pressure is low

because the osmolarity of their blood is low,

and that can have a number of downstream consequences.

I should also mention it can be the consequence itself

of challenges or even deficits in kidney function,

but all of these organs are working together,

so the encouragement here is not necessarily

to ingest more sodium.

It’s to know your blood pressure

and to address whether or not an increase in sodium intake

would actually benefit your blood pressure

in a way that could relieve some of the dizziness

and other symptoms of things like orthostatic disorders,

but of course, to do that in a safe context

and to never play games with your blood sugar

or your blood osmolarity that could set your system

down a cascade of negative events.

Let’s look at what the current recommendations are

for people that suffer from orthostatic disorders,

like orthostatic hypo, meaning too low tension,

orthostatic hypotension,

postural tachycardia syndrome,

sometimes referred to as POTS, P-O-T-S,

or idiopathic orthostatic tachycardia and syncope.

These have the incredibly elaborate names.

Those groups are often told to increase their salt intake

in order to combat their symptoms.

The American Society of Hypertension

recommends anywhere from 6,000 to 10,000.

These are very high levels.

So this is six grams to 10 grams of salt per day,

keeping in mind, again, that salt is not the same as sodium

so that equates to about 2,400 to 4,000 milligrams

of sodium per day.

Again, if you want to learn more about this

and get more of the citations,

I’ll refer you back to this study

on dietary sodium and health,

how much is too much for those with orthostatic disorders.

We will put a link to this in the caption show notes.

So that’s not just in the US.

The salt recommendations

from the Canadian Cardiovascular Society

are 10,000 milligrams of salt per day.

So four grams of sodium is what that equates to

and on and on and on for things like POTS,

for these postural syndromes that result from,

or I should say from these syndromes

that involve low blood pressure when people stand up

or in certain postures.

So I point out this paper

and I point out these higher salt recommendations

to emphasize again, that context is vital, right?

That people with high blood pressure

are going to need certain amounts of salt intake.

People with lower blood pressure

and maybe with some of these postural orthostatic syndromes

are going to need higher amounts of salt.

And for most people out there,

you’re going to need to evaluate how much salt intake

is going to allow your brain and body to function optimally.

And there are some fairly straightforward ways

to explore that.

And there’s some ways to explore that

in the context of what you already know

about thirst and salt appetite

that can make that exploration

one in which it’s not going to be a constant

wandering around in the dark

and where you can figure out what’s right for you.

For most people, a moderate increase in salt intake

is not going to be detrimental

provided that you consume enough fluids,

in particular water, okay?

Meaning if you happen to overeat salt a bit,

you will get thirsty, you will ingest more water

and you will excrete the excess sodium.

There is evidence that the body can store sodium

in various organs.

That storage of sodium may or may not be

a detrimental thing.

In general, excess storage of sodium

in tissues and organs of the brain and body

is not thought to be good for long-term health.

So eating much more sodium than you need

for long periods of time is indeed bad for you.

Earlier, I mentioned that salt

and your hunger and thirst for salt

is homeostatically regulated.

And indeed that’s the case,

much like temperature is homeostatically regulated.

What that means is if you pay attention to it,

if your salt levels are low,

you will tend to crave salt

and salty beverages and salty foods.

And in most cases, you should probably follow that craving

provided those salty beverages and salty foods

are not bringing in a lot of other things

or anything ideally that’s bad for you.

So I think it’s fair to say

that whether or not you’re vegan, vegetarian,

carnivore, omnivore,

that we should all try to limit

our ingestion of processed foods.

My read of the literature is that sure,

some processed foods are acceptable for us

and aren’t going to kill us outright,

but that for most people in the world,

eating fewer processed foods

is just going to be a good thing to do.

So following your salt hunger and thirst in most cases

is going to be beneficial

provided that it’s in the context

of eating healthy non-processed foods

on whatever backdrop of nutritional

and dietary recommendations is right for you.

I simply can’t tell you what to eat and what not to eat

because I acknowledge the fact that some people are vegans

because of ethical reasons related to animals

or some people are vegans because of reasons

related to the climate and the environment.

Other people do it for specific health reasons.

Likewise, I know plenty of people that eat meat

and avoid vegetables, believe it or not.

And I know people that eat both

and they do this often each, I should say,

all citing literature that supports their particular camp

and their particular view.

It’s not a territory I want to get into,

but with respect to salt intake

and the fact that salt intake is homeostatically regulated,

it is the case that if you’re craving salt,

you probably need it.

So for those of you that are sweating excessively

or even if you’re in a very hot environment

and you’re not exercising and you’re just losing,

you’re losing water and salt from your system,

remember also that you can be in a very cold environment,

very cold, dry environments often go together

and you can be losing a lot of fluids from your body

and you will crave fluids and salt even though it’s cold

and you’re not actually noticeably perspiring.

So if you’re exercising a lot,

if you’re in a particular cold, dry environment

or a particular hot environment,

you ought to be ingesting sufficient amounts

of salt and fluid.

A rule of thumb for exercise-based replenishment of fluid

comes from what some episodes back

referred to as the Galpin equation.

The Galpin equation, I named it after Andy Galpin

and I think that is the appropriate attribution there.

Andy Galpin is an exercise physiologist

at Cal State Fullerton, I believe.

And he’s going to be a podcast guest

here on the Huberman Lab podcast.

He’s an exceptional muscle physiologist.

He also lives in the practical realm

where he gives recommendations about exercise

to expert athletes as well as the everyday person.

So the Galpin equation is based on the fact

that we lose about one to five pounds of water per hour,

which can definitely impact our mental capacity

and our physical performance.

And the reason that loss of water from our system

impacts mental capacity and physical performance

has a lot to do with literally the changes

in the volume of those cells, the size of those cells

based on how much sodium is contained

in or outside those cells.

And something that I’ve alluded to before on the podcast

and I’ll talk about more in a moment,

which is that neurons signal to one another

by way of electricity

through something called the action potential.

And that actually requires sodium

and potassium and magnesium.

So the Galpin equation suggests

that we start exercise hydrated with electrolytes,

not just with water.

So that means water that has some sodium,

potassium, and magnesium.

There are simple low-cost ways to do that we’ll talk about.

And the formula for hydration,

the so-called Galpin equation,

is your body weight in pounds divided by 30

equals the ounces of fluid you should drink

every 15 minutes.

That may turn out to be more fluid

than you can comfortably consume

during the activity that you’re performing.

Now, the Galpin equation is mainly designed for exercise,

but I think is actually a very good rule of thumb

for any time that you need to engage mental capacity,

not just physical performance.

Your body weight in pounds divided by 30

equals the ounces of fluid you should drink

every 15 minutes,

does not necessarily mean you have to ingest it

every 15 minutes on the dot.

And I think many activities, physical activities,

but also cognitive activities like Zoom meetings

or in-person meetings or lecturing or running or cycling

are going to make it complicated to ingest

the appropriate amount of fluid

every 15 minutes on the dot.

I’m not going to speak for Andy, for Dr. Galpin,

but I think he would probably agree

that these are averages to shoot for.

And that unless you’re hyper-neurotic,

the idea is to make sure that you’re entering the activity,

cognitive or physical, sufficiently hydrated,

and that throughout that activity,

you’re hydrating regularly.

And it points to the fact that most people

are probably under hydrating,

but not just under hydrating from the perspective

of not ingesting enough water,

that they’re probably not getting enough electrolytes

as well, sodium, potassium, and magnesium.

So I’ve said two somewhat contradictory things.

On the one hand, I said, follow your salt appetite,

follow your salt thirst.

If you’re craving salt,

ingest some salt until you stop craving the salt.

On the other hand, I’ve given you

this fairly specific recommendation

based on the Galpin equation,

that you should ingest your body weight in pounds

divided by 30.

That’s how many ounces of fluid

you should drink every 15 minutes,

which I’m guessing for most people

is going to be more fluid

than they’re currently drinking on average.

And so how could it be that you can have a recommendation

for what’s optimal that’s different

than the amount that you would reflexively drink?

And it has to do with the fact

that a lot of the hormone systems,

like vasopressin, antidiuretic hormone,

other hormones like aldosterone,

and a lot of the neural and hormonal signals

that govern salt and water balance

are fairly slow to kick in.

So for instance, if you eat a fairly salty meal

and you sense that salt, you’ll probably,

meaning you detect it and perceive it,

because the food tastes salty,

you’ll probably want to drink

a fair amount of fluid with it.

Whereas if some of the salt is disguised by other flavors,

something that we’ll talk about in a few minutes

when we talk about the neural representation

of things like salty and sweet,

well, then you might not notice that something’s salty.

And then a few minutes or hours after ingesting that meal,

you might feel very, very tired.

You might even wonder whether or not

it’s because of some blood sugar effect.

Maybe it’s a crash in blood sugar, you might think,

or something else related to that meal,

or maybe you think it’s because of

some other event in your life.

But actually what has happened is you’re dehydrated

because you didn’t recognize

that you needed to drink more fluids.

So I want to acknowledge the contradiction

in the idea that everything is homeostatically regulated

and therefore you are aware of what you need.

And the counter argument that,

ah, you need to follow these strict recommendations,

it’s actually going to be somewhere in between.

And of course, your body and brain can start to adapt

to certain levels of salt intake.

There’s a now fairly famous study

that was done in Germany,

which looked at different phases of salt intake,

meaning they had subjects ingest

either 12 grams of salt per day,

or nine grams per day, or six grams per day

for fairly long periods of time.

And they collected urine for testing.

This was actually a very controlled study.

I’m just going to paraphrase

from the National Institutes of Health report on this study

because they did a very nice write-up of it.

And they say that, you know,

a big surprise of these results is that

whatever the level of salt that was consumed,

sodium was stored and released from the subject’s bodies

in fairly regular weekly and monthly patterns,

meaning people tended to adapt

to a certain level of salt intake.

And then it led to a fairly constant amount

of salt retention and urine fluid excretion.

And that’s because of the various hormones like aldosterone,

which regulate sodium excretion from the kidney,

and glucocorticoids,

which we’ll talk about more in a moment,

which help regulate metabolism.

Glucocorticoids are released from the adrenal glands,

which ride atop the kidneys.

And there’s a very close relationship

between the stress system, glucocorticoids,

and the salt system.

So the reason why your salt appetite

isn’t a perfect readout of how much salt you should ingest

and why it might be helpful to follow

some of these formulas like the Galpin equation,

especially if you’re engaging in exercise,

where you’re going to be perspiring, of course,

is that your body will tend to adapt

to a certain amount of salt intake over time.

And then your appetite for salt

won’t necessarily be the best indication

of how much salt you should ingest or avoid.

Before I move on, I want to really reemphasize the fact

that inside of the Galpin equation,

there is that mention of every 15 minutes.

And people have come back to me again and again

about this saying,

I can’t drink that much water every 15 minutes.

It’s too much volume of fluid in my stomach.

I can’t run with that, et cetera.

Remember, these are averages.

So that’s what you want to average

around a particular activity.

These are not strict recommendations

where a buzzer goes off and every 15 minutes,

you have to chug that exact amount

of electrolyte containing solution.

Another key feature of the study

that I was referring to before,

which incidentally was published

in the Journal of Clinical Investigation,

is that the body regulates its salt and water balance,

not just by excreting sodium,

but by retaining or releasing water.

And this is because of the relationship

between sodium and water that we were talking about before.

And the advantage of this mechanism,

they state here, I’m paraphrasing,

is that the long-term maintenance of body fluids

is not as dependent on external water as once believed.

What the system probably evolved to do

was to adjust to different levels

of sodium availability in the environment.

And that raises a really key element of salt

and its importance in human history

and human evolution and human health.

We haven’t talked too much about this,

and there are several very good books

about the history of salt.

You know, salt was a very valuable

and heavily sought after substance

throughout much of human history,

so much so that there are actually written reports

of people being paid for labor in the form of salt.

And salt, when it’s scarce,

has been quite expensive in certain regions of the world,

especially regions located further away from the sea.

And a friend of mine who has deep roots

within the culinary community told me about traveling

to some somewhat impoverished areas of Europe

some years ago and going into homes

where in the middle of the kitchen table,

there was a fish, a salty fish,

hanging from a thread above the table.

And that because of a lack of availability of table salt,

the common practice was to take any food

that needed some salt for additional flavoring

and to actually rub that food on this salty fish

or to squeeze the fish a bit onto the food substance

in order to get salt from it.

So, you know, that’s a very kind of extreme example.

Nowadays, we kind of take salt for granted,

and most of the discussion out there is about excess salt.

But as I’m pointing out that, you know,

salt for a long time has been a very sought after commodity

and one that people really cherished for their health.

In the episode that I did on metabolism,

I talked about the relationship between salt and iodine.

If you’re interested in iodine

and whether or not iodized salt or non-iodized salt

is best or required,

I’d encourage you to listen to that episode,

which was about, again, metabolism.

Some people may need more iodine intake.

Some people perhaps do not.

Some people might even want to ingest things like kelp.

Some people might not.

So please listen to that episode

if you’re interested in the iodine aspects of salt,

which have direct impact on thyroid hormone

and thyroid function,

which of course relates to metabolism.

Nowadays, there’s a lot of interest in,

and even a kind of proliferation of what I call fancy salts.

So whether or not you should be ingesting sea salts

or whether or not common table salt will suffice.

In most cases, for what we’re discussing here,

common table salt is fine,

but I should point out that sea salt

often contains other minerals, which can be very useful.

And we will do entire episodes on those other minerals.

So sea salt can contain dozens or more of minerals,

some of which can be quite valuable to our health,

others of which are less important

and only need to be consumed in trace amounts,

but you’re not going to get many minerals,

if any, from common table salt.

And that’s why, in addition to the pretty colors

and perhaps some people report

that it actually tastes better,

some of these so-called fancy salts or sea salts,

you might want to consume a more advanced form of salt,

if you will.

Although I suppose it’s actually

the more primitive form of salt,

if it’s actually the one that comes from the ocean.

So we’ve all heard about how excess salt,

it’s bad for blood pressure,

damage the heart, the brain, et cetera.

I do want to give some voice to situations

where too little salt can actually cause problems.

And this has everything to do with the nervous system.

So without getting into excessive amounts of detail,

the kidneys, as we talked about before,

are going to regulate salt and fluid balance.

The adrenal glands, which ride atop the kidneys,

are going to make glucocorticoids like aldosterone.

And those are going to directly impact

things like fluid balance.

And in part, they do that by regulating

how much craving for and tolerance

of salty solutions we have.

And there’s some really nice studies

that have looked at so-called adrenalectomies.

Now, this is an extreme case,

and it’s typically done in animal models,

but it illustrates the role of the adrenals

in salt preference.

Basically, when the glucocorticoid system,

meaning the release of these particular hormones

from the adrenal glands is eliminated by adrenalectomy,

ectomy means removal,

then the threshold for what’s considered too salty

really shifts, okay?

So typically, when the adrenals are intact,

a animal or a human will prefer a mildly salty

to moderately salty solution, if given a choice.

And at some point, it’s so salty

that it just feels aversive.

Just like taking a gulp of seawater

is almost always aversive.

I can’t think of an instance where it’s not aversive.

And actually, drinking seawater can kill you

because of the high osmolarity of seawater.

You certainly don’t want to drink seawater.

Under conditions where the adrenals are missing,

animals and humans will tend to prefer

a higher sodium concentration fluid,

and they will be willing to tolerate

ingesting very high concentrations of sodium.

Now, that’s a very crude experiment

and not one that you want to do, I promise you.

But I mention it because it illustrates

the very direct relationship between the stress system,

which is the glucocorticoid system,

and the salt craving system.

And this actually makes sense.

Earlier, as we were talking about hypovolemic thirst,

when there’s a loss of blood pressure,

usually due to a loss of blood from the body,

there’s a salt craving in order

to bring that blood volume back up.

Because by ingesting salt,

you bring fluid into the bloodstream,

you’re increasing that blood pressure

and you can restore the blood that’s lost.

Now, there are many examples where

if sodium levels get too low in the bloodstream,

either because people are ingesting too little salt,

or they are ingesting too much water

and therefore excreting too much salt,

that it can cause stress and anxiety.

There’s some really nice data that point to the fact

that low dietary sodium can actually exacerbate anxiety

in animal models.

And to some extent,

there’s evidence for this in humans as well.

And that should not come as a surprise.

The whole basis for a relationship

between the adrenal system, these glucocorticoids,

things like aldosterone and the craving for sodium,

is that the stress system is a generic system

designed to deal with various challenges to the organism,

to you, or to me, or to an animal.

And those challenges can arrive in many different forms.

They can be an infection, it can be famine,

it can be lack of water, and so on.

But in general, the stress response

is one of elevated heart rate, elevated blood pressure,

and an ability to maintain movement

and resistance to that challenge, okay?

I’ve said this before, but I’ll emphasize it again.

There’s this common misperception that stress makes us sick.

And indeed, if stress lasts too long,

it has a number of negative effects on our health.

But more often than not, if we’re pushing, pushing, pushing,

we’re studying or taking care of somebody

or traveling like crazy,

we don’t tend to get sick under those conditions.

But as soon as we stop,

as soon as we reduce our adrenaline output,

as soon as we reduce our glucocorticoid output

from our adrenals, then we will get sick.

That’s a very common occurrence.

And it’s because stress actually activates

our immune system in the short-term.

So I’d like to try and dispel this myth

that stress actually suppresses the immune system,

at least not in the short-term.

For long-term stress, it’s a different issue.

You don’t want long-term ongoing stress,

especially of several weeks or more.

Nonetheless, it makes sense that bringing sodium

into the body would be at least one way

that we would be wired to counteract

or to resist stressors, right?

Stressors being the things on the outside coming at us.

So it could be a stressful relationship,

stressful job situation, again, infection, and so on.

It’s clear from a number of studies

that if sodium levels are too low,

that our ability to meet stress challenges is impaired.

Now, that doesn’t mean

to place your sodium intake cosmically high,

but it does point to the fact that if you’re feeling anxious,

perhaps from low blood pressure,

which can also give symptoms of anxiety,

as we talked about before,

but even if it’s independent of low blood pressure,

that slightly increasing sodium intake,

again, I would encourage people to do this,

not in the context of processed foods and drinks,

but ideally in the form of maybe a little bit

of sea salt and water

or salting one’s food a little bit more,

that that can stabilize blood pressure

and one’s ability to lean into stressors and challenges.

And I say this because I think that most people assume

that adding salt is always bad,

when in fact, that’s simply not the case.

There are conditions such as

when we are under stress challenge,

when there is a natural craving for more sodium,

and that natural craving for more sodium

is hardwired into us as a way to meet that challenge.

So it’s hard for me to know whether or not people out there,

especially the listeners of this podcast,

are getting too much, just enough, or too little sodium.

So I can’t know that, I’m shouting into a tunnel here,

you have to decide how much sodium you are ingesting.

But I think that there’s some, for most people,

especially people who are not hypertensive,

pre-hypertensive, there’s some wiggle room to explore

whether more intake of sodium could actually be beneficial

for suppressing some of the anxiety responses

that they might feel under conditions of stress.

Again, more studies need to be done,

certainly more studies in humans need to be done,

but the relationship between stress and sodium intake

and the fact that additional sodium intake may be beneficial

and indeed is naturally stimulated by stress

shouldn’t be necessarily looked at as a pathological event.

I know when some people get stressed,

they crave salty foods,

that’s actually a hardwired biological phenomenon

that you see not just in humans, but in animals,

because this is a very primitive mechanism

whereby your body is preparing

to meet any additional challenges and stressors.

Now we can’t have a discussion about sodium

without having a discussion about the other electrolytes,

magnesium and potassium.

Magnesium is important enough

and an extensive enough topic

that we should probably do an entire episode

just on magnesium.

For purposes of today’s discussion,

I just will briefly touch on some of the forms of magnesium

that we’ve discussed on the podcast before

in different contexts.

I want to emphasize that many people

are probably getting enough magnesium in their diet

that they don’t need to supplement magnesium.

Some people, however, opt to supplement magnesium

in ways that can support them.

And there are many different forms of magnesium.

And just in very brief passing,

I’ll just say that there is some evidence

that you can reduce muscle soreness from exercise

by ingestion of magnesium malate, M-A-L-A-T-E.

I’ve talked before about magnesium threonate,

T-H-R-E-N-O-A-T-E, magnesium threonate,

for sake of promoting the transition into sleep

and for depth of sleep.

And perhaps, again, highlighted perhaps,

because right now it’s mainly animal studies

and ongoing human studies, but the data aren’t all in,

perhaps magnesium threonate can be used

as a way to support cognitive function and longevity.

That was discussed in the episode

with Dr. Jack Feldman from UCLA.

Typically, magnesium threonate is taken 30 to 60 minutes

before bedtime in order to encourage sleep.

You can go to our Neural Network newsletter

and look for the one on sleep,

and you can see the recommendations,

or I should say the options for that,

because again, you should always check with your physician.

Those aren’t strict across the board recommendations.

And then there are other forms of magnesium,

magnesium bisglycinate,

which is somewhat of an alternative to threonate,

not known to have cognitive enhancing effects,

but seems at least on par with magnesium threonate

in terms of promoting transition

into in-depth of sleep and so on.

There are other forms of magnesium, magnesium citrate,

which has other functions.

Actually, magnesium citrate is a fairly effective laxative.

Not known to promote sleep and things of that sort.

So a lot of different forms of magnesium,

and there’s still other forms out there.

Many people are not getting enough magnesium,

many people are.

Okay, so that’s magnesium.

Anytime we’re talking about sodium balance,

we have to take into consideration potassium,

because the way that the kidney works

and the way that sodium balance is regulated

both in the body and the brain

is that sodium and potassium

are working in close concert with one another.

There are a lot of different recommendations

about ratios out there,

and they range widely from two to one ratio

of potassium to sodium.

I’ve heard it in the other direction too.

I’ve heard a two to one sodium to potassium.

The recommendations vary.

One of the sponsors of this podcast, for instance, Element,

which I’ve talked about in this episode and before,

the ratio there is a gram of sodium

to 200 milligrams of potassium, 60 milligrams of magnesium.

So there they’ve opted for a five to one ratio

of sodium to potassium.

And of course, many people opt to make their own

hydration electrolyte formulas.

They’ll put sea salt into some water,

maybe even ingest a potassium tablet.

It all depends on the context.

An important contextual element is your diet.

So for instance, carbohydrates hold water in the body.

So regardless of how much salt

and how much fluid you’re ingesting,

if you’re ingesting carbohydrate

and you drink fluids, water,

some of that fluid is going to be retained in the body.

Now for people that are following low carbohydrate diets,

one of the most immediate effects of a low carbohydrate diet

is that you’re going to excrete more water.

And so under those conditions,

you’re also going to lose not just water,

but you’ll probably also lose sodium and potassium.

And so some people, many people in fact,

find that when they are on a lower or low carbohydrate diet,

then they need to make sure that they’re getting

enough sodium and enough potassium.

And some people do that

by taking 99 milligram potassium tablets

every time they eat.

Some people do that by ingesting more foods

that contain potassium.

And of course, some people who are on low carbohydrate diets

do ingest vegetables, you know,

or other forms of food that carry along with them, potassium.

So it’s quite variable from person to person.

I mean, you can imagine if carbohydrate holds water,

water and salt balance and potassium go hand in hand

that if you’re on a low carbohydrate diet,

that you might need to adjust your salt intake and potassium.

And conversely, that if you’re on a carbohydrate rich diet

or a moderate carbohydrate diet,

then you may need to ingest less sodium and less potassium.

And in fact, a certain amount of water

is probably coming in through the foods you eat as well.

So I don’t say all this to confuse you.

Again, I say this because it all depends on the context.

I’ll give yet another context

that I think is fairly common nowadays,

which is many people are following a pattern of eating

that more or less resembles intermittent fasting

or at least time-restricted feeding.

So they’re eating between particular feeding windows.

And then in the certain parts of the 24-hour cycle,

not just sleep,

but during certain parts of their waking cycle,

they’re also actively avoiding food.

Banking on, I think, either the possible,

I want to say possible,

longevity-promoting effects of intermittent fasting

and or, I should say,

they are banking on the fact that for many people,

not eating is easier than portion control

for certain parts of the day.

And so they find it beneficial to limit calories overall

to a given amount, depending on what their goals are,

by not consuming food for certain periods of the day.

But usually during those periods of the day,

they’re consuming fluids.

And oftentimes those fluids include not just water,

but caffeine.

And caffeine is a diuretic.

It actually causes the excretion of fluids

from the body in part,

because it causes the excretion of sodium.

All of that to say that if you’re somebody who,

for instance, eats your first meal around noon

or one or 2 p.m.

and you’re fasting for the early part of the day

and you’re drinking coffee or tea

or ingesting a lot of water,

you are going to be excreting sodium along with that water.

And so many people, including myself,

find that it’s useful,

especially when I’m drinking caffeine

during that so-called fasting

or non-food intake part of time-restricted feeding,

that I’m making sure to get enough salt

either in the form of something like Element,

an electrolyte drink,

or putting some sea salt into some water,

or certainly anytime one is ingesting caffeine,

replacing some of the lost water

by increasing one’s water intake.

There are some simple rules of thumb around this

that I think can get most people into a place

where they’re more comfortable and functioning better,

which is for every ounce of coffee or tea that you drink,

I should say caffeinated coffee or tea that you drink,

that you consume one and a half times as much water.

So let’s say you have an eight-ounce coffee,

try and drink about, you don’t have to be exact,

but try and drink about a 12-ounce glass of water,

and you might want to put a tiny bit of sodium into that.

By tiny bit, I just mean a tiny pinch of sodium.

Because remember, even if we’re talking

about increasing the amount of sodium intake overall,

the total amount of sodium contained in salt

is sufficiently high that even just a quarter teaspoon

is going to really start to move that number up

towards that range that’s still within the safe range.

But if you keep doing that all day long,

you’re very quickly going to get into

that excessive salt intake range

that is deleterious for health.

So again, if you’re consuming more caffeine,

you’re going to be excreting water and salt and potassium,

and so you’re going to have to find ways

to bring water, salt, and potassium back in.

Again, this has to be evaluated

for each of your own individual situations.

If you’re exercising, fasted,

and you’re doing that after drinking caffeine,

then before, during, and certainly after exercise,

you’re going to want to replenish the fluids

and electrolytes that you lost, including sodium.

So you can imagine how this all starts

to become pretty dizzying,

and yet it doesn’t have to be dizzying.

We can provide some useful ranges

that for most people will work.

And so let’s talk about what those ranges are,

and I’m going to point you to a resource

that explores what those ranges are

in these various contexts of nutrition, exercise, and so on.

The resource is a book that was authored

by Dr. James D. Nicolantonio.

He’s not a medical doctor.

He’s a scientist, so he’s cardiovascular physiology,

as well, I believe, as a doctor of pharmacy.

And the title of the book is The Salt Fix.

The Salt Fix is an interesting read

because it points to, first of all,

the history of salt in society,

and as it relates to health,

it actually emphasizes some of the major missteps,

maybe even pretty drastic errors

that have been made in terms of trying to interpret

the role that salt has in various diseases,

and emphasizes some of the ways in which

perhaps increasing salt

can actually improve health outcomes.

And I think it strikes a pretty nice balance

between what’s commonly known about salt

and what I believe ought to be known about salt,

or at least taken into consideration.

You know, the book does provide certain recommendations,

and I actually reached out to the author.

I’ve never met him in person or talked to him directly,

and I asked him outright, I said,

how much salt do you recommend people take on average?

And he gave, of course, the appropriate caveats

about prehypertension, hypertension, et cetera,

but made a recommendation which I’ll just share with you,

and if you want to learn more

about the support for this recommendation,

you can check out his book.

The recommendation he made was anywhere

from eight to 12 grams of salt a day,

which corresponds to 3.2 to 4.8 grams of sodium.

So going back to the current recommendations

that we talked about before, 2.3 grams of sodium per day,

this is about one and a half times to, you know,

double the amount of sodium that’s currently recommended

in most circles, and what this corresponds to

is about one and a half to two teaspoons of salt per day

to arrive at that 3.2 to 4.8 grams of sodium.

Again, this is the recommendation that was passed along

for most people, most conditions,

barring, you know, specific health issues.

Now, what was also interesting is he pointed

to a sodium to potassium ratio,

which is four grams of potassium,

and he also mentioned 400 milligrams of magnesium

and pointed out, and I generally agree here

that many people are deficient in magnesium.

So again, that was a 3.2 to 4.8 grams of sodium,

four grams of potassium.

You might think, well, gosh, that’s one and a half

to two times the current recommendation,

but we can go back to that study that was mentioned earlier

in the episode, the 2011 study,

where I described this sort of J-shaped curve

in which when you look at the occurrence

of these negative health events,

they were fairly low at low sodium intake,

lower still at slightly higher sodium intake,

much in line with the recommendations that are made

or that Dr. D. Nicolantonio passed along to me,

and then they increased quite,

those health risks increased quite substantially

as one moves out past, you know,

six grams of sodium, seven grams of sodium per day.

That’s when things really do seem to get hazardous

and really, it makes sense, I think,

given the consensus around this

to really avoid very high salt intake.

So the salt fix describes the rationale

behind those recommendations.

The salt fix also describes in quite beautiful detail

the relationship between salt intake, potassium intake,

and the relationship to the sugar consumption system.

I’d like to pick up on this idea of the relationship

between salt and sugar,

because I think that one key aspect of the way

that salt can work and can benefit us or can harm us

has to do with the way that sodium and sugar are regulated

and actually perceived by the brain

and how under conditions of certain levels of sodium intake,

we might be inspired to seek more sugar

or to crave sweets more or less.

So up until now, we’ve been talking about salt

as a substance and a way to regulate fluid balance

and blood volume and so on.

We haven’t talked a lot about salt as a taste

or the taste of things that are salty.

And yet we know that we have salt receptors,

meaning neurons that fire action potentials

when salty substances are detected,

much in the same way that we have sweet detectors

and bitter detectors, and we have detectors of umami,

the savory flavor on our tongue.

And earlier at the beginning of the episode,

I talked about the fact that we have sweet receptors,

neurons that respond to the presence of sugar

or even non-caloric sweet things in the gut.

And that signals up to the brain through the vagus nerve.

And those signals converge on pathways

that relate to dopamine and so on.

Well, we also have salt sensors at various locations

throughout our digestive tract.

Although that the sensation and the taste of salt

actually exerts a very robust effect

on certain areas of the brain

that can either make us crave more or sate,

meaning fulfill our desire for salt.

And you can imagine why this would be important.

Your brain actually has to register

whether or not you’re bringing in salt

in order to know whether or not

you are going to crave salt more or not.

And beautiful work that’s been done by the Zucker Lab,

Z-U-K-E-R, Zucker Lab at Columbia University,

as well as many other labs,

have used imaging techniques and other techniques

such as molecular biology

to define these so-called parallel pathways.

Parallel meaning pathways that represent sweet

or the presence of sweet taste in the mouth and gut.

Parallel pathways meaning neural circuits

that represent the presence of salty tastes

in the mouth and gut and so on.

And that those go into the brain,

move up through brain stem centers

and up to the neocortex,

indeed where our seat of our conscious perception is,

to give us a sense and a perception

of the components of the foods

that we happen to be ingesting

and a sense and a perception of the fluids

and the components of those fluids

that we happen to be ingesting.

Now, parallel pathways, as I’m describing them,

are a fundamental feature of every sensory system,

not just the taste system, but also the visual system.

We have parallel pathways for perceiving dark objects

versus light objects,

for perceiving red versus green, et cetera.

This is a fundamental feature of how we are built

and how our nervous system works.

And in the taste system, much like in these other systems,

these pathways are indeed parallel,

but they converge and they can influence one another.

And I think the simplest way to put this

is in the context first of the visual system,

whereby your ability to detect the color red

has everything to do with the fact

that you have neurons in your eye

that absorb long wavelengths of light

that we call reds, red wavelengths of light,

which are longer wavelengths than say blue light,

which is shorter wavelength.

But it is really the comparison of the electrical activity

of the neurons that absorb red light

with the activity of the neurons that absorb green light,

which actually gives you the perception of red.

So that might seem a little counterintuitive,

but indeed it’s not.

It’s actually because something is red

and has less greenness that we perceive it

as more red than the green.

And this is actually the way

that your entire nervous system works

is that we aren’t really good at evaluating absolute levels

of anything in the context of perception.

It’s only by comparison.

And actually there’s a fun experiment that you can do.

I think you could probably find it easily online.

You could also do this experiment at home.

You can stare at something that’s red or green

for that matter for a while.

So you make an active decision to not blink

and to stare at something that’s red.

And then you look away from that thing

and you’ll actually see a green after image

of that red object.

Conversely, if you look at something that’s green for a while

and you stare at it and you look away,

you will see the red after image of that thing.

Now the taste system doesn’t have quite the same

aftertaste type effect, but nonetheless the pathways,

the parallel pathways for salty

and the parallel pathways for sweet and bitter and so on

can actually interact.

And this has important relevance in the context

of food choices and sugar craving.

One of the things that’s common place nowadays

is in many processed foods, there is a business, literally,

a business of putting so-called hidden sugars.

And these hidden sugars are not always

in the form of caloric sugars.

They’re sometimes in the form of artificial sweeteners

into various foods.

And you might say, well, why would they put more sugar

into a food and then disguise the sugary taste

given that sweet tastes often compel people

to eat more of these things?

Well, it’s a way actually of bypassing

some of the homeostatic mechanisms for sweet.

Even though we might think that the more sweet stuff we eat,

the more sweet stuff we crave,

in general, people have a threshold whereby they say,

okay, I’ve had enough sugary stuff.

You can actually experience this.

If you ever feel like something is really, really sweet,

take a little sip of water with a little bit of lemon juice

in it or vinegar, and it will quickly quench

that overly sweet sensation or perception.

It will disappear almost immediately.

There’s actually a practice in fancy meals

of cleansing the palate through the ingestion

of different foods.

And that’s the same idea that you’re cleansing the palate.

You’re actually neutralizing the previous taste

so then they can bring yet another dish

to overindulge you in decadence and so forth.

So these sensory systems interact in this way

by putting sugars into foods

and hiding the sugary taste of those foods.

Those foods, even if they contain artificial sweeteners,

can activate the sorts of neurons that we talked about

at the beginning of the episode, like the neuropod cells

that will then signal to the brain to release more dopamine

and make you crave more of that food.

Whereas had you been able to perceive

the true sweetness of that food,

you might’ve consumed less.

And indeed, that’s what happens.

So these hidden sugars are kind of diabolical.

Why am I talking about all of this

in the context of an episode on salt?

Well, as many of you have probably noticed,

a lot of foods out there contain a salty-sweet combination.

And it’s that combination of salty and sweet,

which can actually lead you to consume more

of the salty-sweet food than you would have

if it had just been sweet or it had just been salty.

And that’s because both sweet taste and salty taste

have a homeostatic balance.

So if you ingest something that’s very, very salty,

pretty soon your appetite for salty foods will be reduced.

But if you mask some of that with sweet,

well, because of the interactions

of these parallel pathways,

you somewhat shut down your perception

of how much salt you’re ingesting.

Or conversely, by ingesting some salt with sweet foods,

you mask some of the sweetness of the sweet foods

that you’re tasting,

and you will continue to indulge in those foods.

So salty-sweet interactions can be very diabolical.

They can also be very tasty,

but they can be very diabolical

in terms of inspiring you to eat more of a particular food

than you would otherwise if you were just following

your homeostatic salt

or your homeostatic sugar balance systems.

And the beautiful imaging work that’s been done

by the Zucker Lab and other labs

has actually been able to reveal

how some of this might work by showing, for instance,

that a certain ensemble,

meaning a certain group of neurons,

is activated by a sweet taste

and a non-overlapping distinct set of neurons just nearby,

sitting cheek to jowl with those other neurons,

would be activated by salty tastes

and yet others by bitter tastes, et cetera.

So there’s a separate map

of these different parallel pathways,

but that when foods or fluids are ingested

that are both salty and sweet,

you get a yet entirely different ensemble

of neurons activated.

So your brain, whether or not it’s for your visual system

or your auditory system or your taste system,

has a way of representing the pure form of taste,

salty, sweet, bitter, et cetera,

and has a way of representing their combinations.

And food manufacturers have exploited this to a large degree.

I mention all of this

because if you’re somebody who’s looking to explore

either increasing or decreasing your sodium intake

for health benefits, for performance benefits,

in many ways, it is useful to do that

in the context of a fairly pure,

meaning unprocessed food intake background,

whether or not that’s keto, carnivore, omnivore,

intermittent fasting or what have you,

it doesn’t really matter.

But the closer that foods are to their basic form and taste,

meaning not large combinations

of large amounts of ingredients

and certainly avoiding highly processed foods,

the more quickly you’re going to be able to hone in

on your specific salt appetite and salt needs,

which as I’ve pointed out numerous times

throughout this episode

are going to vary from person to person,

depending on nutrition, depending on activity,

depending on hormone status

or even portion of your menstrual cycle for that matter.

So if you want to hone in

on the appropriate amount of sodium for you,

yes, blood pressure is going to be an important metric

to pay attention to as you go along.

And the parameters for healthy blood pressure ranges

are readily available online.

So I’ll let you refer to those

in order to determine those for yourself.

But in determining whether or not

increasing your salt intake might be beneficial

for instance, for reducing anxiety a bit

or for increasing blood pressure

to offset some of these postural syndromes

where you get dizzy, et cetera,

for improving sports performance or cognitive performance,

I can only recommend that you do this

in a fairly clean context

where you’re not trying to do this

by ingesting a bunch of salty foods

or salty sweet foods, et cetera.

And indeed many people find, and it’s reviewed a bit

and some of the data are reviewed in the book,

the salt fix, that when people increase their salt intake

in a backdrop of relatively unprocessed foods

that sugar cravings can indeed be vastly reduced.

And that makes sense given the way

that these neural pathways for salty and sweet interact.

Now thus far, I’ve already covered quite a lot of material

but I would be completely remiss

if I didn’t emphasize the crucial role

that sodium plays in the way that neurons function.

In fact, sodium is one of the key elements

that allows neurons to function at all.

And that’s by way of engaging

what we call the action potential.

The action potential is the firing

of electrical activity by neurons.

Neurons can engage electrical activity

in a number of different ways.

They have graded potentials, they have gap junctions.

There’s a whole landscape

of different electrophysiologies of neurons

that I don’t want to go into just yet.

At least not in this episode.

But the action potential is the fundamental way

in which neurons communicate with one another.

They’re sometimes called spikes.

It’s just kind of nomenclature that neuroscientists use.

I’m just going to briefly describe the action potential

and the role that sodium plays.

And this will involve a little bit of chemistry

but I promise it will be accessible to anyone

even if you don’t have a chemistry or a physics background

or electrophysiology background.

Neurons have an inside and an outside

and inside are things like your genetic material.

They have a bunch of things floating around in there

that allow those cells to function.

And they tend to have this wire extending out of them.

Sometimes a very long wire,

sometimes a short one that we call the axon.

And at the end of that wire, that axon,

they release little packets of chemicals

that either cause the next neuron to fire action potentials

or prevent the next neuron from firing action potential.

So they kind of vomit out these little packets of chemicals

that either inspire or suppress action potentials

in other neurons.

The way that that whole process occurs

is that a given neuron needs to

change its electrical activity.

So normally neurons are hanging out

and they have what we call a negative charge.

And the reason they have a negative charge

is that the inside of the cell

has things floating around in it

like potassium, a little bit of sodium,

and some stuff like chloride.

These are literally just,

just imagine these as little balls of stuff.

And if they have a negative charge on them,

then the inside of the cell

is going to tend to be more negative.

And outside of the cell, it turns out,

you’re going to have a bunch of stuff

that’s positively charged.

And one of the main factors

in creating that positive charge is sodium.

Sodium carries a positive charge.

So you have neurons that you can just imagine,

for sake of this discussion,

you can just imagine as a sphere

with a little wire sticking out of it.

They, you can put a little minus on the inside for negative.

You can put a little plus on the outside for positive.

And when that neuron is stimulated by another neuron,

if the stimulation, the electrical stimulation,

is sufficiently high,

meaning enough little packets of neurotransmitter

have been vomited onto its surface

at sufficient concentration,

what happens is little pores, little spaces,

little gaps open up in the membrane of that cell

that separates the inside from the outside.

And because it’s positive,

there’s a lot of positive charge outside

and there’s a lot of negative inside.

It’s like a boulder running downhill.

All this stuff tends to rush downhill.

It tries to create even amounts of charge.

So it’s negative on the inside, positive on the outside.

And what happens is sodium rushes into the cell,

carrying a lot of charge into the cell.

And as a consequence, the charge of that cell

goes from negative, actually very negative,

to quite positive.

And if it hits a certain threshold of positive charge

because of all the sodium ions going into the cell,

then it fires what’s called an action potential.

And it vomits out its own set of chemicals

onto the next neuron.

And so it sets off a chain of,

one neuron goes from negative to positive,

vomits out chemicals onto the next one.

The next one, the next neuron that binds to receptors

or enters the cell,

and that cell goes from negative to positive charge,

vomits its contents onto the next cell,

and so on and so forth.

Sodium rushing into the cell, therefore,

is the way that the action potential is stimulated.

In other words, sodium is the way

that neurons communicate with one another.

Now, the neurons don’t stay in a positive charge.

Otherwise they would just keep vomiting out their contents.

Blah, blah, blah.

But they need to maintain some of that,

and they need to go back to preparing to do it

the next time and the next time by resting a bit.

And it turns out that the way they restore their charge

is by pushing that sodium back out of the cell.

There are mechanisms in place to do that,

things like the so-called sodium-potassium pump.

There’s a change in the levels of potassium

across the cell membrane, and so on and so forth.

If you want to look at a demonstration of this,

you can put into a web browser the action potential.

You’ll find some beautiful descriptions there

on YouTube and elsewhere.

Maybe sometime on Instagram,

I’ll do a description with a diagram,

because I realize a number of people

are just listening to this.

I can’t do that here.

I won’t do that here,

because I want everyone to be able

to get the same amount of material,

regardless of whether or not they’re watching

and or listening to this.

But the point I’d like to make,

at least as it relates to this episode on salt,

is that having sufficient levels of salt in your system

allows your brain to function,

allows your nervous system to function at all.

Again, this is the most basic aspect

of nervous system function.

And there are cases where this whole system gets disrupted.

And that brings us to the topic of sodium and water balance.

As many of you have probably heard,

but hopefully if you haven’t,

you’ll take this message seriously.

If you drink too much water,

especially in a short amount of time,

you can actually kill yourself, right?

And we certainly don’t want that to happen.

If you ingest a lot of water in a very short period of time,

something called hypernatremia,

you will excrete a lot of sodium very quickly

and your ability to regulate kidney function

will be disrupted.

But in addition to that,

your brain can actually stop functioning.

So people have actually consumed water to excess,

especially after sports events and so forth.

And if that water doesn’t contain sufficient electrolytes,

you can actually shut down neurons ability

to function at all by disrupting this balance

of sodium and potassium

and the amount of extracellular sodium

and neurons ability to signal to one another

through action potentials.

And I can’t emphasize the importance

of action potentials enough.

They are the way that I can lift my pen right now.

They’re the way that I can speak.

They’re the way that you breathe.

They literally control all aspects

of your nervous system function.

Now it takes quite a lot of water intake

before you excrete enough sodium

that your nervous system is going to shut down.

And I certainly don’t want to give the impression

that simply by ingesting more sodium,

your neurons will work better.

But it absolutely is the case

that if you don’t ingest enough sodium,

that your neurons won’t function as well as they could.

And that if your sodium levels are made too low

by hemorrhage or by ingesting so much water fluid

that you excrete excess amounts of sodium

or through any other mechanism that is,

then indeed your neurons won’t be able

to fire action potentials

and your brain and nervous system simply won’t work.

And that’s one of the primary reasons

why dehydration leads to confusion

and dizziness and lack of coordination.

And I’ve talked about this a bit

in the episode on endurance,

but there are instances in which, you know,

competitive athletes have come into the stadium

to finish a final lap of a long endurance race

and are completely disoriented

and actually can’t find their way to the finish line.

You know, it might sound like kind of a silly,

kind of crazy example,

but there are examples of people having severe mental issues

and physical issues post exercise

when that exercise involved a ton of sweating

or hot environments or insufficient ingestion of fluids

and electrolytes,

because included in that electrolyte formula,

of course, is sodium.

And as you just learned,

sodium is absolutely crucial for neurons to function.

So to briefly recap some of what I’ve talked about today,

we talked about how the brain monitors

the amount of salt in your brain and body

and how that relates to thirst

and the drive to consume more fluid and or salty fluids.

We also talked a little bit about the hormones

that come from the brain

and operate at the level of the kidney

in order to either retain

or allow water to leave your system.

Talked a little bit about the function of the kidney itself,

a beautiful organ.

We talked about the relationship between salt intake

and various health parameters

and how a particular range of salt intake might be optimal,

depending on the context

in which that range is being consumed.

Meaning, depending on whether or not you’re hypertensive,

prehypertensive or normal tension.

We talked about fluid intake and electrolyte intake.

So sodium, potassium and magnesium

in the context of athletic or sports performance,

but also in terms of maintaining cognitive function.

Talked about the Galpin equation,

which you could easily adapt to your body weight

and to your circumstances.

Of course, adjusting the amount of fluid

and electrolyte intake upwards,

if you’re exercising or working in very hot environments.

Downwards, maybe if you’re in less hot environments

where you’re sweating less and so on.

We also talked about the relationship

between the stress system and the salt craving system

and why those two systems interact

and why for some people who may suffer a bit from anxiety

or under conditions of stress,

increasing salt intake,

provided it’s done through healthy means,

might actually be beneficial.

We also talked about conditions

in which increasing salt intake might be beneficial

for offsetting low blood pressure

and some of these postural syndromes

that can lead people to dizziness and so forth.

These are things that have to be explored

on an individual basis.

And of course, have to be explored

with the support of your doctor.

I mentioned the salt fix,

which I think is an interesting read,

keeping in mind that a lot of the information in there

runs counter to the typical narrative

that you hear around salt,

but nonetheless has some very interesting points

that you might want to consider

and certainly will broaden your view of the history of

and the applications of salt

as it relates to a great number

of health and performance metrics.

We also talked about the perception of salt,

meaning the perception of salty tastes

and how the perception of salty tastes

and the perception of other tastes like sweet

can interact with one another

to drive things like increased sugar intake

when you’re not even aware of it.

And indeed, how the combination of salty and sweet tastes

can bias you towards craving more,

for instance, processed foods

and why that might be a good thing to avoid.

And of course, we talked about salt

and its critical role in the action potential,

the fundamental way in which the nervous system

functions at all.

So my hope for you in listening to this episode

is that you consider a question.

And that question is, what salt intake is best for you?

And that you place that question

in the context of your fluid intake.

You place that in the context of the diet you’re following,

the amount of caffeine you might be ingesting

and the diuretic effects of caffeine.

And crucially, that you place that in the context

of the electrolytes more generally,

meaning sodium, potassium, and magnesium.

Someday there will be an online program or an app,

I imagine, where one could put

a bunch of different parameters in about,

their particular health status, their particular diet,

their particular exercise, et cetera.

Maybe it would all be run by AI algorithm or something

where it would monitor all of that for us.

And then it would spit out for us a precise amount

of sodium that we should take in each day.

Unfortunately, no such tool or device exists right now.

And so all of us have to figure out

the appropriate amount of sodium intake for ourselves.

And that has to be done

under these contextual considerations.

Who knows?

Maybe one of you will design such an app or such a device.

I think it would be very useful.

If nothing else, today’s discussion ought to

illuminate the fact that some strict recommendation

of salt intake cannot be made universally

across the board for everybody.

There’s just simply no way that could be done.

And yet, I think most of what we’ve learned about salt

in the general discussions around health

are that it’s this evil substance.

Nothing could be further from the truth.

It’s an incredible substance.

Our physiology is dependent on it.

Our cognition is dependent on it.

Indeed, our mental and physical health

and our performance in essentially all aspects of life

is dependent on it.

And I hope I’ve been able to illuminate

some of the beautiful ways in which the brain

and the bodily organs interact

in order to help us regulate this thing

that we call sodium balance.

And the fact that we have neurons in our brain

that are both tuned to the levels of salt in our body

and positioned in a location in the brain

that allows them to detect the levels of salt in our body

and to drive the intake of more or less salt

and more or less fluid and other electrolytes

really just points to the beauty of the system

that we’ve all evolved

that allows us to interact with our environment

and make adjustments according to the context

of our daily and ongoing life.

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