Using Salt to Optimize Mental & Physical Performance | Huberman Lab Podcast #63

- Welcome to the Huberman Lab Podcast,

where we discuss science and science-based tools

for everyday life.

[authoritative music]

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 are 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 a lot of information

and actionable items.

I'm pleased to announce

that I'm hosting two live events this May.

The first live event will take place

in Seattle, Washington on May 17th.

The second live event will take place

in Portland, Oregon on May 18th.

Presale tickets for these two events are now available

at hubermanlab.com/tour.

I should mention that

while I do hope to visit other cities in the near future

to do more live events,

right now,

these are the only two live events I have scheduled,

at least for the six months,

so once again, if you go to hubermanlab.com/tour,

you can access the presale tickets.

I hope to see you at these live events,

and as always, thank you for your interest in science.

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 Bohorquez' lab

at Duke University.

The Bohorquez 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 this 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 Bohorquez 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 Bohorquez 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,

nonartificial, noncaloric 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, noncaloric 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 noncaloric 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 of 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 would, 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 noncaloric 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 Bohorquez 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 Bohorquez 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 where 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.

Our first sponsor is Athletic Greens, now called AG1.

I've been taking AG1 since 2012,

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The reason I started taking AG1

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I try and eat really well, but I'm not perfect about it,

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The probiotics are particularly important to me

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important for immediate and long-term health,

things like immune system function,

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I believe in ingesting appropriate amounts of salt,

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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,

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'll 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 couple 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 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,

so the estimates vary,

but anywhere from 1/3 to maybe even 1/2

or even 2/3 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,

so 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 holes in it,

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

and substances can move freely in

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 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 cerebrospinal 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 cerebrospinal fluid.

There are 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 onto urine,

to hold onto 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 of 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 cerebrospinal 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 in one another

about what's happening out there.

They're not saying, "Psst!

"Hey, there's too much salt in the bloodstream.

"Let's do something about it."

All they receive are 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,

organum vasculosum of the 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 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, with 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's 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 onto its fluid stores.

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 onto 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.

The 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 nonmonogamy

in a species of animal called the prairie vole.

You can check out that episode.

I believe vasopressin in the nonmonogamous 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 supraoptic 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 MD,

an MD, excuse me,

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,

prehypertension, 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.

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.

It's a 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 the 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 in 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.

There are a lot of data in here, but is Figure 1,

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 2 grams per day,

but then continues to go down

until about 4.5

to 5 grams per day

that, 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 7 to 8 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 2 grams per day,

you run fewer health risks,

but the number of risks continues to decline

as you move towards 4 and 5 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 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 1/2 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 nonprocessed 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 are 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 hazard,

low incidence of hazardous outcomes,

cardiovascular event, stroke, et cetera,

but the ingest, according to that plot,

the ingestion of 4 or 5 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 100 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

and 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,

asked 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 anec-data,

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 6 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'll put a link to this in the caption show notes,

so that's not just in the U.S.

The salt recommendations

from the Canadian Cardiovascular Society

are 10,000 milligrams of salt per day,

so 4 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, 'kay?

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, a'ight?

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, nonprocessed 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 I, 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 hyperneurotic,

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 underhydrating,

but not just underhydrating

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've 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 counterargument that,

ah, you need to follow these strict recommendations

is 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 now a 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 9 grams per day

or 6 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 a big surprise of these results

is that whatever the level of salt that was consumed,

sodium was stored and released from the subjects' 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 regulates 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 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, right?

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 dependent, is not as dependent on external water

as once believed, right?

What this 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.

Haven't talked too much about this,

and there are several very good books

about the history of salt.

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 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 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 noniodized 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 common, 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 they actually taste 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 from,

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're 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.

It 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, 'kay?

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 stressful relationships,

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, prehypertensive,

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,

'cause 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 a 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

and 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, 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,

LMNT, 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,

and 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

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, and 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,

or, 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 1:00 or 2:00 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 nonfood intake part of time-restricted feeding,

that I'm making sure to get enough salt,

either in the form of something like LMNT,

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 1 1/2 times as much water,

so let's say you have an 8-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 1/4 teaspoon

is going to really start to move that number

up towards that range that's still within the safe range,

but you're going to, 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 DiNicolantonio.

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.

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 8 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 1 1/2 times

to double the amount of sodium

that's currently recommended in most circles,

and then, what this corresponds to

is about 1 1/2 to 2 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 specific health issues.

Now, what was also interesting is

he pointed to a sodium-to-potassium ratio,

which is 4 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,

4 grams of potassium.

You might think, "Well, gosh,

"that's 1 1/2 to 2 times the current recommendation,"

but we can go back to that study

that was mentioned earlier in the episode,

that 2011 study,

where I describe 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. DiNicolantonio passed along to me,

and then, they increased quite,

those health risks increased quite substantially

as one moves out past 6 grams of sodium,

7 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 noncaloric 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 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 Zuker Lab,

Z-U-K-E-R, Zuker 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 seed 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 are 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 or 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,

but 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 afterimage

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 afterimage 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 commonplace 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 have 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 Zuker 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 nonoverlapping 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 taste 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 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 key to a 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 home 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.

Now, 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,