Welcome to the Huberman Lab Podcast,
where we discuss science
and science-based tools for everyday life.
I’m Andrew Huberman,
and I’m a professor of neurobiology and ophthalmology
at Stanford School of Medicine.
Today, we are discussing cannabis,
also referred to as marijuana.
Cannabis includes many different compounds
that have profound impact on the brain and body.
So while many of you have probably heard of THC,
there are also compounds in cannabis
such as CBD, and of course,
there are different types or strains of cannabis,
including sativa strains and indica strains
and hybrid strains.
And believe it or not,
nowadays there is also an entire literature,
meaning a scientific and medicinal literature
about type 1, type 2, and type 3 strains.
I’ll explain what all of that is and how they work.
I’ll talk about some of the medicinal applications
of different strains of cannabis
and combinations of cannabis strains,
as well as some of the potential health hazards
of cannabis use.
I want to emphasize that any discussion about cannabis
has to be framed within the context
that the legality of cannabis varies tremendously
depending on where you are in the world.
So depending on which country you’re in
and even which state you’re in
or which area within a country,
possessing and using and certainly selling cannabis
can be either highly illegal or entirely legal
or decriminalized or largely overlooked.
You, of course, are obligated to know
what those local laws are for you,
where you live and where you travel.
With that said, today’s discussion really will include
a full picture as to where cannabis
and the various and even very specific compounds
within cannabis can be extremely useful
in the treatment of some ailments
and where certain compounds in cannabis
can be extremely dangerous for certain individuals to use,
in particular, individuals that have preexisting
genetic propensity for psychosis.
That theme is going to come up again and again,
but we are also going to talk about the role of cannabis
in anxiety, in depression,
both positive and negative effects.
We’ll talk about sex differences
in terms of women versus men
and how they react differently to cannabis.
And I would be entirely remiss
if I didn’t include a conversation about cannabis,
meaning THC, CBD, hybrid strains, et cetera,
in creativity and different modes of thinking
because as many of you probably know
or at least have heard about,
cannabis can impact the way that we think,
the types of memory systems we can access,
and what’s called convergent and divergent thinking,
which is one way of conceptualizing
what is commonly referred to as creativity.
So today’s discussion is going to include
a lot of information,
but I promise to make it clear and accessible to all of you,
regardless of whether or not you have a background
in biology or not.
And today’s discussion will also be quite nuanced.
You’ll find me routinely reading directly
from specific research papers,
something that of course we always do on this podcast.
But today I’m really going to dig into
some of the finer points of the methodology in papers
and some of the statistics that were used
and the specific populations of people that were studied.
Because as it turns out,
there are instances that we will discuss
in which the use of cannabis
can be immensely beneficial to one group
and yet can be entirely detrimental to another group,
even at equivalent dosages
and depending on a number of different factors.
So we will discuss what those factors are.
Just to give you a brief overview
of the kind of structure I’m going to put on today’s episode,
we will review, of course, cannabis and its various forms.
I’ll talk about some of the biology,
but we are going to really drill into how dosage,
that is the concentration of THC relative to CBD,
impacts whether or not cannabis
is going to have one effect or another.
We will also talk about the frequency of use,
daily use, multiple times per day use,
weekly use or monthly or occasional use,
we will also talk about different professions
and how some people may have a little bit more leeway
in terms of whether or not they decide to use cannabis
or any of its various component chemical constituents,
that is CBD or THC, et cetera.
And for other professions,
it might be entirely inappropriate
because of the particular kinds of cognitive tasks
those professions demand.
We will also talk about genetic predisposition,
again, sex differences, hormone effects.
And I will also touch on
what I think is the most important variable
in determining whether or not cannabis
is right or wrong for you.
And that is your age at which you are considering
starting or continuing use or ceasing use.
What I can assure you
is that by the end of today’s podcast,
you will have a quite thorough understanding of cannabis,
how it works, what it does,
what its potential benefits can be,
what its potential hazards are,
and whether or not it’s right for you
and the people that you know.
Before we begin,
I’d like to emphasize that this podcast
is separate from my teaching and research roles at Stanford.
It is, however, part of my desire and effort
to bring zero cost to consumer information about science
and science-related tools to the general public.
In keeping with that theme,
I’d like to thank the sponsors of today’s podcast.
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Let’s talk about cannabis.
And when we refer to cannabis,
we are indeed referring to marijuana or the marijuana plant.
Now, cannabis plants come in different strains
or different varieties.
And those different strains
are indeed different genetic strains.
So just as animals and humans
have different genetic backgrounds
and they can be crossed to one another
to yield further genetic variation in the offspring,
plants can be hybridized to one another
in various ways through grafting
or through the use of different types of seed combinations,
et cetera, in order to generate different strains.
There are also naturally occurring differences
in the strains of plants,
and the cannabis plant is no exception.
So for instance, in the context of a discussion
about cannabis and its medicinal uses
and recreational uses,
we need to distinguish between the sativa variety,
the indica variety,
a variety called ruderalis that’s not often discussed,
and hybrids of sativa, indica, and ruderalis.
Before diving into the different strains of cannabis
and how they impact the brain and body
both similarly and differently,
I want to emphasize that the cannabis plant
contains a number of different psychoactive compounds.
Now, the most powerful of those compounds is THC.
The technical name for it
But THC, as I’ll refer to it,
is just one of the psychoactive
and biologically active compounds within cannabis plants.
There’s also CBD,
which is technically referred to as cannabidiol,
and cannabidiol, CBD, is known to be used
for things like pain management, anxiety management,
and other medicinal purposes.
We will talk about the efficacy of CBD for those purposes,
as well as some of, believe it or not,
some of the dangers of CBD,
depending on where it’s sourced and the dosage, et cetera.
So we’ve got THC, CBD, and also CBN, or cannabinol.
CBN is less often discussed.
You’re going to hear a lot less
about CBN-containing products out there,
but it is relevant to today’s discussion,
so it will come up a bit.
Now, I will be sure to provide more specificity
to what I’m about to say,
but very broadly speaking,
THC is largely responsible
for the psychoactive effects of cannabis.
That is the changes in mood,
the changes in bodily state and sensation, et cetera.
Whereas CBD, and to some extent CBN,
have profound effects on the brain and body,
but they don’t tend to give people the sensation
of altered perception, altered mood, et cetera.
Some people might say they are not the component of cannabis
that quote-unquote gets you high.
Although today we will really drill
into what the high itself represents
in terms of chemical systems in the brain and body.
And what we will soon learn
is that what we think of as being high
actually includes a number of different changes
in the brain and body,
some of which can be best explained by CBD, not by THC,
which runs counter to what most people out there
know and believe.
So broadly speaking, we have THC, CBD, and CBN,
but I want to point out that the cannabis plant
has over 70, seven zero,
70 different psychoactive compounds,
many of which still have not been studied
in isolation and in detail.
So there’s a big future of research for cannabis
and for THC and THC-related psychoactive compounds,
as well as for CBD and CBN.
Today, we’re mainly going to focus on THC and CBD,
as I mentioned before.
I should also point out that the cannabis plant
has over 400 biologically active compounds.
So these are biologically active compounds
that may or may not have psychoactive properties,
that may or may not be useful for pain relief, et cetera.
Again, there is a vast landscape for exploration
of the cannabis plant and of hemp
for what they include that could be beneficial to us
or detrimental to us.
So again, a lot more work to do.
Today, we’re going to really try and stay on target
with what we already know
and where there are certain exciting mysteries
or intriguing mysteries about what we ought to explore more.
I will certainly highlight those.
Let’s go back to the different strains
of the cannabis plant, sativa, indica, and ruderalis,
and explore how each of those
differentially impacts the brain and body.
Because therein, I think we can start to learn
a lot about this incredible plant
that is the cannabis plant.
And whether or not you are a user of cannabis
or whether or not you are entirely opposed to cannabis use,
understanding how cannabis works in the brain and body
itself is absolutely fascinating
and can teach you a lot about how your brain and body work
at a basic level,
and can tell you a lot about how your brain and body
will react to different life events
and how your mood is established and stabilized
and how your appetite is established and stabilized,
and so on.
So we have the three major strains of cannabis,
sativa, indica, and ruderalis.
And for sake of today’s conversation,
we can pretty much cross off ruderalis.
It’s not often consumed,
and components of ruderalis are not often consumed
for medicinal or recreational purposes.
Let’s focus on sativa and indica.
People will consume the sativa variety of cannabis
either by edible or by smoking cannabis,
or they will consume the indica variety of cannabis,
again, by edible or by smoking cannabis,
or sometimes they will take it in a transdermal form
or a sublingual form.
There are a bunch of different ways
to get the cannabis into the body,
but there’s a clear distinction between sativa and indica
that actually shows up first in the structure of the plant.
At their extremes, meaning in a pure strain of sativa,
it tends to be a taller plant,
a longer stalk, believe it or not.
And actually the length of the leaves
is quite a bit longer.
Whereas the indica plant tends to be more short and stout.
And for those aficionados out there,
I’m sure you know a lot of the other specific features
of sativa versus indica.
But already what we’re talking about
is the same plant, cannabis,
with two very different morphologies or shapes.
You might say, well, why is this interesting
or important to how it affects me
or affects other people
for medicinal or recreational purposes?
Well, it turns out that even though they are the same plant,
these two different genetic varieties,
because of the way that they grow
and the way they capture sunlight,
and the way, believe it or not,
that the different plants within that strain
interact with one another,
because believe it or not,
plants are interacting with one another,
they actually bring different elements
of the psychoactive compound to different components
within the leaves and the so-called buds.
The takeaway is that when consumed,
and when I say consumed, I want to be very clear,
I don’t necessarily just mean oral consumption
or eating cannabis sativa by edible.
I also mean smoking it,
and that could be, you know, people will,
just like with tobacco,
the way that they bring the psychoactive components
into their bloodstream and into their brain and body
is to essentially heat the dried leaves
of the cannabis plant.
Then the heat liberates
some of the psychoactive components
that when inhaled into the lungs,
because the lungs include a lot of vasculature,
a lot of basically blood vessels and capillaries,
that the psychoactive components
are actually directly absorbed
from the lungs into the bloodstream,
and they can cross into the bloodstream
and permeate throughout the body
and cross the so-called blood-brain barrier.
So in other words,
burning the plant liberates the smoke
that contains the psychoactive compounds,
and those are inhaled into the lungs
and then get into the brain and body
and act on the brain and body.
And the major effect of sativa varieties
are to create a high, if you will,
and I’m putting this in air quotes
for those of you that are listening,
but to also act as a stimulant.
The sativa varieties tend to make people
feel kind of invigorated, somewhat alert.
It doesn’t tend to be as much of a sedative
as some of the other varieties.
Some people report heightened sense of focus
or heightened sense of creativity.
We will talk a little bit later on
as to whether or not they actually
are achieving heightened levels of focus and creativity
or whether or not they just perceive themselves
to have heightened levels of focus and creativity.
The sativa varieties tend to make people
feel a little bit less susceptible
to pain and noxious stimuli,
which are basically stimuli that you don’t like.
So the sativa varieties are often prescribed
or are used in the recreational context
for pain management and relief.
Basically, the sativa variety is known to include
a sort of head-biased effect.
So here we’re talking about subjective effects.
And of course, these will vary
from one individual to the next.
Some people will smoke cannabis sativa
or ingest cannabis sativa orally,
and will feel an entirely different array of effects.
But most people, the majority of people
experience a sort of head-centered, high alertness,
focus, and a sense that they’re more creative.
Contrast that with the indica varieties of cannabis.
And when people smoke or eat or ingest indica varieties,
the psychoactive components of indica,
and again, this is pure indica,
so not hybridized with sativa at all,
but just pure indica,
tend to lead to more full-bodied effects.
People report feeling more complete full-body relaxation,
more of a sedative effect.
Indica cannabis is often prescribed
and or used recreationally in order to achieve
a state of sleep or to help relieve anxiety.
So less of a stimulant effect.
And we will talk about why,
literally the underlying neural circuits
that lead to the sativa variety,
causing more of a elevated mood and a head high, if you will,
and the indica varieties being more full-body relaxation.
One of the ways to remember the distinction
between the effects of cannabis sativa and cannabis indica
was relayed to me by a friend who actually was a chronic,
meaning every day, all day,
consumer of marijuana.
He basically smoked marijuana for 20 years
before quitting about four or five years ago.
And he said that indica is often referred to as in the couch,
meaning laid back in the couch.
And that can help you remember
that the indica varieties of cannabis
do tend to be more sedative in their effects.
Okay, so there’s sativa and there’s indica,
and then now there are hybrid strains.
So marijuana growers and people who specialize
in creating novel varieties of the cannabis plant,
again, I’m using the words cannabis and marijuana
more or less interchangeably here.
They are very good at creating new strains of plant
that might be 25% sativa and 75% indica or vice versa,
or 50-50 or 90-10.
Essentially what’s happening nowadays
is that through plant biology, plant genetics, I should say,
growers are getting quite efficient
at creating a variety of different strains
of the marijuana plant that give rise to very nuanced
and distinct effects on brain and body.
In fact, so much so that there’s now a new nomenclature,
a new language emerging around cannabis
and the development of novel strains of cannabis
for medicinal and or recreational purposes.
And while this might sound a little bit medical
or a little bit clinical to some people,
believe it or not, this is the nomenclature
that’s now typically used.
People still refer to the sativa, indica,
and hybrid strains, but there’s now also a description
of so-called type one, type two, and type three strains
for any given sativa, indica, or hybrid strain, okay?
So just to put this clearly in your mind,
you’ve got sativa varieties, that is pure sativa varieties.
You have indica varieties, again, pure indica,
and then you have hybrid varieties.
And beneath each of those, you have type one, type two,
and type three strains of indica, sativa,
or hybrid varieties.
What are type one, type two, and type three?
Well, type one, type two, and type three strains
are strains that have varying amounts
or ratios of THC to CBD.
So for instance, type one strains,
so for instance, you could have a pure sativa type one,
or a type one pure sativa, or a type one indica.
Those are going to have the greatest amount of THC
relative to CBD.
And I really want to emphasize this,
understanding the ratio of THC to CBD
can help explain a lot or even predict a lot
about how a given strain of cannabis will impact somebody.
For instance, because THC is largely responsible
for the typical psychoactive components of cannabis.
So what I mean here is if somebody’s ingesting sativa
and it routinely makes them feel more energized,
elevates their mood,
gives them a heightened sense of creativity,
if that’s what they experience,
and they’re taking a type one version of that,
that means that it’s quite rich in THC and very little CBD.
However, if they were to take a type one version of sativa
and it feels far too strong, like too much energy,
or they felt like there were too much in their head,
nowadays, there are strains of sativa
that have been genetically engineered.
And I don’t mean by an engineer tinkering away
with gene engineering in a kind of CRISPR creating mutants,
but literally by hybridizing,
crossing different plants to one another, okay?
Creating in a natural context,
the same way plants in the outside world
would sometimes hybridize to one another.
Creating a variety that’s perhaps type two,
which is going to have less THC and more CBD,
or a type three, which is going to be very high CBD
and very little THC.
And the same is also true for the indica varieties.
So I want to make sure that everyone understands this
because it becomes very important
for understanding the biology of cannabis
and predicting positive versus negative effects of cannabis.
Sativa has this kind of stimulant-like effect
and tends to be more of a head high, if you will.
Indica tends to be more full body
than lead to more in the couch,
as I referred to it before, pun intended.
Deep relaxation, reduced insomnia, et cetera.
Now within each of those sativa and indica,
you have type one, type two, and type three.
And that has everything to do with how much THC,
which is the dominant psychoactive compound,
versus CBD, which has other effects mainly on the body,
but not so much on the brain
and modes of thinking and mood, et cetera.
How much THC versus CBD is present.
And again, type one is THC dominant,
type two, kind of equal ratios, if you will,
of THC and CBD and type three tend to be high CBD.
Okay, so already we’ve got some categorization here
that hopefully isn’t overwhelming to you,
but this turns out to be extremely important
if you want to understand how cannabis works
and predict the effects of cannabis.
Okay, so somewhat surprisingly,
we’re going to set aside cannabis.
We’re going to take what we know about sativa, indica,
type one, type two, type three, CBD, et cetera.
We’re just going to set that aside for a moment.
Why would we do that?
Well, we have to ask ourselves,
why would any of these plants,
why would any of these compounds, THC, CBD,
sativa, indica, et cetera,
why would any of that have any effect on us at all?
And this discussion that we’re about to have
very much resembles the discussion that we had
on a previous episode about nicotine.
Because as many of you know,
nicotine is a commonly used substance.
In fact, if we were to look at
the three most commonly used drugs,
alcohol will be at the top of the list.
Many billions of people regularly use alcohol
or occasionally use alcohol.
Many billions of people also use nicotine.
It’s the second most consumed drug.
So more than 1 billion
and probably closer to 2 billion people consume nicotine.
And then the third most consumed drug
is cannabis in one form or another.
And many of you are probably shouting,
what about caffeine?
What about caffeine?
Well, in the context of drugs
and in particular addictive drugs,
caffeine doesn’t quite rise to the list.
But if we were to look at caffeine
and include in that list,
caffeine would be above all of those.
Okay, but the most commonly used drugs are alcohol.
Second after that is nicotine and then cannabis.
Nicotine, as some of you may know,
if you listened to the episode on nicotine,
but even if you didn’t,
nicotine comes from the tobacco plant.
And there are a few other plants that include nicotine.
And typically it’s brought into the brain and body
by smoking tobacco, dipping tobacco, snuffing tobacco,
or vaping nicotine.
Nicotine exists in the outside world in these plants,
the tobacco plants.
But the reason it has an effect on the body
is that there are so-called nicotinic receptors in the body.
Now those nicotinic receptors were named
after nicotine, the compound,
but they existed in the brain and body,
not because of the existence of a tobacco plant,
but because there are other chemicals in the body
that naturally occur, namely acetylcholine,
that bind the nicotine receptor.
Those chemicals such as acetylcholine
that bind the nicotinic receptor in your brain and body
create an enhanced sense of focus, et cetera, et cetera.
But nicotine from tobacco binds that same receptor,
but with much greater affinity
and therefore also creates a state of focus,
but a much greater one than we can achieve without nicotine.
Okay, so you can see the nicotine episode
if you want to learn more about that.
In a very similar way, all of our brains and bodies
from the time that we are conceived, believe it or not,
very shortly after conception, if we want to be accurate,
very early conception, when you were in the womb
and still now, if you’re listening to this,
you have what are called cannabinoid receptors
because you also have endogenous cannabinoids.
What do we mean by that?
You have receptors which are like little parking spots
that are present on cells in your brain and body.
And what we call a ligand,
which is basically just a chemical that’s released,
parks in that receptor
and causes a number of different biological effects.
Cannabis contains compounds
that also bind to those receptors.
But here I want to make a really clear distinction.
We have what are called endogenous ligands.
Those that just mean chemicals from within us
that we make naturally,
even if we never go near the cannabis plant
or any other source of cannabis,
we have chemicals that are created in us
that park in those receptors
and cause biological effects on mood, on perception,
on the immune system, on hunger, et cetera.
Again, without ever going anywhere near cannabis,
we have these endogenous cannabinoids.
Endogenous cannabinoids are floating around in us
or I should say they are released in us in particular ways,
bind to these receptors and cause changes in mood,
appetite, et cetera.
They have many different effects on the brain and body.
We will talk about those.
But just like with nicotine,
there are substances in the outside world.
In this case, cannabis contains these substances.
So things like THC and like CBD
that when ingested by smoking or vaping
or by ingesting edibles
also will park in those same receptors,
the cannabinoid receptors and lead to biological effects.
Now it’s a little bit misleading
because we call them cannabinoid receptors
as if they were there to bind cannabis.
Or just like we call the nicotine receptors
it makes it seem as if they were there
in order to bind nicotine from tobacco.
But that’s not the way our brains and bodies evolved.
Our brains and bodies evolved for these receptors
to make use of chemicals that exist within us
called, again, endogenous chemicals.
And those endogenous chemicals lead to certain effects,
as I mentioned before.
The key thing here,
if you haven’t understood anything I’ve said up until now,
please understand this.
The key thing is that THC and CBD
and the other components of cannabis
bind to those receptors,
those endogenous cannabinoid receptors,
the ones that we naturally make,
with much greater affinity
and exert a vastly greater potency
and effect on mood and perception, et cetera,
than do our endogenous cannabinoids.
Another analogy that one could take
in order to understand this
would be hormones like testosterone and estrogen.
Many people, I would say all people,
make testosterone and estrogen to varying degrees.
It’s going to depend on whether or not you’re male, female,
your age, whether or not you’ve gone through puberty,
et cetera, et cetera.
But let’s just take testosterone, for example.
There is testosterone circulating in your body.
That’s true if you’re male or female.
And there are receptors called androgen receptors.
We could even call them testosterone receptors.
And the testosterone binds to those receptors
and has effects on cells.
It causes hair growth, changes the voice.
It can affect libido.
It affects all sorts of things in the brain and body,
depending on which organ and tissue you’re talking about.
But of course, there are people
that take synthetic testosterone
or derivatives of testosterone.
And some of those derivatives, for instance,
in the bodybuilding community, in the sports community,
they will take things like Dianabol.
These are modified versions of testosterone
that can bind to the testosterone receptor
with much greater affinity,
or I should say the androgen receptor,
with much greater affinity
and have supraphysiological effects,
effects that would essentially never be seen
from testosterone that was endogenously, excuse me,
endogenously released within the body.
We could say the same thing for estrogen.
There are estrogen receptors, they bind estrogen, okay?
But if someone were to take synthetic estrogen
or to ingest a plant compound
that contains various estrogenic compounds,
and those plants certainly exist out there,
they can have supraphysiological effects on those receptors.
Why am I telling you this?
Well, many people believe that because cannabis,
marijuana is a plant, and plants grow out of the ground
and they’re naturally occurring,
and because we have receptors in our body
that are there without the need to engineer them
from some external source, right?
They’re in our genome, it programmed for it,
and we’re born with these things
and we keep these things our entire life.
Many people mistakenly think,
ah, you know, these plant compounds are safer for us
or better for us or are somehow appropriate
for us to ingest, but that’s simply not true.
And here I’m not saying that cannabis
is always a bad idea for people.
There are certain populations and certain people
for which it can be relatively safe recreationally,
that’s the truth, and there are other populations
for which it can be downright dangerous
recreationally or medicinally.
And of course, there are medicinal purposes
that are being explored and we’ll talk more about that.
But this is vital to understand
because I think that when we hear,
oh, it’s from a plant, it’s natural,
and then you also have a receptor
for these endogenous cannabinoid receptors,
and therefore the marriage of those two, right?
The coming together of the chemical THC or CBD
or both with these receptors is somehow supposed to happen
as if this was a purpose of having these receptors,
but it’s simply not the case in the same way
that the nicotinic receptors are not there
because nicotine is good for us.
They’re there because there are compounds
that exist within us that are good
to bind to those receptors from time to time.
Now, here’s the key thing about,
I guess today I’m saying there are a lot of key things,
but here’s another key thing about understanding cannabis
and the way that it works,
which is that THC and CBD,
when they’re brought into the brain and body
by smoking or edible, et cetera,
they bind to those receptors,
those endogenous cannabinoid receptors,
and they tap into the same systems
that your endogenous cannabinoids would tap into,
the ones that affect mood and energy
and creativity and relaxation, et cetera,
but they do so with thousand-fold greater potency.
And as a consequence of that,
your endogenous cannabinoids are out-competed.
They really get no opportunity
to interact with those receptors.
And understanding that can lead
to a very clear understanding of why, for instance,
when people use cannabis to relieve anxiety
or they use cannabis to enter a certain brain state
for creativity or to enter sleep,
why a dependence on cannabis starts to emerge.
Because if they don’t ingest cannabis,
and again, ingest could mean smoke,
to bring THC in or CBD in or ingest orally
or even transdermal or tincture
or one of the other varieties.
If they don’t do that,
then what happens is not only are the receptors
not stimulated to the same degree
or with the same potency that they normally are,
but the endogenous cannabinoids
can no longer have their effect.
So people experience heightened levels of anxiety,
disrupted mood, disrupted brain state, and so on.
Now, again, I want to be very clear
that I’m not trying to paint a picture of cannabis
as all bad or even partially bad.
What I want to do today is give you
as much information I can as to how cannabis works,
how its different component parts work,
how the different types of cannabis work,
and point to some of the valid medicinal uses
and some of the recreational uses,
and then lay out the landscape for you
as to who is really most at risk
in terms of psychoactive components,
immune components, and so on and so forth
so that you can make the most informed choice for you.
I am not here to tell you what to do or what not to do.
As I like to say, do as you wish, right?
I mean, don’t do as you wish
if it harms other people or yourself,
but do as you wish, but know what you’re doing.
So that’s really my goal here.
So as we begin to dive further into the biology,
I think you’ll start to get a clearer picture
of why cannabis is so effective in some contexts,
but also why it can create such massive suffering
in other contexts because of the way
that it out-competes
your own natural endogenous cannabinoid systems.
So let’s talk about those endogenous cannabinoid systems,
what they are and how they work,
because that will give us a lens
into what the higher potency or maximum impact
of the various cannabis plant varieties and strains
and THC and CBD and so forth, how and why those work.
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So what are the endogenous cannabinoids,
these chemical substances that everybody makes?
You make them, I make them.
You’ve been making them basically
from the time that you were conceived,
and you are going to make them until the time that you die.
Whether or not they have the impact
and the biological functions that I’m about to describe
will depend a lot on whether or not
you are using your own endogenous cannabinoids
to park in those receptors that you also have
from birth until death,
or whether or not you are tickling those receptors
or strongly activating those receptors
using some external source like cannabis, THC, et cetera.
The two main endogenous cannabinoids
that we want to consider are anandamide,
which we refer to as EAE, so anandamide,
and another one, which is arachidonoylglycerol,
arachidonoylglycerol, which we will abbreviate 2AG.
So let’s just take EAE and 2AG, lump them together,
and talk about the endogenous cannabinoids
just to make it simple.
But if you want to do the deep dive on anandamide
versus 2AG, please be my guest.
The endogenous cannabinoids are released from neurons.
What are neurons?
Neurons are nerve cells,
and nerve cells should be conceptualized like this.
You have presynaptic neurons and postsynaptic neurons.
Presynaptic neurons basically contain little vesicles,
little bubbles full of neurotransmitter,
which are chemicals,
and when neurons are stimulated electrically,
and that could be from a thought,
it could be from the desire to move,
it could be because of a drug,
it could be because you’re hungry,
the relevant neurons will vomit out
or will fuse, as we say, those little packets,
those little bubbles of neurotransmitter
into the gap between the pre- and postsynaptic neuron.
We call that a synaptic cleft or the synapse.
It’s a little gap, a little space,
and the neurotransmitter flows across that synapse,
and some of it will park in little parking spots
that we call receptors on the postsynaptic neuron side.
Depending on which neurotransmitter it is
and a bunch of other things,
not worth going into right now,
the parking of that chemical
in those neurotransmitter receptors
will either cause that neuron on the postsynaptic side
to itself release neurotransmitter elsewhere,
or it will quiet it down,
so-called excitation and inhibition.
That’s kind of neurotransmission in a nutshell.
If you don’t understand it, no big deal.
It’s not going to prevent you
from understanding today’s discussion.
If you understand even a small fraction
of what I’ve just said,
then it’s going to allow you to understand
not just today’s discussion, but a lot of neuroscience
with a lot more nuance and depth of understanding.
The key thing to know about the endogenous cannabinoids
is that unlike most neurotransmitters,
they are released from the postsynaptic side.
So what happens is neurotransmitter
goes from presynaptic neuron to postsynaptic neuron,
but under certain conditions,
the postsynaptic neuron itself releases a chemical,
and that chemical goes backward,
what we call retrogradely to the presynaptic neuron,
binds to receptors there and changes the probability
that the presynaptic neuron will release neurotransmitter.
Put simply, endogenous cannabinoids
tend to decrease the probability
that a neuron will release neurotransmitter.
They are sort of a break on the system.
They are a way of shutting down
the communication between neurons, regulating it,
not to make it completely quiet,
but to adjust the levels with a lot of nuance.
Now, the other thing that the endogenous cannabinoids do
is sort of a mind bender,
because we’re talking about cannabis
and a commonly known feature of cannabis
and marijuana consumption
is disruptions in short-term memory.
And there is essentially zero debate
as to whether or not that occurs.
And we’ll talk about the mechanisms a little bit later.
And yet, endogenous cannabinoids,
the chemicals that you naturally release
from these postsynaptic neurons
that travel retrogradely back to the presynaptic neuron
actually can lead to strengthening of connections
between the presynaptic neuron and the postsynaptic neuron
through a process called long-term potentiation or LTP.
They can also cause what’s called depression
of communication between a presynaptic neuron
and a postsynaptic neuron.
Long-term depression has nothing to do with depression
as a psychological state or as a illness.
Long-term potentiation and long-term depression
simply refer to the probability that one neuron
will be able to stimulate and activate another neuron.
And as I just told you,
the endogenous cannabinoids can either turn up the dial
or turn down the dial.
They can either increase the probability
or decrease the probability
that a given connection between neurons
will function more or will function less.
So if you think about the communication between neurons
as a crosstalk, as a conversation,
well, the endogenous cannabinoids
can dictate whether or not that conversation
is likely to occur or not to occur.
Think of them as either putting someone
at the top of your text chain in your phone,
which would be long-term potentiation,
or essentially blocking their number,
which would essentially be long-term depression.
So if you’re getting the impression
that the endogenous cannabinoids
are working in a number of different ways
and it’s not very straightforward, you’re right.
In fact, that’s the message that I’d like you to take away.
The endogenous cannabinoids
are sometimes increasing neuronal communication.
This can lead to increases in mood
or increases in the likelihood
that someone will talk a certain way
or behave a certain way or feel a certain way.
They can also lead to decreases in synaptic transmission,
that is communication between neurons,
in ways that will make somebody’s mood lower
or will make them less hungry or more hungry.
And here’s the really key thing.
There are two kinds of endogenous cannabinoid receptors
referred to as CB1 and CB2.
And we can say with confidence
that CB1 is highly enriched in the nervous system
and especially within the brain.
It’s found not everywhere,
but almost everywhere in the brain
and elsewhere in the nervous system.
So spinal cord and other aspects of the nervous system.
CB2, the cannabinoid receptor,
CB2 is largely located in the tissues of the body,
including the immune system, the liver,
even the genitals, et cetera.
So what this means is that the endogenous cannabinoids
are having these sorts of effects
on neurons that I talked about,
but they are also having effects on immune cells,
on reproductive organs, on liver, on digestion,
on hunger, et cetera,
through mechanisms that are divorced
from the function of the nervous system of neurons.
Now, in reality, no system of the brain and body
is divorced from the nervous system
because the nervous system is controlling everything.
It was really the master controller
and everything’s feeding back to the nervous system.
So it’s a two-way street.
But the simple way to think about a CB1 receptors
are mainly in the nervous system
and CB2 receptors are mainly in the body
and endogenous cannabinoids.
Again, EAE, anatomide, and 2AG, arachidinoyl glycerol
are impacting CB1 and CB2 receptors.
Today, we’re mainly going to talk about CB1 receptors
because they are the ones that are responsible
for most of the familiar effects of cannabis.
But the key takeaway at this point
is to really understand that the major effects
of your endogenous cannabinoids on these receptors,
in this particular CB1, are very nuanced.
It depends on context, it depends on which neurons.
Sometimes increasing communication between neurons,
sometimes decreasing it.
And then along comes cannabis.
And that cannabis, again, can arrive by smoking,
by vaping, by edible.
And cannabis contains THC and CBD
that potently bind the CB1 receptor.
And now the effects of the CB1 receptor
being occupied by THC or being occupied by CBD
are not very nuanced.
In fact, they are very predictable.
And especially important is to understand
that they are so strong,
and they park in that receptor with such affinity,
with such force and precision and stubbornness
and refusal to leave that receptor,
that they completely outcompete
the endogenous cannabinoid system.
In fact, they leave the endogenous cannabinoid system
which in some cases may be a good thing,
but in most cases is going to lead to problems
of various kinds.
And we’ll talk about what sorts of problems.
And again, I feel obligated to say,
this is not me saying don’t ingest cannabis or THC or CBD.
That’s not what I’m saying.
What I’m saying is, if you evaluate the potency,
that is, in technical terms,
it would be the affinity with which these compounds,
THC and CBD and CB1, bind to these endogenous receptors.
That would be like a howitzer gun, like a cannon going off,
as compared to endogenous cannabinoid,
whether or not it’s EAE or 2AG,
which is more like a cap gun level of activation,
at least in this analogy.
So now you have what, at least I would like to think,
is a fairly complete understanding
of the different varieties of cannabis,
at least at a broad sweep,
and the different biological effects that they can have,
at least in terms of the major receptors
and in retrograde signaling, et cetera, et cetera.
Now let’s take a step back into the real world.
And evaluate or think about what happens
when somebody smokes cannabis or ingests cannabis
by way of edible or tincture or something of that sort.
Cannabis is very fast to enter the bloodstream.
In fact, within 30 seconds,
it’s going to enter the brain
and permeate throughout the brain and body.
That’s very, very fast.
I mean, when you contrast that with something like alcohol
or even nicotine, depending on how the nicotine is delivered,
that is a very fast delivery of the psychoactive
and biologically active compound,
which in this case is THC and CBD
and probably some other things as well.
So within 30 seconds,
it reaches the brain and bodily tissues.
And within 30 to 60 minutes,
it’s going to reach its peak concentrations
and have its peak biological effects.
Those aren’t always the same thing,
but in the case of cannabis,
and again here, I’m using cannabis
as a kind of umbrella term for THC and CBD,
the effects are going to peak at about 30 to 60 minutes
after bringing those compounds into the body
in some way or another.
And the effects tend to last
anywhere from three to four hours,
although there’s some variation on that
depending on individual metabolism,
whether or not somebody is familiar with the compound,
believe it or not, psychologically familiar,
but also biologically familiar
or whether or not it’s a first-time use
or occasional use and so on.
THC and CBD and other components of cannabis
are highly what we call lipophilic.
That is, they have an affinity toward
and they can actually pass through fatty tissues.
Now, every cell in your body,
but especially neurons have a double layer of fat
on their outside.
And of course, when people hear fat,
they always think, ooh, fat’s bad, fat’s bad.
Most of the world seems to want to lose fat or bodily fat.
Here, we’re talking about the fatty membrane,
the barrier around each tissue.
And in this case, we’re talking particularly about neurons.
And THC and CBD and the other components of cannabis
are highly lipophilic.
So they can get into essentially all cells
just simply by flowing into them.
They will also remain in those cells for a long time.
So I know that a number of people,
depending on whether or not they get tested
for work or for sport or otherwise,
for cannabis or CBD and THC,
don’t take this as a strict number,
but typically if one ingests CBD or THC,
smokes cannabis, ingests by orally, et cetera,
it doesn’t matter.
It’s going to stay in that fatty tissue
and can be detected for at least as long
as 80 days after ingestion.
And there’s a whole industry as to
how to accelerate the clearance.
And I should just tell you that just losing bodily fat
isn’t going to eliminate it from your system,
maybe partially in those fat cells,
but certainly intravisceral fat and other fatty tissue
that’s in and around the brain and body
is going to harbor that THC molecule and the CBD molecule
for quite a long while, at least 80 days.
Okay, so if someone smokes cannabis or they ingest cannabis,
very rapidly gets into the bloodstream
and the components that are psychoactive
get into the bloodstream and are immediately able
to access neurons and other cells
and start having these effects of parking
at those endogenous cannabinoid receptors
and impacting the signaling between neurons,
which leads to the subjective effects of cannabis,
including THC and CBD.
So let’s talk about what those
different subjective effects are.
Again, this is going to vary depending on whether or not
people are ingesting sativa varieties of cannabis.
Just to remind you, those tend to be elevated,
mood, alertness, talkativeness.
People who take sativa varieties tend to talk a lot more
than they would otherwise.
Again, there are exceptions to this.
Of course there are exceptions.
I’m sure there are people out there shouting,
although I guess if you’re the quiet people
who don’t talk too much, you’re probably not shouting,
or if you’re not, you’re not doing a sativa joke intended.
But in any event, there are exceptions,
but there are also general rules.
And the sativas tend to meet people
sort of mood elevated, energetic,
again, the sort of head high.
And indica varieties tend to do the opposite,
more of a sedative, relaxant, et cetera.
Why and how would they do that?
Okay, well, without going into an extensive deep dive
into the different neurotransmitter systems
of the brain and body,
what we know for sure is that CB1 receptors
are present on an enormous number of different neurons
in brain structures and neural circuits,
so that the sativa varieties that act as sort of a stimulant
making people feel happy,
because in general, they do tend to elevate mood,
at least at certain dosages.
Talkative tend to make people feel
like they have ideas that are interesting,
that they might want to share,
tend to narrow their context,
so tend to increase focus.
This is something that’s not often discussed about cannabis,
but it can, especially the sativa varieties
can increase people’s level of focus to particular things,
something they’re watching or something they’re doing,
or music allows them to narrow their sense of focus.
That’s going to occur by activation of CB1 receptors
in the so-called prefrontal cortex,
which is just behind the forehead.
And the prefrontal cortex acts as a strong modulator
of so-called limbic circuitry and other circuitry
that is more stress-oriented.
The way to think about the stress and limbic circuitry,
such as the amygdala, which many people have heard about,
is that they aren’t really circuits for fear and stress.
They are circuits that are constantly evaluating
one’s own internal state, heart rate, et cetera,
and what’s happening externally.
And sorry to say, but the default of those systems
is to detect danger, the sort of threat detection systems.
And then the prefrontal cortex largely acts
as a brake on those systems,
sort of like the reins pulling back on a steed of horses
that would otherwise just kind of take off.
And so the sativa varieties tend to increase CB1 activation
in the prefrontal cortex and in other circuitry
that then leads to a kind of overall reduction in stress
because of the way that prefrontal circuitry
can reduce activation of the amygdala.
Now that, of course, does not explain
why some people become very stressed and very paranoid
when they smoke sativa varieties
or other varieties of cannabis
or ingest other varieties of cannabis.
We will talk about the paranoid effect
and why that occurs and who might predict
that would occur to them in a little bit.
But I just want to give you a sense of how this is working
because as I mentioned before,
THC and or CBD are going to bind that CB1 receptor,
let’s say in prefrontal cortex,
and neurons of prefrontal cortex is going to bind there.
And then there’ll be a retrograde signaling
back to the presynaptic neuron.
And in the case of prefrontal cortex,
what’s happening is it’s increasing transmission,
increasing the release of neurotransmitter
in the prefrontal cortex.
However, at the same time,
the very same THC and CBD that was brought into the system
is binding the very same type of receptors, CB1 receptors
in other brain structures, such as the amygdala
and causing retrograde signaling
back to the presynaptic neurons in the amygdala,
but it’s quieting the activation of those neurons.
So this is interesting, right?
We have the same compounds, THC and or CBD
brought into the body and brain binding the same receptors,
in this case, the CB1 receptors,
but depending on where those receptors are located
and which brain areas we’re referring to,
they are either causing heightened levels of alertness
and activation of systems that are designed
to make you talkative and alertness and mood, et cetera,
focus, or they’re causing suppression of those circuitries.
So we have kind of a seesaw effect here
where the same compound is increasing mood and alertness
and focus in the prefrontal cortex
and is decreasing stress and threat detection
in the amygdala.
And that’s one of the reasons why,
especially the sativa varieties of cannabis
allow people to enter these states of focus.
Some might even say flow,
although I don’t want to go into
what flow states really are,
that’s for a different discussion.
And it’s very poorly defined as it is.
And I certainly don’t want to give people the impression
that cannabis increases flow states
because that’s not always the case.
And certainly most often it’s not going to be the case.
But the idea here is that this molecule comes into our brain
and is shifting everything towards a state of focus,
elevated mood, of heightened sense of importance
about whatever it is that we happen to be doing.
And now, of course, whatever we could happen to be doing
could be writing a song, writing poetry,
communicating with somebody,
but it could also be something as trivial
as watching cartoons or watching a movie,
which is not trivial in its own right,
but in terms of thinking about the creative aspects
or the creativity stimulating aspects of cannabis,
not sort of productivity oriented.
So narrowed focus, elevated mood,
more relaxed and yet energetic.
That’s the major effects of the sativa varieties,
except, and this is a really big bold face,
triple underlined except, except in some individuals,
depending on dosage,
but also depending on preexisting neural circuitry
and propensity for anxiety,
some people ingest or smoke sativa varieties.
And regardless of whether or not it’s a type one,
type two, or type three variety, okay?
Regardless of the ratio between THC and CBD,
people will experience intense anxiety and paranoia.
Now, how do you predict
who will experience intense anxiety and paranoia
and who will experience intense relaxation,
focus, and sense of creativity
from ingesting or smoking a type one, type two,
or type three sativa?
Well, there is no way to predict that.
And there’s a lot of kind of what I would call street lore
or dorm room lore or kind of pure, not peer reviewed,
but sort of peer discussed,
I mean, among friends and people and acquaintances,
lore out there that what one needs to do
is simply smoke more, right?
Or just ingest more, you hear that.
Oh, well, listen, if it makes you paranoid,
you simply need to use more.
That is absolutely categorically false.
Everything we know about the way that THC and CBD work
is that they tend to potentiate,
that is increase the effects of these different systems
at given synapses and in different areas
of the brain and body.
That is, if someone experiences paranoia or anxiety
from a given strain of the marijuana plant
or from ingesting an edible in a particular way
or a particular kind of edible,
that person is very likely to experience the same effect
every time they ingest that strain or variety.
This is part of what’s led to this enormous industry.
I mean, there are a number of different reasons,
but this is part of what’s led to this enormous industry
of highly customized cannabis,
where people will spend some time
really seeking out the different strains of cannabis
and hybrids of cannabis that work best for them
and work best for them in particular contexts.
I wish I could tell you that if you are a person
who is between five foot seven and six feet tall
and you have blue eyes or brown eyes
that the sativa varieties are going to be right for you
or that the sativa varieties
are going to give you panic attacks.
I can’t do that.
The only way to determine it would be
to actually experience ingesting those or smoking those,
which is certainly also not what I’m suggesting, right?
That’s up to you.
I’m not telling you what to do or what not to do,
but there are no good predictors.
In fact, if you look in the literature,
it is not at all clear that people
who have a heightened level of anxiety
when they do not smoke cannabis
will experience cannabis as less paranoia inducing
or more relaxing.
That’s simply not the case.
Now, what we can say for sure
is that general categories of effects,
such as increased focus and reduced anxiety
are largely due to activation of areas
like the prefrontal cortex.
Now, unlike other compounds like nicotine or alcohol
or neurotransmitter systems like dopamine,
when we talk about the cannabinoid system
and I say effects, biological effects, psychoactive effects,
I want you to keep in mind always,
please, please, please keep in mind
that those effects can be varied
and often opposite in direction.
So let’s just give an example of that.
I just mentioned that when people smoke or eat sativa,
that it tends to lead to one specific set of,
or generally leads to one specific set of effects,
heightened focus, mood, et cetera.
Whereas when they ingest or smoke indica
and its components, right?
Again, we’re still talking about THC and CBD
in varying ratios, but now indica cannabis,
and you say, well, why would it improve
the transition time to sleep?
Or at least give people the impression
that it improved the transition time to sleep.
We’ll talk about what indica actually does
for sleep in a little bit.
But indica also tends to suppress activation
of the amygdala and threat detection centers in the brain.
Again, binding the same CB1 receptors
and those retrograde signaling mechanisms
I talked about before.
But it also tends to shut down the hippocampus,
an area of the brain associated with memory,
which is why indica varieties lead to pronounced,
or I should say profound defects in short-term memory,
and sometimes in long-term memory as well,
if it’s consumed over long periods of time.
We’ll talk about short, medium, and long-term consumption,
occasional consumption going forward.
So what I’d like you to take away
from this component of the discussion is,
first of all, the mechanism of action
by which cannabis impacts the brain and body,
but in particular, the brain,
is going to be through CB1 receptors.
And those CB1 receptors can lead to either an acceleration
or a break on particular biological mechanisms.
And there are going to be a constellation
of different accelerations and breaking
of different neural systems in the brain and body,
depending on whether or not people ingest sativa or indica
or some hybrid strain.
And perhaps most importantly,
even if you didn’t understand anything that I’ve said
about the biology of these different strains
and the receptors,
please do understand that there is no way to predict
what the effect of a given strain will be
on an individual.
There has been extensive exploration
as to whether or not people who are so-called mellower
or more anxious or any number
of different personality dimensions will respond
in one way or the other.
But in fact, there is no way to tell.
Layer on top of that,
the fact that dosing THC and CBD
can be fairly straightforward in the form of edibles,
right, because there can be,
at least if it’s a controlled source,
a defined number of milligrams of THC,
a defined number of milligrams of CBD.
That’s true for ingestibles.
It’s much harder to gauge that
from the smokable forms of cannabis,
especially if those smokable forms of cannabis
are obtained through sources
where there isn’t a lot of clear information
about the total amount of THC in that product.
Now, this is all changing quite a lot nowadays
because of the commercialization of THC and CBD products
and cannabis in a number of different areas,
including in the United States.
But still many people are ingesting cannabis,
THC, CBD through sources
where they don’t really know how much
they’re bringing into their system.
And so whether or not someone gets
incredible anxiety relief,
enhanced sense of mood and focus
and wellbeing, pain relief, et cetera,
or whether or not they have full-blown panic attacks,
et cetera, is very hard to predict
based on dosage information alone.
Now, of course, we can create broad categories
and we’re going to talk about studies
that create broad categories of low dose,
moderate dose and high dose,
frequent use and infrequent use.
But unlike alcohol, unlike nicotine,
we can’t really point to specificity
of X amount of alcohol, grams of alcohol per week,
which is safe, or X amount of alcohol, which is not safe.
And so I know a lot of people out there are wondering,
you know, how often can they smoke cannabis
or how often can they eat cannabis or THC or CBD
and any number of its different forms and products safely?
Well, we have to really define what safely means
and we have to really acknowledge
that there’s a pretty loose set of controls
over what one is bringing into their brain and body
as they ingest THC and CBD.
But even under conditions in which it’s very controlled,
it’s very hard to predict what those effects will be.
So before moving into specifics of taking cannabis
or not taking cannabis, who should, who shouldn’t,
what the medicinal purposes are
and what some of the newer exciting data point to,
I just briefly want to make a list.
And I promise very briefly, I know I’m not often concise,
but I do try to be thorough for your sake.
I want to make a very brief list
of the different brain areas that are impacted
by THC and CBD and why THC and CBD
have the various effects they do.
When somebody smokes or ingests cannabis,
doesn’t matter what the THC or CBD ratio is,
if they experience deficits in memory,
and that’s almost always present,
that’s going to be because of reductions
in electrical activity within this brain region
we call the hippocampus.
Hippocampus means seahorse, it’s shaped like a seahorse.
Anatomists like to name things after what things look like,
but hippocampus memory,
memory is reduced in particular short-term memory.
That’s true regardless of whether or not
one is using sativa, indica, or some hybrid.
In general, the prefrontal cortex is going to be activated
by the sativa varieties, which is going to increase thinking
and narrowly constrain focus to some activity.
And that’s more commonly associated
with the sativa varieties.
The indica varieties, as I mentioned before,
tend to lead to a suppression of activity
in prefrontal cortex, believe it or not,
and turn off thinking and planning.
This is why indica varieties are often used for relaxation
and for promoting sleep.
Regardless of whether or not sativa or indica variety,
and again, regardless of the ratio of THC to CBD,
there is a general suppression of neural circuits
within the so-called basal ganglia and cerebellum.
Basal ganglia and cerebellum are areas of the brain
that are involved in action planning and withholding action.
So that would be the basal ganglia,
so-called go-no-go circuitry.
And the cerebellum, which is involved in balance,
but also motor planning and motor sequencing.
This is why people who smoke marijuana,
regardless of the strain,
will tend to be less physically mobile.
Other common effects are reddening of the eyes,
dryness of the mouth.
That’s actually caused by the same general mechanism,
which is a reduction in the secretion of saliva
and of sort of tears and lubrication of the eyes
from the lacrimal glands of the eyes
because of the presence of largely CB2,
but also CB1 receptors in the mouth and on the eyes.
And there tends to be,
especially with certain strains of cannabis,
increase in appetite, so-called munchies.
And that has everything to do
with very, very high density of CB1 receptors
in the hypothalamus,
and in particular areas of the hypothalamus,
like the arcuate nucleus of the hypothalamus,
other areas as well, of course,
that have tons of CB1 receptors,
bind THC and CBD,
and activate the neurons that strongly stimulate appetite
through two mechanisms.
One is a cognitive mechanism of creating a preoccupation
with food and anticipation of taste,
as well as the experience of taste.
So the narrowing of focus to what you want to go eat,
right, you really crave, I don’t know, pizza,
it seems to be high fat, high carbohydrate foods,
but really crave pizza,
and narrowing of focus
so that you’re not thinking about anything else,
but also signaling from the hypothalamus to the gut,
to neurons within the stomach itself
that regulate blood sugar.
So there are strong effects on blood sugar of THC and CBD
that generally lead to increases in appetite.
So two parallel mechanisms,
one within the brain, one within the body,
Okay, so there’s an array of different effects.
And as I mentioned before,
CB1 receptors are present all over the nervous system
in the brain, the spinal cord.
In fact, the presence of CB1 receptors in the spinal cord
largely explains the fact that THC and CBD,
to some extent, although it’s not very well studied,
can provide some pain relief.
I say some because a lot of people perceive
or believe that they experience more pain relief
from cannabis than they actually do.
It actually has a lot to do with a perceptual shift
to basically focusing on other things,
but there does seem to be some antinosusceptive,
meaning anti-pain effects of cannabis, THC in particular,
and that is exerted largely through effects
on CB1 receptors in neurons of the spinal cord.
So a broad array of effects are taking place,
regardless of what strain you take
and whether or not you eat the cannabis
or you smoke the cannabis.
And the broad array of effects can be explained
by the fact that that retrograde signaling
can lead to activation or suppression of activity
in various neurons.
So now I’d like to take a step back
from the biology of cannabis and THC and CBD
and all the signaling and receptors, et cetera,
and really just focus on cannabis use.
And wherever possible, I will point to the specific strains
that have been studied and the ratios of THC to CBD.
But I have to say that unfortunately,
most studies of marijuana, of cannabis,
while they have been very careful to detail
the amount of THC, low dose, medium dose, or high dose,
and actually getting very specific,
right down to the number of milligrams
or even how much circulating THC is present
after somebody smokes a joint or ingests cannabis,
most studies have not distinguished
between sativa and indica strains.
And that’s unfortunate because in the real world,
people are distinguishing between sativa and indica strains
in their patterns of use and what they prefer
and what they don’t prefer,
even what they prefer to smoke during the day
or ingest during the day versus night.
Believe it or not, there are people
who are using certain strains during the day
and other strains at night.
But the science has yet to catch up to that,
or I should say more accurately,
the general public and the themes that are emerging
and the practices that are emerging around cannabis,
especially in states where it’s decriminalized or legalized
are occurring at such a rapid rate
that there’s absolutely no way
that the science could keep up.
This is a naturally occurring experiment,
not to say that it’s natural, like people should do it,
but it’s an experiment that’s happening in real time
in the real world, much faster than controlled studies
within university laboratories
and other laboratories can keep up.
So at this point,
I think it’s appropriate to ask ourselves,
why do people even use cannabis?
I mean, what are they trying to achieve?
Is it always about not feeling pain?
Is it always about reducing anxiety?
Well, sometimes it is,
but oftentimes people are using cannabis
in order to achieve a particular state.
And we could use a broad brush and say,
well, they just like being high.
But while that may be true in a lot of circumstances,
and I have to believe it actually is true
in a lot of circumstances,
there are a lot of people who use cannabis
in a very directed way,
or they get quote unquote high in order to achieve states
that to them are particularly attractive.
And one such state is a state of creativity.
And this brings us to a broader theme,
which is, does cannabis increase creativity?
And if so, is it the THC, the CBD,
what’s the appropriate ratio
or the best ratio for accessing creativity?
This is an interesting and important discussion, I believe,
because creativity is one of the more sought after
and more elusive states that humans can experience.
And yet, if you look at human evolution,
you look at our progression
in terms of technology development and culture
and music and poetry, et cetera,
we really can look to creativity as the state
that fostered so much of that evolution.
So whether or not you’re into technology
or you’re into art or music,
whether or not you’re just somebody
who wants to expand their understanding
or their experience of life in some way,
creativity is a fundamentally important state
to try and access and to try and access regularly
and to try and tap into
in order to eventually produce something,
in order to create something of meaning that exists,
not just in that creative state,
but to yourself after that creative state has gone away.
So the painting that you paint in the creative state,
hopefully is a painting that still inspires
and has impact after you exit that creative state
and that will inspire others.
And this could be true for any number of different things,
not just painting.
So does cannabis increase creativity?
The short answer is it depends.
First of all, we need to define creativity.
Here we are thinking as scientists,
if not already scientists.
And there are basically two modes of thinking
that are associated with creativity.
And they don’t completely explain creativity,
but if you look in the research,
the psychology research and the neuroscience research,
you’ll hear about convergent thinking
and divergent thinking.
Convergent thinking is taking loose ideas
and kind of braiding them together,
finding a common thread,
synthesizing and organizing those different ideas
into some common or specific framework
in order to get or create some specific outcome.
So convergent thinking is basically the person in the room
who’s listening to all the ideas and taking them all in.
Maybe it’s a panel of how should we get a certain product
out to market?
Or what are the different motifs that we should include
in a piece of music?
Or what should we do in terms of re-architecting
a given physical space?
Taking in those different opinions,
those different ideas from different people,
and then synthesizing them and coming up with one
or a small subset of coherent ideas
that incorporate some or all of the ones that they heard.
Okay, so that’s convergent thinking.
It doesn’t have to involve a panel of people
talking to you.
I use that as an example of what goes on
inside your own head
when you are engaging in convergent thinking.
You’re thinking, well, so-and-so said this,
and I think that,
and you’re kind of braiding them through
and trying to get some common theme,
some common vector to emerge from that.
Divergent thinking, on the other hand,
is best described as brainstorming.
It’s exploring ideas and continuing to move
into the variation and the vastness of ideas
in hopes of eventually being able to converge
on some novel idea or framework, okay?
So these are similar and related,
but typically the creativity process
involves first brainstorming and divergent thinking,
and then in order to arrive at something,
to actually create something, right,
the verb create,
not just thinking about what you might create,
which occurs during divergent thinking,
but actually creating something,
a specific painting, a specific song,
a specific body of literature,
a specific scientific project or experiment, and so on.
That usually involves convergent thinking.
Now, these can be explored in the laboratory,
and they can be explored in the laboratories
through sets of different types of questionnaires
or even tasks that you can give human subjects,
and this has been done extensively,
and across the entire body of data,
and by that I mean literally hundreds of studies
that have explored the relationship
between particular neural circuits and neurochemicals,
convergent and divergent thinking,
we can arrive at a principle,
and the principle involves a molecule
that many of you have heard about before,
which is dopamine.
Dopamine is a neuromodulator,
it’s involved in motivation,
and it tends to direct our attention
to things outside of us,
but it’s also closely related to convergent thinking
and divergent thinking and to the creative process,
and therefore it should come as no surprise
that diseases of the nervous system,
excuse me, such as bipolar disorder,
of which we’ve done an episode all about bipolar disorder,
or mood disorders that impact the levels of dopamine,
either make it way, way too high,
or way, way too low,
strongly impact whether or not people will be creative,
and I think the short takeaway
that makes the most sense in terms of framing this,
and we cover this on the episode on bipolar disorder,
sometimes called bipolar depression,
is that in professions
where there’s a lot of creativity required
in order to succeed,
so again, musicians, composers, artists, et cetera,
you tend to find more manic depression,
and manic depression, at least in the manic states,
the hyperactive states,
are correlated with elevated levels of dopamine.
Likewise, it has been seen over and over throughout history
that individuals that have mild forms of schizophrenia
or even full-blown schizophrenia,
many famous painters, for instance, or musicians,
they are known to have elevated levels of dopamine
and they are quite creative.
Now, that doesn’t mean everybody who’s creative
has elevated levels of dopamine,
although it’s likely that their levels of dopamine
are at least not diminished,
and it doesn’t mean that non-creative people
have low levels of dopamine,
so don’t get carried away with the interpretation here,
but the point is this.
Dopamine levels strongly relate to the probability
that you can engage in convergent and divergent thinking,
and they do so in the following way.
When dopamine levels are high,
divergent thinking is more likely.
That is, when people have a lot of dopamine
circulating in their system,
they tend to be very expansive with their ideas,
they tend to brainstorm a lot,
they tend to be comfortable and even want to,
or reflexively, throw out a lot of ideas
that sometimes even seem a little disconnected.
Some people might think of this
as kind of attention deficit, but it’s not.
It’s really the idea of throwing out disparate ideas, right?
You know, you hear sometimes,
you throw things against the wall and see what sticks.
Well, these people, that’s obviously an analogy,
but people are throwing lots of things against the wall
and seeing what stick,
and then seeing how the things that stick fit together.
That’s divergent thinking,
and elevations in dopamine
tend to increase divergent thinking.
However, they tend to do this
in a kind of an inverted U-shaped way.
For those of you that are watching on YouTube,
I’m just drawing kind of a hump, obviously,
and for those of you listening,
just imagine a U, the shape of a letter U,
and then just flip it upside down
so it looks like a bump.
Turns out that when dopamine levels are very low,
there’s a low probability of divergent thinking.
When dopamine levels are high, as I mentioned before,
there’s a high level or probability of divergent thinking.
But when dopamine levels go very, very high,
then there’s, again, a reduction in divergent thinking.
In other words, there’s a kind of a sweet spot
of elevated dopamine for divergent thinking.
And again, divergent thinking is critical
for the creativity process,
because creativity, by definition,
is taking a novel set of ideas
and arranging them in a particular way,
or taking existing ideas and arranging them in a novel way
that then you eventually converge on some new product,
new idea, new song, et cetera.
Now, convergent thinking follows a very different pattern.
When dopamine levels are high,
convergent thinking is not very likely.
And when dopamine levels are low,
convergent thinking is very likely.
So here, using arguably a very reductionist view,
we’re looking at all of this thing of,
we’re calling creativity
through a very neuroscience-y reductionist lens,
we can say this.
The creative process involves going into a state
where you’re willing to consider a lot of options,
many of which seem distantly
or not even connected to one another.
And dopamine facilitates that divergent thinking state
in which you are perfectly happy,
and in fact, experience a kind of a joy or elation,
a comfort and a pleasure
in organizing all these different ideas
that to anyone else might seem not that related.
But when your dopamine levels are elevated,
these all seem like great ideas
and that maybe there are connections there, right?
You’re not accepting all of them as true and valid
and interesting and combining them,
but there’s this idea that it’s worth
entertaining the possibility, at least for moments.
And then as dopamine levels drop,
there is the process of convergent thinking,
which is taking options down off the wall,
saying, no, no, that doesn’t fit with that,
doesn’t fit with that, but ah, that fits with that,
and that can work, that feels right or sounds right
or looks right.
That’s the creativity process.
And so I think this is not just important
for understanding cannabis,
which we’ll get back to in a moment,
but it’s important for understanding creativity
and brain states in general.
Brain states are not, as we would say,
a square wave function.
You don’t just drop into a trench of creativity.
Creativity is not an event, it’s a process.
And what I’m telling you is that it’s a process
that involves divergent thinking and consideration
of a lot of different ideas.
That’s correlated with high, but not too high dopamine.
And then one has to transition
into a state of convergent thinking,
which is really homing in on the ideas
that seem to have validity or that could have validity
and getting rid of everything else.
And that’s associated with low dopamine.
It’s more about logical implementation and consideration
as opposed to thinking about and considering everything.
So let’s now return to the question
of whether or not cannabis
and its different components increase creativity.
And when you look at the literature on this,
you find studies that very clearly point to a yes,
it increases creativity.
And it’s not surprising, therefore,
that cannabis can increase dopamine transmission,
that is dopamine levels in certain brain areas,
in particular brain areas involved in thinking and planning.
Okay, so cannabis increases dopamine in these areas,
elevated dopamine increases divergent thinking,
and divergent thinking is associated with creativity.
And there are studies that support the idea
that cannabis can increase creativity.
However, there are at least as many studies
that say that cannabis does not increase creativity,
that cannabis increases consideration of multiple ideas,
perhaps through elevation of dopamine and related systems,
but that ultimately the ideas that converge from that
are not truly creative ideas.
At least they don’t meet the criteria
for creative brainstorming
and extraction of ideas that are truly novel.
So it doesn’t increase creativity.
So which one is it?
Well, fortunately, there’s an entirely
distinct set of literature
that has taken all the other literature into consideration.
And here’s where we arrive.
So there’s a really nice study
that explored creativity in cannabis users.
And we will provide a link to this study.
First author is Emily LaFrance,
and the title of the paper,
so somewhat amusing in its own right,
which is, it starts with a question,
inspired by Mary Jane, of course,
Mary Jane being one of the kind of old school versions
of our ways of talking about cannabis or marijuana.
Nowadays, people refer to it mainly as pot,
has other names too, of course.
And the title of the paper is inspired by Mary Jane,
mechanisms underlying enhanced creativity in cannabis users.
And I really like this study for a couple of reasons.
First of all, they looked at people who did not use cannabis
as well as people who use cannabis.
So they had two different groups,
but they did not evaluate creativity of the cannabis users
while they were under the influence of cannabis.
They looked at the level of creativity
in these cannabis users
when they were not under the influence of cannabis
and asked whether or not their ability to be creative
was enhanced by cannabis.
Now we’re going to compare this to studies
in which people come into the laboratory
and actually use cannabis,
and then they evaluate creativity under that context.
But this study has some unique takeaways
that I think are really interesting.
First of all, they did, yes,
see evidence for enhanced creativity.
And when I say enhanced creativity,
I mean within the context of this divergent thinking thing
that I talked about a moment ago.
And when I say enhanced,
I mean significantly greater than in non-users,
so people that don’t use cannabis.
So right now I can imagine
that all the cannabis users are cheering,
yes, cannabis increases creativity,
makes people more creative than they would be otherwise.
Well, this is interesting.
We have to ask ourselves how that was accomplished.
And it turns out that one of the major ways
in which it was accomplished is that cannabis users,
even if they are not under the influence of cannabis,
are far more open to novel ideas,
and they have a more explorative and sort of reduced anxiety
or I should say lower anxiety mode of thinking
when they explore novel ideas,
which is essential for divergent thinking.
So they observe both enhanced divergent
and convergent creative type thinking in cannabis users.
And the source of that they conclude is,
and here I’ll just quote,
cannabis users higher levels of openness to experience
are responsible for their enhanced self-reported creativity
and convergent thinking test performance.
So it’s not necessarily that cannabis
is increasing the capacity of the brain areas
that are associated with creativity,
but rather cannabis appears to be increasing an openness
and probably doing that in part through lowering anxiety
in particular people.
And that openness is leading to inclusion of more ideas
during the divergent thinking process, right?
They’re willing to consider throwing up more things
on the wall to see if they stick, so to speak.
So in their conclusions,
they have a really nice statement.
Again, I’ll just read from the paper
because they said it better than I ever could.
Quote, while mainstream media has propagated the idea
that cannabis expands the mind and enhances creativity,
our results show the link between cannabis and creativity
is largely a spurious correlation,
meaning that it’s not the case
that cannabis increases creativity,
but, and I inserted the but in this quote,
but driven by differences in personality
that are related to cannabis use.
For example, openness to experience
that are related to both cannabis use
and augmented creativity.
This is a real chicken-egg argument.
What do I mean by that?
What I mean is this paper finds
that people who are more open to experience
are more likely to use cannabis
and people who use cannabis
are going to be more open to new experiences.
And that combination of features, openness to experience
and what that openness to new experiences brings
enhances the convergent and divergent thinking
that is characteristic of the creative process.
So in short, cannabis increases creativity,
but through changes in personality
that tap into the creative process
rather than directly impacting the neural circuits
that for instance, turn on creativity.
And I have to say this study is really important
because by exploring cannabis users
not while under the influence of cannabis,
they were able to tap into this very important,
what I believe to be fact.
Because if you think about a study
in which you would have one group using cannabis
and another group not using cannabis,
and then you give them some tasks
that taps into creativity, you will see effects.
And very likely you’ll see effects
where cannabis might even increase
divergent convergent thinking and creativity
that those results have actually been published
many times before.
But given the varied effects of cannabis and THC
that we talked about earlier
through all that complex signaling stuff,
you can imagine that there will also be other studies.
And in fact, there are where divergent
and convergent thinking and creativity
is not assisted by cannabis
and might even be reduced by ingesting cannabis.
However, if one considers that divergent thinking
is absolutely crucial to the creativity process
and the range of things that one will explore
will be enhanced by openness
and by reduced levels of anxiety.
So a willingness to explore different options,
some of which might seem completely crazy,
and cannabis increases the personality types
and reduces the anxiety that create that sense of openness.
Well, then it makes perfect sense
why cannabis would increase creativity
in certain individuals, but not directly.
And this study, the one I just referred to,
which I should say was published
in the journal Consciousness and Cognition,
and again, we’ll provide a link to it,
did a wonderful job of teasing out
this impact of cannabis on personality,
which then impacts creativity.
So if somebody asks you, or if you’re wondering,
or if you feel like cannabis increases creativity,
in some sense, the answer is yes,
but the answer is yes because of the ways
that it shapes openness to new ideas.
And can, I should say can, because not in everybody,
but can in some individuals reduce anxiety.
What this means is that if you are somebody
who experiences anxiety or increased levels of focus
from cannabis, regardless of the strain,
and here I have to imagine people
are exploring different strains
if they’re exploring them at all,
exploring different modes of delivery,
smoking or ingestible, et cetera.
If you’re somebody who experiences anxiety,
it’s very likely that you won’t have the increased openness
to experience and divergent ideas
that will facilitate creativity.
However, if you are somebody
who achieves heightened levels of relaxation
and reduced levels of anxiety from cannabis,
regardless of which strain we happen to be talking about,
well then, yes, it will position you
to be in a heightened state of creativity,
at least as defined by convergent and divergent thinking.
One of the more characteristic,
or I should say stereotype qualities
of people that smoke a lot of marijuana
or ingest cannabis through other means
is their changed patterns of speech.
In fact, there’s a kind of a lore in the clinical realm
that you can predict or get some strong indication
as to whether or not somebody is a cannabis user
or pot smoker based on their voice
and their particular tone of voice
and their lack of inflection.
There’s a lot of speculation here,
but fortunately it’s been studied.
So I’d like to discuss now
whether or not cannabis can impact patterns of speech,
both acutely, meaning while under the influence of cannabis
and over time in chronic cannabis users.
And when I say chronic cannabis use,
I want to be very specific what I mean.
Chronic cannabis use does not necessarily mean
that people are smoking cannabis
or ingesting cannabis every day.
Although certainly if they are,
that qualifies as chronic use.
Chronic use is regular use over time
of anywhere from twice a week or more.
So using cannabis once a month
would not be considered chronic use,
even if it’s for many, many years.
Using cannabis or ingesting cannabis in some way or form
twice a week would be considered chronic use.
And then of course,
some of you out there are going to ask me to split hairs
and say, well, what if somebody uses it twice a month?
Well, listen, the clinical literature
and the scientific literature don’t get that specific.
And of course, there are an infinite number of ways
to arrange one’s cannabis use,
everything from zero, none at all,
to constantly every day, all day and everywhere in between.
But think of chronic use as twice a week or more.
Think of occasional use as less than that
and realize that within the realm of chronic use, excuse me,
that or more can be anywhere from twice a week
to every day to just in the evenings, et cetera.
The effects of chronic use of cannabis,
as I just defined it, on speech have been studied
because of this characteristic drawing out
of certain syllables, a slowing of speech,
and in many cases, a total change or alteration
in the way that people speak and use language,
both when under the influence of cannabis
and when not under the influence of cannabis,
if they are chronic users.
And here, we really want to distinguish
between THC and CBD and just make it really simple
and say that CBD is not responsible
for most of the psychoactive effects of cannabis,
whereas THC is.
And again, the ratio of CBD to THC
is going to be relevant there,
but let’s just think about cannabis and THC
as one in the same for this portion of the discussion,
realizing that, of course,
they are not exactly the same thing.
There’s an excellent study entitled
Adults with History of Recreational Cannabis Use
Have Altered Speech Production.
And we will provide a link to that.
First author, Adam Vogel, really liked this paper.
It was published in the journal
Drug and Alcohol Dependence.
We will provide a link to it for you
if you’d like to peruse it in more detail.
The title itself,
Adults with a History of Recreational Cannabis Use
Have Altered Speech Production,
tells you pretty much everything you need to know,
except there’s some important nuance in here
because as I mentioned earlier,
people who smoke sativa varieties of cannabis
oftentimes will become more talkative, much more talkative.
However, whether or not people tend to rely
on sativa cannabis use or indica cannabis use,
there is a very consistent finding
that people who are chronic users,
again, twice a week or more,
recreational use or medicinal use,
undergo pretty profound changes in the way that they speak,
but in a very specific set of ways.
Now, first of all,
the changes in speech shouldn’t surprise us at all
because both sativa varieties of cannabis
and indica varieties of cannabis
impact those brain centers involved in movement,
the basal ganglia.
Remember the go-no-go circuitry,
the circuitry that makes you want to do things
and the circuitry that makes you want to withhold action,
and it tends to shift the body and brain
toward more inaction.
And cannabis impacts CB1 receptors in the cerebellum,
which is involved in motor planning, execution, and balance.
So regardless of whether or not people are using cannabis
of the sativa or the indica variety,
there are disruptions in motor circuitry.
And as you may have heard,
if you listened to our episode
with Rockefeller professor, Dr. Eric Jarvis,
who works on speech and movement,
speech is movement, right?
The movements of the mouth, the movements of the hands,
those are intimately related in terms of our speech.
In fact, the centers of the brain
involved in hand movements
are part of the speech areas and vice versa.
Eric actually pointed out
that if you put your hands behind your back,
provided you normally do have use of your hands,
it actually will reduce your fluidity of speech.
And so I’m going to put them back in front of me now.
The point is smoking marijuana
or consuming marijuana by edible changes one’s speech
and does it in a very specific way.
And in this study by Adam Vogel and colleagues,
they explored a huge different variety of aspects of speech.
And this can be done using spectral processing,
which is fancy nerd speak
for looking at how much inflection there is
or looking at how long people hold vowels
or consonants, et cetera.
And again, these are people
not under the influence of cannabis,
but rather people who tend to be
under the influence of cannabis
when not participating in the study.
In other words, chronic recreational cannabis users.
So what are the two major shifts that cannabis causes
on our patterns of speech?
Well, the first one is a change
in what’s called spectral tilt.
Again, that’s fancy nerd speak
for vocal effort and intensity.
So I’m not a pot smoker, I confess.
But if I were to say the sentence,
vocal effort and intensity
are important components of speech.
That’s the way I would say that sentence
if I was striving to enunciate very carefully
and to accent certain words and syllables.
A pot smoker or somebody who uses recreational cannabis
fairly often would have reduced spectral tilt,
AKA vocal effort intensity,
and might say spectral tilt is vocal effort and intensity.
And it differed between groups
and appeared to change in line
with the duration of abstinence from cannabis use.
That I think is not a far cry
from the change in spectral tilt that they observed here.
In addition, there are changes in verbal timing.
That is pronunciation of words
and accenting particular syllables of words
in people that consume cannabis or smoke cannabis.
So rather than emphasize particular words within a sentence,
so again, I’ll just use a sentence from the paper
so that you can gain more knowledge from the paper.
Cannabis, and I’ll say it the way that I would say it
since I’m not a cannabis user.
is the most commonly used illicit drug in the world
with approximately 4% of adults aged 15 to 64 years
reporting recent use.
And the citation is from the United Nations
Office on Drugs and Crime, 2019.
So that would be the way
that I would typically read that sentence.
And having gone into the data in this paper
and of course evaluated references therein,
and listen to some of the spectral analysis
that they include as data,
you can literally go into these papers online
and hear recordings of people who are cannabis users
or non-cannabis users.
And I’ll try and give you a clear sense
without picking an extreme example
of how somebody who’s a fairly consistent
or even occasional cannabis user
might read that very same sentence.
is the most commonly used illicit drug in the world
with approximately 4% of adults aged 15 to 64 years
reporting recent use.
And the citation comes from the United Nation
Office on Drugs and Crime, 2019.
Now you’ll notice that wasn’t a dramatic difference.
And of course I could have taken the liberty
to pick an extreme example of the sort
that they did occasionally observe
in evaluating subjects for this paper.
I could have said something like cannabis,
marijuana is the most commonly used illicit drug.
But frankly, that would have been selecting
an outlier example and I don’t want to do that.
I don’t want to skew the data as they say.
Rather, if you heard the first time I read the sentence
and the second time I read the sentence,
what’s mainly different is the difference
in the amount of enunciation and accenting
of particular words and symbols within a sentence.
So the total content that’s delivered is exactly the same.
And while I wasn’t measuring my pace,
the overall rate of communication is essentially the same,
but there’s less sort of lilting and falling of the voice
and less accenting.
That’s the major consistent effect of cannabis use.
Now, of course, there are examples of people
who are using a lot of cannabis
and it impacts brain centers involved
in movement and speech.
So much so that they really do have the really drawn out
kind of, and oftentimes this will be detected in the laugh.
You know, there’s this sort of stereotypical stoner laugh
as it’s sometimes called, rather than say,
or that’s a fake laugh, obviously.
It’s hard to make myself laugh
if something’s not actually funny.
I have to think of something funny.
When people will say, like, that’s a bit more
of the way I might laugh, like,
sort of the inspiratory laugh or the,
which is expiratory laugh.
People who use cannabis chronically will often do that.
Which is sort of the back of the throat.
It’s sort of this, the,
it’s neither inspiratory nor expiratory laugh.
And believe it or not, there’s an entire literature
on inspiratory inhaling versus expiratory laughs.
And there’s also a literature on cannabis
altering the pattern of inspiratory and expiratory laughs.
It almost sounds like a sarcastic laugh
when in fact they may not be feeling sarcastic at all.
And I have a very close friend and colleague
who’s a phenomenal neurosurgeon and neuroscientist
by the name of Dr. Eddie Chang.
He’s the chair of neurosurgery at UCSF
and his lab and him are expert in the study
of neuroscience controlling language and speech.
And he often tells me that he can predict
with almost certainty whether or not somebody
is a regular cannabis user based not just
on the patterns of speech that they use,
but even just by recording specific neurons in their brain
that underlie the laugh reflex
and certain patterns of speech.
So this idea that cannabis use changes your ability
to speak and enunciate clearly does appear to be true.
And the stereotype that cannabis use tends to create more
of a drawl or kind of a, if you will, a laziness
in the laugh and some of the reflexive enunciations
that people use does also appear to be true.
And I say all that, of course, with the caveat
that many people out there will know individuals
or perhaps you yourselves are individuals
that may use cannabis,
but that have incredible articulation,
probably better than mine and better than other people
out there who speak for a living.
So I’m not saying that 100% of people
that use cannabis regularly can’t speak well or clearly,
that’s simply not what I’m saying.
And I don’t want to communicate that idea at all,
but it is the case that people who are regular cannabis
users are impacting the neural circuits involved
in movement, movement also controls speech
and therefore cannabis is impacting speech.
Now I’d like to turn our attention
to whether or not cannabis can increase sexual activity,
sexual desire and or sexual function.
So we’re going to be talking about libido,
about sexual desire and about effects
of cannabis on hormones.
And while this might sound like a discussion
that’s purely oriented towards recreational use of cannabis,
that is people using cannabis to heighten
or increase their sense of arousal for sexual activity,
it actually ventures into the clinical realm too,
meaning there have been excellent peer-reviewed studies
that I’ll describe to you in a moment,
exploring the use of cannabis or THC more specifically
for something called hypoactive sexual desire disorder,
which refers to a persistent or recurrent deficiency
or absence of sexual fantasies and thoughts
and or desire for or receptivity to sexual activity.
This is a disorder that is fairly common
anywhere from six to 9% of people, both males and females.
It used to be considered higher prevalence
in females than in males,
but now those numbers seem to be evening out.
So basically there are anywhere from six to 9%
of people out there who have very diminished sexual desire.
And so a number of those people are interested
in figuring out ways to increase
their amount of sexual desire.
And of course there are people in the general population
who may not have hypoactive sexual desire disorder,
who are interested in using cannabis recreationally
in order to increase their desire for
or their experience of sexual activity.
Now, first we have to acknowledge that sexual desire
and activity is a complex set of processes,
meaning it’s not just one event, sex, the verb,
it involves arousal, it involves sex, the verb,
and it involves a whole set of mindsets and emotional states
that vary tremendously between individuals.
But once again, we can distill out a few basic principles
and I should emphasize these are by no means
the only chemicals in neural circuits involved
in the sexual arc, as we’ll call it,
desire, the act of sex, et cetera,
but they are central to it, they are vital to it.
They would be considered what I would call necessary,
but not sufficient, okay?
So there’ll be other chemicals involved too,
but the main chemicals in neural circuits
are those involved in dopamine.
So the so-called mesolimbic reward pathway
in particular brain structure called nucleus accumbens,
which we’ll talk about more in a moment,
is vital to all motivated behaviors
and to the seeking out of all particular types
of pleasurable experiences and sex is no exception.
So when we hear that the nucleus accumbens is activated,
that almost always means that dopamine has been released
in that area and other areas of the brain and body,
and we can consider dopamine central
to the desire for, pursuit of, and act of sex.
In addition to that, there are molecules like oxytocin,
which are involved in pair bonding
and they’re going to be neural circuits
specific to the oxytocin circuitry.
But in terms of sexual arousal and sexual behavior,
it’s really the dopamine pathway in this nucleus accumbens,
which are especially vital.
That allows us to address the question,
does cannabis increase, decrease,
or have no effect on sexual desire
and or the ability to have sex?
And therein, we will find some very interesting answers
because once again, it will point to the fact
that the effects of cannabis on different individuals
can be highly divergent.
Meaning in one set of individuals,
cannabis will make them far less anxious.
And in another set of individuals,
the same strain of cannabis at the same dosage
will make them extremely anxious.
The same can be said also of sexual activity.
And this was beautifully illustrated
in the context of sexual desire
in the journal Psychopharmacology
in a paper published in 2017.
The title of this paper is
Individual Prolactin Reactivity
Modulates Response of Nucleus Accumbens to Erotic Stimuli
During Acute Cannabis Intoxication, an fMRI Pilot Study.
So I’ll give a little bit of definition
to some of the terms in the title
that will make it easier for you to understand the paper,
but then I’ll just march through the results
because they are very straightforward
and easy to understand and very interesting.
fMRI is just Functional Magnetic Resonance Imaging.
So basically subjects in this experiment
came into the laboratory.
They were either people who had not used cannabis before
or who had used cannabis before.
They were placed into a brain scanner,
one of these fMRI devices.
It looks like a tube that people are backed up into
and then they can view images in there
and their brain can be imaged
without having to remove any skull
or drill into the skull, no neurosurgery.
The participants in this study
were grouped according to whether or not
they had experienced any aphrodisiac effects
during the intoxication with cannabis.
So that would be the first group, group A.
They literally called it group A for aphrodisiac.
And then the second group,
and this is the only thing I don’t like about this study
is rather than call it group B,
they called them group non-A,
which is just gets a little confusing.
So I’ll try and simplify all this.
There are two groups and one group experiences
sexual arousal when under the influence of cannabis.
The other group does not.
And it turns out this is a very commonly observed
divergence of effects of cannabis.
Some people experience a lot of sexual arousal
from cannabis and THC in particular,
and some people do not.
In fact, they experience suppression of sexual desire.
And it’s always been a little bit mysterious
as to why that is.
Well, in this study,
they showed people in both groups, erotic images,
and they measured sexual arousal
through a number of different measures.
We won’t go into all that.
It was largely subjective.
There’ve been other studies where they’ve actually
measured things like erections in males
and vaginal lubrication in females.
These are so-called autonomic responses
that people can’t lie about, so to speak,
and that tap into other aspects
of the so-called sexual arousal process.
In this study, they also took blood samples
to look at the concentration of things like cannabinoids.
So this is a really nice study
in that they actually measured how much THC
was in the bloodstream in different individuals
who reacted to these erotic stimuli in different ways.
And they measured hormones,
namely cortisol, which is a stress hormone,
which tends to negatively correlate
with sexual arousal, and prolactin.
And the interesting takeaway from the study was
that for people, and it didn’t matter
if it was males or females,
because they looked at both,
for people that experienced elevated prolactin levels
under cannabis intoxication, that’s how they refer to it,
people take cannabis, they measure prolactin.
Some people had elevated prolactin, some people did not.
For the people that had elevated levels of prolactin,
they did not observe activation of brain areas
associated with sexual arousal.
In this case, the right nucleus accumbens,
so you have two nucleus accumbi, I guess they’d be called,
one on each side of the brain,
and the activation of that brain area
is strongly associated with dopamine and with arousal
and sexual arousal in particular in this study.
And if people had elevated prolactin,
they did not experience activation of nucleus accumbens,
and they did not report feeling sexually aroused
to those pictures, at least not to the same degree
as the other group.
So some people’s prolactin levels go up
when they ingest cannabis,
and those people do not achieve elevated levels
of sexual arousal when under the influence of cannabis,
even if they’re looking at erotic stimuli.
That makes sense because prolactin
is mutually inhibitory, as we would say,
it’s kind of in a push-pull with dopamine.
When dopamine levels are high,
prolactin levels tend to be low.
And when prolactin levels are high,
dopamine levels tend to be low.
The other group, so-called group A,
that experienced elevated levels of sexual arousal
when under the influence of cannabis
and viewing erotic stimuli,
that group did not show elevated levels of prolactin
in response to cannabis.
So this, I believe, resolves a longstanding controversy
in the field, which is,
does cannabis increase sexual arousal?
Well, it depends.
If you fall into the category of person
who has elevated levels of prolactin
in response to cannabis, then no,
actually cannabis will suppress
your sexual response and desire.
If, however, you are in the category of person
that does not have elevated levels of prolactin
in response to cannabis,
well, then erotic stimuli can potentially,
and in fact do, increase sexual arousal
in the majority of individuals.
Now, many of you are probably hearing this
and wondering whether or not you fall
into one category of individual or another.
And the key thing here to understand
is that levels of prolactin heading into the study
did not predict, did not predict,
whether or not people would respond to cannabis
with elevated or non-elevated
or even reduced levels of sexual arousal.
It was whether or not people’s prolactin levels went up
or did not go up that predicted whether or not
their levels of arousal would go up or not.
So if you are somebody who, yes,
does experience elevated levels of sexual arousal
and function when under the influence of cannabis,
well, that’s very likely that cannabis
does not increase your prolactin levels,
at least not to a significant degree while you’re taking it.
And if you are somebody who does not experience increases
in sexual arousal or function
or even diminished sexual arousal and function
when under the influence of cannabis,
it’s very likely the cannabis
is increasing your levels of prolactin.
Unfortunately, there’s no way to know or predict
based on some other measure.
I think the outcome measure that is increased
or not increased or even reduced sexual arousal
is really the litmus test by which one can figure that out.
While we are on the topic of the effects of cannabis
on sexual function and hormones like prolactin,
it’s probably worth mentioning
that cannabis has been studied extensively
for its impact on other hormones.
And we can summarize those literature in the following way.
And here I’m referring to studies only on adults.
We will talk about the developing brain and body
in a little bit, but it is very clear
that smoking cannabis increases prolactin levels.
Very, very clear.
Now you might say, didn’t you just describe a study
about a set of individuals whose prolactin didn’t increase?
And as a consequence, their level of sexual desire went up?
Yes, there are a subset of individuals
for which that’s true.
But people who smoke cannabis
do experience increases in prolactin.
And that’s especially pronounced
in people that smoke cannabis more than twice a week.
So this is important.
Prolactin, as I referred to earlier,
is reciprocal or mutually inhibitory with dopamine.
One way to think about this is in the context
of the normal sexual arousal arc,
whereby dopamine is increased
when people are sexually aroused,
but then after orgasm, both in males and females,
prolactin levels skyrocket.
This is actually what creates the so-called refractory period
for males during which they cannot achieve erection again
for some period of time.
That relates directly
to how long the prolactin increase lasts, okay?
Prolactin is also increased in new parents of all species,
including humans, which at least partially explains
some of the reported or typical reductions
in sexual desire and activity in new parents.
Now there are other reasons for that too, sleep deprivation,
but nature is smart and has arranged a set of hormones
and circuits in the brain and body
such that when tending to a newborn
is the most important thing, it relegates.
It reduces the importance of producing more children
and sexual activity in those moments and days and weeks,
So when prolactin levels are up, dopamine levels are down.
Smoking marijuana more than twice a week
significantly increases prolactin.
There are fewer studies exploring
whether or not edible marijuana has the same effect,
although the preliminary evidence suggests that it does not.
I get into this in a lot more detail in a future episode,
all about hormones with Dr. Kyle Gillette,
who’s been on this podcast before,
but he verified that in my read of the literature
is that the edible forms of marijuana, cannabis,
probably again, let’s put an asterisk next to this,
but it appears do not have as much
of a prolactin elevating effect
and therefore not as much of a dopamine suppressive effect
and therefore not as much
of a testosterone suppressing effect.
And that gets to the issue of testosterone.
Does cannabis marijuana suppress testosterone?
And this is a very controversial literature and here’s why.
Some studies say, yes, it suppresses testosterone
in males and females.
And keep in mind that testosterone in females
is vital for libido and cognitive function,
cellular repair, et cetera.
So it’s not just important in males, of course.
However, other studies say that cannabis
does not decrease testosterone.
And it seems to depend on whether or not
the cannabis is brought into the system
by way of smoking or edible.
And it seems to depend on whether or not
the cannabis is used chronically by an individual or acutely.
And here, I just want to zoom out and say
that studies on cannabis or drugs of any kind in humans
are really complicated.
If you think about it,
someone has to come into the laboratory
and let’s say you want to study chronic cannabis use.
Well, you can’t keep them in the laboratory all the time.
So you have to rely on their self-report
of how often they use cannabis and in what form.
And you can’t really control from one individual
to the next of how much cannabis and THC
they’re bringing into their system.
One person might smoke cannabis out of a bong
and take big, deep, lungs full bong inhalations or such.
Other people might smoke joints.
Other people might use edibles.
It becomes very complicated to know what people have done
and that they’re reporting it accurately.
And no joke here,
especially if marijuana is impacting
the short-term memory systems.
They might not actually remember.
They might not be tracking it that well.
Contrast that with studies of the acute use of cannabis
and THC where people who are not regular users
come into the laboratory and now suddenly
with institutional guidelines and safety protocols
are under the influence of THC and cannabis.
Well, now you’re dealing with a person
who may not have experience with the elevated heart rate
and blood pressure that’s characteristic of cannabis
because it is a stimulant,
at least when initially brought into the system,
even if it might eventually lead to relaxation.
So now you’ve got someone who’s anxious
or somebody who’s not anxious, who’s deeply relaxed,
and you’re trying to study these effects.
So it’s a moving target of sorts.
It’s very complicated to study marijuana and cannabis
and its various derivatives in this way.
Now you can probably appreciate better
as to why there’s so little nuanced data
about sativa versus indica
versus different ratios of CBD and THC.
It’s really difficult to do these studies
in the first place.
That said, the general rules are smoking marijuana
increases prolactin in men and women,
which will reduce dopamine and testosterone.
Smoking marijuana chronically,
meaning more than twice a week,
does appear to reduce testosterone significantly
and elevate so-called aromatase enzymes,
which are the enzymes that convert testosterone
This might partially explain the effect
that occurs in about 35% of males,
which is gynecomastia,
which is a development of breast tissue in males,
in particular, young males
who have elevated levels of testosterone
or who are taking exogenous testosterone
for testosterone replacement therapy,
or if they’re taking high doses, anabolic steroids,
or in females, the increase in breast size,
which is due to additional estrogen
from testosterone converted to estrogen.
So it does appear that marijuana and cannabis
increase estrogen, reduce testosterone,
increase prolactin, especially in chronic users.
Now, I’m sure that some people out there will say,
well, their testosterone levels are exceedingly high
or they are fine,
meaning the constellation of symptoms
associated with low testosterone and elevated estrogen
are not present in them.
That probably means one of two things, or both.
They either had elevated levels of testosterone
to begin with, so their ceiling was higher,
so bringing it down didn’t have that much of effect,
or that they have very low levels
of aromatase in their system.
There is some anecdotal evidence
that smoking particular parts of the marijuana plant,
in particular, the seeds,
can increase aromatase
and the conversion of testosterone to estrogen.
I think in the old days, the lore was
the seeds make you sterile,
and I think that was related to what I just told you,
this increase in conversion of testosterone to estrogen.
There’s a vast literature
on the effects of cannabis on fertility.
It does seem, yes, it does seem to alter sperm motility
and sperm health and function
when taken chronically more than twice per week,
in particular, high doses of high-potency THC.
This is something we will cover in far more detail
on a future episode all about fertility.
And in females, there’s an increase in estrogen
as a consequence of smoking marijuana
and increasing prolactin and estrogen in parallel.
Whether or not that’s detrimental isn’t clear,
although I point out that elevated estrogen and prolactin
can be associated, again, can be associated,
not necessarily, and certainly not causative,
but can be associated with elevated levels
of or frequency of breast cancer detection.
So cannabis and its effects on hormones
are not without consequence.
There are effects of cannabis on cortisol.
In some individuals, it greatly increases cortisol
due to the anxiety and paranoia it can create,
and in other individuals, it reduces cortisol.
Again, we have these divergent effects,
but I want to be very clear.
The effects on prolactin, meaning elevated prolactin,
the effects on testosterone, meaning,
at least most studies point to reduced levels of testosterone
and increased estrogen, that seems to be true
for most all individuals that chronically use cannabis,
whereas the effects on cortisol tend to be divergent.
Cannabis increases cortisol in some individuals
and decreases cortisol in others.
In general, increases in cortisol that are ongoing
are not healthy for us, and so on.
And then, of course, there are other effects on hormones,
and I’ll just briefly summarize those,
that THC in particular, not CBD, but THC in particular,
is known to be strongly inhibitory
for something called gonadotropin-releasing hormone.
This is a hormone that’s released from the brain,
from the hypothalamus, that then feeds onto,
or I should say signals to the pituitary gland,
which is also near the roof of your mouth,
a lot of stuff happening near the roof of your mouth,
it turns out, biologically.
And reduced levels of gonadotropin-releasing hormone,
caused by cannabis use,
reduced levels of LH, luteinizing hormone, and FSH,
which reduced levels of testosterone
and sperm production in males,
and egg health and ovulation
and menstrual function in females.
Now, I’m sure there are a number of women out there
who will say they have perfectly normal menstrual cycles
despite using cannabis.
I’m certainly not going to dispute that.
But if you are somebody who’s trying to maximize fertility
or regulate or balance hormones,
marijuana and cannabis reduces GNRH,
that is the gonadotropin released from the hypothalamus,
and thereby reduces luteinizing hormone
and follicle-stimulating hormone,
which are released from the pituitary
and travel in the bloodstream
to support normal ovarian function and health
and normal testicular function and health
in females and males, respectively.
Up until now, I’ve been discussing
the biological and psychological effects of cannabis.
Now I’d like to shift our attention
to some of the negative health effects of cannabis
and shine light on some of the individuals
or groups out there that need to be especially wary of
and probably avoid cannabis use entirely,
including ingestion of cannabis by way of edible.
And I frame things that way
because I think there is an increasingly large number
of people out there that appreciate
that smoking tobacco or smoking cannabis,
vaping tobacco, yes, vaping tobacco or vaping cannabis,
each and all have negative health consequences
on the lungs and on the so-called endothelial cells
of the body, the cells that make up the vasculature,
the capillaries and blood vessels.
If you don’t already know this,
I’ll make it very clear and I’ll make it very brief.
Whether or not you smoke or vape, tobacco or cannabis,
you are severely impairing the function
of endothelial cells that make up the capillaries
and blood vessels of your brain and body.
And that is known to decrease cognitive capacity over time,
increase probability of strokes,
severely impact lung function,
and also lead to things like peripheral neuropathies.
It leads to sexual dysfunction
because of lack of blood flow to the genitals,
can lead to other aspects of reproductive damage,
including to the ovaries and testes.
Essentially, there is no other way to state it
except that smoking and vaping
have negative health consequences
that are independent of the substances
that people are trying to get into their bloodstream
by smoking or vaping.
So people smoke and vape tobacco
and people smoke and vape cannabis.
And in both cases,
if we just set aside the direct effects of tobacco
and the direct effects of cannabis,
we can confidently say that the process of smoking,
of inhaling smoke into the lungs, and yes, also vaping,
bringing the chemicals that transport nicotine,
or in this case, cannabis into the lungs by way of vaping,
are both severely detrimental to endothelial cells.
I think a few years ago, when vaping wasn’t as prominent,
there was this question and this idea
that maybe vaping was going to be far healthier
or at least not as bad as smoking.
But now we can see a huge number
of negative health effects of vaping,
some of which are distinct from the effects of smoking.
So if you’d like more information on smoking versus vaping,
please see the episode that I did on nicotine.
We will also do an entire episode
all about vaping in the future.
But there’s really no way to slice it and dice it
or candy coat it.
The fact of the matter is that smoking has clear
and severe negative health consequences,
regardless of whether or not you’re smoking tobacco
or cannabis, THC, and vaping has negative health
consequences, whether or not you’re using the vape
to bring in nicotine or THC
or some combination of THC and CBD.
That’s simply the way it is.
With that said, now I’d like to focus our attention
on the direct effects that cannabis has,
either by way of THC action or by way of CBD action
in terms of positive or negative health effects
on the brain and body.
And we’re going to explore that first as a function of age.
And the reason we’re going to do that is related to a fact
that I mentioned at the beginning of the episode,
which is that the CB1 and the CB2 receptors,
the two receptors for cannabis to which THC and CBD and CBN
and all other psychoactive compounds in cannabis bind to,
to have their actions are present throughout development.
Believe it or not,
they are present very soon after conception
and the CB1 and CB2 receptors actually play a critical role
in the development of the fetus.
Now you might wonder why that is,
because of course the developing fetus
doesn’t necessarily expect to see cannabis
or to be exposed to cannabis and THC and CBD.
But as you recall, endogenous cannabinoids are present
in the adult brain and body and endogenous cannabinoids,
it turns out, are also present in the developing fetus.
In fact, endogenous cannabinoids are present
at much greater levels in the developing fetus
than they are after a child is born.
And levels of endogenous cannabinoids
actually go down across development.
I find this really interesting.
What this means is that endogenous cannabinoids
and activation of the CB1 and CB2 receptors
are an integral part of neural development.
And this is going to become especially relevant
in considering whether or not pregnant mothers
should or should not use cannabis or CBD.
And it also points to some very interesting biology
in terms of how the brain develops
and how the body develops.
Now, the development of the brain and nervous system
and body is a fascinating and vast literature,
certainly far too vast to cover in today’s episode,
especially at this late hour, as it were.
But we will have a future episode
all about brain development.
In terms of the effects of cannabis,
it’s sufficient to say that cannabinoid receptors
are present and active in the developing fetus.
They’re present and active in the newborn.
They’re present and active in adolescence.
And across that time, from conception until adolescence,
endogenous cannabinoids are mainly responsible
for the actions of those cannabinoid receptors.
During that time, the cannabinoid receptors
are having very specific effects
that are distinct from their effects later in life.
And those effects can largely be explained
in terms of neural development.
Again, we don’t have time for an entire lecture on this now,
but during development,
your body was a collection of a bunch of cells.
It’s actually called a blastula,
which means a ball of cells.
And then those cells actually have to grow out connections
and duplicate themselves.
And this is a very interesting process
by which neurons initially are situated far apart,
and then they grow out connections
and make contacts with one another.
They remove certain connections,
depending on what kind of life events you’re exposed to.
If you have a wonderful event early in life
or a traumatic early life,
those connections change, et cetera.
The important point for today’s discussion
is that the CB1 receptor in particular
is expressed on every neuron in the developing brain
and has been shown to be important
for every aspect of neural development,
from the proliferation of cells,
meaning getting enough cells to create a brain,
to the outgrowth of the so-called axons,
the little wires that connect up neurons with one another,
to the steering, the direction in which those axons go
in development, which is essential.
And even so far as to explain the connections
that form between neurons, the so-called synapses,
and then how those synapses work.
So the basic statement here is that endogenous cannabinoids
and CB1 receptor activation are critical
for every aspect of brain wiring and development.
With that in mind, the statement I’m about to make
is absolutely terrifying, at least to me,
and frankly, it should be terrifying to you as well.
And the statement is the current statistics
on cannabis use in pregnant mothers
is absolutely shocking.
The most recent survey of pregnant mothers
in the United States show that 15%, one five,
15% of pregnant mothers report using cannabis
in some form or another, either smoking it
or more likely ingestion of an edible,
because they are aware of the negative effects
of smoking on the developing fetus,
ingestion of an edible to increase THC
and or CBD during pregnancy, which to me,
I have to say as a developmental neurobiologist is,
frankly, it’s scary.
It’s absolutely scary because that CB1 receptor
is not just a minor player in neural development,
it is absolutely central to every critical aspect
of brain wiring and development.
Now, the long-term implications
or even the short-term implications of this 15%
of mothers self-reporting the use of cannabis
at some point during pregnancy are not yet known.
This is, as we would say,
an experiment that’s ongoing,
but I’d be remiss if I didn’t point out these data
and just implore you, please, please, please,
if you are pregnant or considering getting pregnant,
you’re a cannabis user, whether or not you’re using edibles,
if you’re a CBD user, please do whatever is necessary
to not ingest cannabis or smoke cannabis
or ingest CBD during pregnancy.
Now, there may be certain clinical indications
by which your physician and your OBGYN
and the pediatrician that will eventually be
the pediatrician for your child will prescribe CBD,
although it’s hard to imagine what those are.
I contacted a number of different pediatricians and OBGYNs
and not a single one said they would ever suggest
and in fact would strongly discourage their patients
from using cannabis during pregnancy.
But I think that the advent of edible forms of cannabis
and the combination of THC and CBD in certain products
and the fact that most people view CBD as safer
because it does not include as, or does not have,
I should say, the psychoactive effects that THC does
has led to a situation where you have 15%
of pregnant mothers using cannabis
at some point during pregnancy
and maybe even frequently throughout pregnancy
and the effects on the developing fetus
are completely unknown, but recall that cannabis
and THC and CBD out-compete, meaning they park
in the receptor for endogenous cannabinoids
and prevent endogenous cannabinoids
from having their normal level and pattern of action.
So this is absolutely critical.
I cannot encourage you enough, or rather I should say,
I cannot discourage enough the use of cannabis
and any related compounds in cannabis,
edible or smoked, certainly not smoked,
but even edible during pregnancy.
And certainly in breastfeeding, lactating mothers,
the same is also true.
Recall that cannabis and THC and CBD
are incredibly lipophilic.
They are fat-soluble and they get into cells very readily
and they cross the blood-brain barrier,
they cross the blood-placental barrier.
So when I encountered this statistic,
I had to kind of wipe my eyes a few times.
I could not believe it.
And yet I cross-checked that number
with a few other studies.
A few others have come in a little bit lower at,
you know, somewhere like 13 to 14%,
and a few have come in a little bit higher,
but the average of 15% is both striking and shocking.
So I don’t know how to make the message more clear.
I hope that is clear.
Please do not use any cannabis, THC,
or related things, including CBD, smoked or edible
if you’re pregnant, lactating, et cetera.
Now we are at the point where we need to consider
some of the negative health effects of cannabis
that have been well-documented in peer-reviewed studies.
And before I do this,
I want to return to a point that I made earlier,
which is that nothing I am about to say
relates directly to issues of legality.
If we consider alcohol, for instance,
alcohol is legal in most areas of the world.
It’s certainly legal in the US,
and yet there’s an age limit for its use.
Typically, it’s not available to people
until they’re 21 or older.
It’s not to say that certain people
don’t use it before age 21, but it’s not legal.
It is illegal to buy or possess alcohol,
consume alcohol before age 21.
And I think with good reason,
because the brain is still developing.
Likewise, we can have a informed discussion about cannabis
and its various components
that can fully acknowledge the reality,
which is that one of the major harms of cannabis
in the past has been the legal ramifications
of cannabis being illegal.
That’s a statement that is no longer controversial.
And this is not a discussion
about legalization or non-legalization.
If you look to the scientific literature,
the epidemiological literature,
there are wonderful data out of Carleton University
and elsewhere in Canada,
showing that many of the negative effects
of marijuana and THC
are due to the criminal justice system itself.
That is the creation of illicit drug businesses,
the creation of organized crime,
the creation of a number of different features
related to the illegality of cannabis.
And again, this isn’t the topic of today’s episode,
but that should be acknowledged.
And at the same time, we need to acknowledge
that when a compound, a drug,
or whatever you want to call it, becomes legal,
there’s a tendency to assume
that it’s safe and safe for everybody.
And with respect to cannabis and THC,
and perhaps even CBD, but certainly for THC
and cannabis that’s smoked or vaped
or consumed in edible form,
that is simply not the case.
There are clear data pointing to negative health effects
of cannabis use and THC use,
which again is not to say that there are not
positive effects on mood, anxiety, pain relief, et cetera.
Those are out there and they exist.
And we will mention some of those, of course,
and we’ve talked about some of those,
creativity, for instance, et cetera.
But if we do not acknowledge the negative health effects
that are documented in the literature,
then we are overlooking some very important data,
especially as it relates to the development of psychosis
in certain individuals.
So with that said, there are very strong data,
and I will provide links to these resources,
pointing to the fact that for people
who are chronic users of cannabis,
that is using it twice a week or more,
that over time their levels of anxiety actually increase.
And this is true even for individuals
that are using strains of cannabis
that while under the influence of cannabis reduce anxiety.
Over time, meaning over the course of 12 or more months,
there is a well-documented effect of the anxiety relief
that cannabis and THC initially brought
being less and less potent.
That is people need to smoke more of it or ingest more THC
in order to achieve the same level of anxiety relief.
And in some cases, a switch from anxiety relief
to increase in anxiety.
And again, that’s increase in anxiety,
not just when the drug is not being consumed,
but also while under the influence of the drug.
Why would that be?
We have to go back to our understanding
of the CB1 receptor and the potency with which THC
binds to that CB1 receptor.
When THC is brought into the system over and over again,
meaning twice a week or more,
the binding of THC to that CB1 receptor
eventually causes a sort of habituation or attenuation
of the entire process of binding the receptor
and creating the psychoactive effects.
So initially it creates anxiety relief,
but over time the affinity for the receptor doesn’t change.
Meaning it can still park in that slot
with a lot of affinity, a lot of strength,
but there are fewer receptors available.
And then the signaling that’s downstream of those receptors
becomes less and less robust.
Now, this is a topic we didn’t get into
in too much detail today
because I didn’t want to include
even more biological detail,
but the CB1 receptor is a so-called
G-protein coupled receptor.
That’s a mouthful, but a G-protein coupled receptor
basically is like a bucket brigade.
So while some receptors in the brain and body
are such that when something, a chemical binds to them,
that receptor has a direct action,
like it opens and allows stuff to rush into the cell,
increases the excitability of the cell,
so-called fast effects.
These G-protein coupled receptors,
and CB1 is a G-protein coupled receptor.
They are more like a bucket brigade
where they kick off a process through one molecule
that then is handed off to another molecule
that this then is handed off to another molecule.
It’s a long chain or cascade of events.
Those long chains or cascades of events
have a lot of opportunity for regulation, for adjustment.
You know, receptor systems in the brain and body,
especially receptor systems like the cannabinoid system
that are used to being kind of tickled, not punched,
you know, tickled by endogenous cannabinoids
every once in a while, some binds, has an effect,
but certainly not bound with incredible potency
and over and over again as they are
when THC is coming into the system.
Well, those systems eventually over time,
they adjust themselves so that the body and those cells
can achieve so-called homeostasis.
So when people are using THC more than twice a week,
what ends up happening
is those G-protein coupled receptors
in the downstream signaling mechanisms
start to adjust themselves
and it requires more and more drug.
So either higher dosages or more frequent use.
And a lot of the positive effects,
the so-called decrease in anxiety,
increased focus, increased creativity,
some of that starts to wane, it starts to dissipate
and people wonder why they have to use so much cannabis
just to achieve a fraction of the effect
that they used to be able to achieve with even a lower dose.
So anxiety is getting worse over time
and that’s anxiety during the drug use
and outside of the drug use.
Some people work around that or try to work around that
by using varying strains of cannabis
or changing the pattern of delivery from smoking to vaping
or from vaping to edible and from edible to transdermal.
Anyway, they go through a lot of gymnastics
and writhing and seeking,
but nonetheless, anxiety increases over time.
Also, it’s very clear that depression increases over time
and especially, this is surprising to me,
but especially for individuals that were not depressed
at the outset of their use.
In other words, they didn’t start using cannabis
because they were depressed,
but rather the depression starts to emerge
as a consequence of the cannabis and THC use.
So that’s serious.
In fact, we now know
based on really solid epidemiological evidence
that depression is not a strong predictor
of seeking out cannabis.
It doesn’t drive terribly many people
to seek out cannabis use,
but cannabis use itself makes people four times likelier
to develop a chronic major depression.
So anxiety is increasing, depression is increasing,
and this turns out to be especially relevant,
important to young people.
Why do I say that?
Well, if you look at the data,
and again, I think some of the strongest data
are data to come out of the Canadian system.
They’ve done some really beautiful controlled studies.
I really hope to invite some of the people
who arranged and ran those studies
as guests onto the Huberman Lab podcast.
But if you look at the data out of Canada,
or you look at some of the data
out of Northern Europe and the US,
what you find is that the probability
that somebody will use cannabis
and then go on to use it chronically
correlates very strongly with age.
So for instance, some of the highest degree of cannabis use
is among individuals 16 to 24 years old.
In fact, in individuals who are 16 to 24 years old,
and in particular in students
and people who are working, surprising,
more than in unemployed populations,
being young, 16 to 24, at least to me that’s young,
and being a student or working,
doubles the likelihood that somebody
is going to use cannabis on a regular basis,
twice or more per week.
The typical age of initiating cannabis use nowadays
is about 19 years old, so 18.7.
And about 20% of people in that age bracket
of 16 to 24 years old are using cannabis daily,
either by vaping, by smoking, or by edible.
That’s an enormous number, at least by my read,
it’s an enormous number.
And here’s why it’s of really serious concern.
During the ages of 16 to 24,
the cannabinoid receptors are still available.
They are not being as strongly driven
by endogenous cannabinoids,
but by ingestion of THC and or CBD,
there are downstream effects
on the signaling within those cells
that all the data point to creating a much,
much higher likelihood of developing major depression,
severe anxiety, or psychosis at later ages.
So to be very clear,
cannabis use between the ages of 16 to 24
in both males and females is increasing anxiety,
increasing depression in the immediate years,
and within the one year’s time or so,
so much so that people are using cannabis ongoing
in an attempt to reduce that anxiety
and reduce that depression.
But in addition to that, the cannabis use,
and because of the signaling mechanisms involved,
are predisposing those individuals
to psychosis later in life.
If you look at individuals
who start using cannabis even younger,
age 14 or even as young as 12,
the probability of psychosis later in life,
in particular schizophrenic or schizophrenic-like episodes,
more than doubles.
So this is of really serious concern.
And this is completely aside
from any so-called positive effects
or beneficial effects of cannabis
that people might derive from occasional use as adults,
meaning people older than 25.
So for the person who’s older than 25,
who eats an edible every once in a while,
or who smokes cannabis every once in a while,
and people love to make the argument,
it’s not as bad as alcohol,
which frankly is a terrible argument,
because if you saw our episode on alcohol,
alcohol is pretty bad.
But even so, it’s just not a good argument.
Saying that something is good
because it’s not as bad as something else
is simply just not a good or valid argument,
at least not biologically speaking.
The use of cannabis in young populations
is very strongly predisposing people to psychotic episodes.
And we know the mechanism by which this occurs.
This occurs by a thinning of the so-called gray matter.
And it’s called gray matter
because with neurons, nerve cells,
they have a so-called cell body.
That’s the part that contains the DNA
and manufactures all the neurotransmitters, et cetera.
And those are shipped out to the other parts of the neuron
that include the axon, the wires between axons.
And those axons under the microscope,
because they have a lot of fatty tissue around them,
and this is healthy fatty tissue
that allows electrical transmission to be fast,
that fatty tissue,
those portions of the cells are called white matter.
So you have gray matter and white matter.
Gray matter are the so-called cell bodies
where the DNA and all the stuff is manufactured.
White matter are the axons or the wires
through which all the key components are shipped out
to the synapse, et cetera.
And I do say wonderful
because this is part of a large-scale consortium
and we will provide a link to the paper.
This was published in Translational Psychiatry
just this year.
Point to the fact that adolescent cannabis use
accelerates the thinning of the prefrontal cortex
and the gray matter in particular.
So what this means is while during normal development,
the gray matter, the prefrontal cortex,
and all the cells there are indeed intended,
it’s a normal process for it to thicken
and then thin a little bit as connections are adjusted
and people learn and mature and grow up.
This is part of the normal healthy maturational process,
independent of cannabis use.
When kids, because these really are kids,
use cannabis and it doesn’t matter
the mode of cannabis delivery,
whether or not it’s vaping or smoking or edible,
that gray matter thins at a much, much greater rate.
And the reason I like this paper
published in Translational Psychiatry this year so much
is that they link the amount of cannabis use,
heavy, moderate, light, or no cannabis use
to the rate of prefrontal cortical thinning.
And it’s absolutely clear from these data
that the more often young people,
meaning individuals between the age of 14 and 25,
the more often they consume or smoke or vape cannabis,
the faster and the more extreme that cortical thinning is.
And the cortical thinning is occurring
in exactly the area of the brain
that’s involved in planning,
in control over one’s emotions, in reflexes,
in organizing one’s life in a number of different ways,
anywhere from cleaning one’s room, literally,
knowing what goes where,
to making plans that extend out through the day,
through the week, through a year,
essentially becoming a functional human being
involves using your prefrontal cortex
in a variety of different contexts
and different sort of time domains,
the time domain of an hour, the time domain of a day,
making plans and being able to execute plans
is fundamental to being a healthy human being.
And it’s absolutely clear from these data
that the more cannabis one uses,
the more impaired those neural circuits are.
There’s simply no other way to view these data.
In fact, so much so that even small amounts of cannabis use
are associated with rates of cortical thinning
and degrees of cortical thinning
that are really detrimental and concerning
for normal cognitive processes.
If you were somebody who smoked marijuana
or consumed cannabis in any form or another
does that mean that your prefrontal cortex
can never be rescued, that it can’t come back?
Well, the short answer is
it probably can be rescued to some degree.
It will depend on how much cannabis you were using
and how often and what strains of cannabis, et cetera.
There’s really no traveling back in time.
As my graduate advisor used to say,
time machines are broken.
At least for now, we don’t have time machines.
So all you can really do is try and emphasize,
first of all, quitting cannabis in any form
and focusing on behaviors that emphasize endothelial cell,
blood flow, health to the brain.
So that would be cardiovascular exercise,
adequate nutrition, not smoking nicotine.
And there are a number of other things that one can do.
We will do an entire episode all about trying to reverse
the effects of cannabis and other drug use
We don’t have time to do a deep dive on that right now,
but all the things that standardize
and kind of promote health, adequate sleep,
good social connection, regular cardiovascular
and weight training exercise, healthy nutrition,
what that represents to you,
healthy metabolic function and weight, et cetera.
Those are all going to facilitate some recovery
of brain function in particular prefrontal cortical function
by way of all the positive effects
that those behaviors and choices have.
But with that said, if you are in the age bracket
that I’ve been referring to,
this 14 to 25 year old age bracket,
and you are a occasional even or chronic cannabis user,
you should be very, very careful and concerned
about the long-term effects that could potentially have.
That statement is bolstered by another statistic,
which is that unlike a lot of other drugs,
the rate of cannabis use is strongly related
to how dangerous people perceive cannabis to be.
And that might seem obvious on the one hand,
if you think something is very, very dangerous,
you would expect that the probability
that somebody would use it would be very, very low.
And if they think something is safe,
the probability would be high.
But that isn’t necessarily the case.
If you think about it, cannabis is a unique instance
in which nowadays we are hearing,
yes, it’s becoming legal in a number of areas.
And we talked earlier about why that’s probably
a good thing in most circumstances,
but that we aren’t just hearing that cannabis is safe,
or it’s not just being implied that cannabis is safer,
but many more people are talking
about the positive effects of cannabis
without a lot of discussion
about the negative effects of cannabis.
And I realize that saying this is going to upset
some people out there,
because I know that there are a number of people
who fought very hard for the legalization process,
and I want to acknowledge that.
I also want to acknowledge the many known positive effects
of cannabis in adults with very occasional use,
provided it is delivered safely
and in the safe context and setting and with legality.
That is entirely distinct from the issue
of whether or not cannabis is safe
for the developing brain and body.
Again, I’m not demonizing anybody for using cannabis,
but I want to make the point very simply and very directly.
It is far and away a different circumstance for the brain,
for an individual to be 25 years or older
and using cannabis in whatever form occasionally,
or maybe even frequently,
than it is for a young person aged 14 to 25
to be using cannabis, either by smoking or vaping,
or by edible or any other form on the brain and body.
It’s absolutely clear that the brain continues to develop
at least until age 25,
and that a huge number of systems
related to mood regulation, so-called executive function,
the ability to organize one’s thoughts,
plan, and execute plans,
essentially to become a functional human being,
that’s one portion of becoming a functional human being,
but certainly an essential one.
All of that relies on the fine-tuning
of this neural circuitry
that we’ve been talking about up until now.
And it’s abundantly clear
that cannabis and THC in particular
dramatically disrupt those processes.
So if this isn’t clear enough just from my statements,
I’d like to point to a particular paper.
This is one of the more impactful papers
in this area in recent years.
This is a paper published in Lancet Psychiatry in 2022.
Title is, Association of Cannabis Potency
with Mental Ill Health and Addiction, a Systematic Review.
There are a number of very important points
in this very fine paper.
Lancet Psychiatry is one of the premier
medical journals out there.
And they evaluated a huge number of studies.
They actually looked at more than 4,000 studies.
They selected the ones that were only the most rigorous
in terms of study design and analysis
and rigor of conclusions.
And they looked at how early use of cannabis
impacted later probability of development of psychosis
and other psychiatric conditions.
And the takeaways from this study are very clear.
First of all, chronic cannabis use,
so more than twice per week,
has consistently been associated
with mental health disorders.
I’m pulling some phrases directly from the paper.
Heavy cannabis use, meaning cannabis use
more frequent than twice per week,
has been associated with four times the risk of psychosis
later in life, in particular,
schizophrenia and bipolar-like episodes.
Now, we’ve done an episode on bipolar disorder,
so-called bipolar depression.
We have not yet done one on schizophrenia,
but both bipolar disorder and schizophrenia
have a very, very strong genetic component.
There’s a 30, three, zero, 30 times greater likelihood
that you’ll have bipolar disorder
if you have a first relative who has bipolar disorder.
And then it’s also the case that using cannabis,
especially during adolescence and the teen years
and up until age 25,
create a four times greater risk of psychosis
for those that have a predisposition
to bipolar disorder and or schizophrenia.
Now, I don’t hear very much about this in the media.
This paper got some attention
and then it sort of got swept away.
I don’t think that was an intentional sweeping way.
There’s just a lot of events in the world,
as you well know.
But I think it’s a particularly important set of findings
because obviously in looking at so many studies,
it distills out the strongest findings that are out there
and really pulls the consistent messages
that are arriving from all these different studies.
And as they point out, and again, I’m paraphrasing here,
this is the first systematic review
of the Association of Cannabis Potency.
And all of the data point to a very clear conclusion,
which is the more potent the THC concentration,
the higher probability of developing psychosis
or a major depressive episode
or a major anxiety disorder later in life.
That should be of particular concern
because we know, we are absolutely clear about the fact
that with the advent of all these new strains of cannabis
and with the engineering and availability of cannabis
at much higher potency, meaning THC potency,
the risk of psychosis is going up and up
and is likely to continue going up
unless something is done to reduce the frequency
of cannabis use to zero, ideally,
or to very low frequency, very low potency
in adolescents and teens and people age 25 or younger.
I know a lot of people don’t want to hear this message
because first of all, it’s alarming.
And second of all, as I mentioned earlier,
the statistics tell us that the greatest number of people
that are starting to use cannabis
are in the age bracket of 16 to 24.
Many of them are functional in other areas of life.
They are students, they are employed, et cetera.
But when you couple that with the fact
that the most frequent adopters of cannabis use
are in this age bracket of 16 to 24,
they’re twice as likely to use as other individuals
or to start using cannabis as our other individuals,
plus the general perception out there
because of the way that cannabis is discussed in the media
and by sports figures and by celebrities
and by politicians, et cetera,
that it’s not as bad as alcohol and maybe not that bad
and maybe even has health benefits,
then you’re essentially setting up a system
where young people are far more likely to adopt
and continue cannabis use without realizing
these serious health consequences that await them later.
With all of that said, I of course, again,
want to acknowledge that there have been
well-demonstrated effects of cannabis for reducing pain,
in particular in chemotherapy and in the context
of reducing nausea in people suffering
from cancer or chemotherapy.
There is a well-known effect
that one can generally point to as positive
using cannabis for things like glaucoma,
for lowering intraocular pressure
and offsetting the loss of neurons
that would lead to blindness,
although there are other tools, of course,
that don’t involve cannabis use
that can accomplish that as well.
So-called intraocular pressure lowering drugs or drops.
There is a list of probably a dozen or more psychological
and bodily ailments that can be aided by cannabis use,
in particular edible cannabis use of particular strains.
I, of course, I’m going to address each
and every one of those in episodes where I’m talking,
for instance, about eye disease or about chronic pain.
I am in no way, shape or form trying to rob
the incredible efforts of the laboratories
and people that have worked very hard to study
and establish the valid uses of cannabis
for treating various ailments
and that continue to study cannabis
in order to try and ameliorate the symptoms
of different ailments.
But today I really wanted to emphasize
the biology of cannabis.
Some of the often discussed effects,
I guess one could call them positive effects,
things like enhanced creativity,
and really point to the nuance
and actually the divergence of people who take cannabis
and some experience heightened levels of creativity
and some do not.
Some people experience heightened levels of sexual arousal
and some people experience the exact opposite
and so on and so forth.
Rather than focus on all the potential positive
and sort of emerging positive data about cannabis
in different medical contexts.
And at the same time,
I strongly feel that it’s important
to acknowledge the shocking,
because there’s really no other way to describe it,
the shocking effects of cannabis use
on the developing fetus and the fact that so many pregnant
and lactating mothers are using cannabis.
I mean, that number 15% still has me dizzy
with kind of disbelief,
and yet we need to acknowledge this
and address this immediately.
And I think it’s vital to understand that cannabis use
through any delivery mechanism,
smoking or vaping or edible or otherwise,
is very, very concerning.
In fact, dangerous to the developing brain,
certainly for the fetal brain and for the baby brain,
but also for the adolescent brain
and for the teen and young adult brain,
not just because of the effects that it can have
in the immediate term,
those slow creeping increases in anxiety and depression
brought on by cannabis use,
but also the time release, if you will,
on the development of psychosis
and other types of major psychiatric disorders
later in life.
I acknowledge we’ve covered a lot of ground today,
and yet there’s still far more ground
that we could have covered
and that we will indeed cover in future episodes.
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So once again, thank you for joining me
for today’s discussion all about cannabis.
And as always, thank you for your interest in science.