I'm Dr. Chris Masterjohn of
chrismasterjohnphd.com,
and you're listening to Episode 56 of
Mastering Nutrition, Part 4, our fourth and
final part of the four-part series Nutrition in Neuroscience.
Welcome back to the safari.
I am your tour guide, taking you through the
wonderful world of the leading
neuroscience textbook known as Neuroscience,
pointing out all the things relevant to nutrition.
In Part 1 we talked about how to nourish the basic mechanisms of a neuron's ability to
transport information from one place to another.
In Part 2 we talked about the neurotransmitters, all the major ones and how they relate to
nutrition.
In Part 3 we talked about our five senses with a special detour into pain management.
And now in our fourth and final installment, we talk a little bit about autonomic control
of our involuntary processes, and we mostly talk about higher-order cognitive functions.
We have a deep discussion of dopamine, often misunderstood as a pleasure chemical, about
a signal-of-value calculation in the basal ganglia, how it integrates signals of value
ranging from emotional inputs from the amygdala, memory inputs from the hippocampus, subjective
preference, historic experience of the rewards of different choices, and comparisons of different
choices, all coming in from the cortex to signal whether something has enough value
to invest energy into it.
In fact, we look at movement disorders of the basal ganglia, like Parkinson's disease
as fundamentally not a problem with movement but a problem with a perception of the value
at a subconscious level, a perception of the value of investing energy in controlling movement.
We talk about the tonic and phasic dopamine pools and how they regulate our ability to
let go and our ability to focus; the critical importance of methylation and nutrients like
folate, vitamin B12, choline, and glycine in that process; the critical importance of
GABA in suppressing the things that dopamine doesn't signal has value in order to make
the dopamine signal of value actually be meaningful.
We talk about autonomic control of many of our involuntary processes; the sympathetic
nervous system mediating the fight-or-flight response and the parasympathetic nervous system
regulating the rest-and-digest response; the relative roles of acetylcholine and norepinephrine
in those processes and the importance of nitric oxide to the sexual functions of the autonomic
nervous system; the nutrients that support those and how they might be manipulated if
you're always stuck in the rest-and-digest mode or if you're always stuck in the fight-or-flight
mode; a little speculation on the role of spinal problems, misalignments and tightness,
in screwing up the autonomic nervous system.
Sleep and circadian rhythms, the importance of vitamin A, blue blocking, morning sun exposure,
vitamin B6, oxidative stress; why you can't ever mimic your natural melatonin rhythm with
melatonin supplements; why circadian entrainment, light and dark practices, light hygiene might
be the most important thing to preventing you from getting up in the middle of the night
and peeing but why salt might help, too; whether the timing of carbohydrate, protein, and choline
supplements makes a difference for your daytime wakefulness, your nighttime sleepiness, your
deep sleep, and your REM sleep; possibility that glycine and magnesium could help get
rid of conditioned fear responses, the things that we shouldn't be fearful of.
And final thoughts on consciousness.
Are we a ghost in the machine, or are we just a machine?
Is there a soul behind our awareness, and does science have anything to say about it?
And then the default mode network, something suppressed by psychedelics and certain types
of meditation practices, something that goes dysfunctional in autism and schizophrenia
but is fundamentally about our inward, introverted-directed processes, contrasted with the executive control
network, which is all about our relationship to the outside world and our extraverted functions.
I talk about how things that had nothing to do with people skills but allowed me to flex
my extroverted muscles, like exploring the outside world on my own, helped me with my
people skills, and I speculate because this is because all of our extraverted functions
fall under this executive control network to some degree, just like all of our introverted
functions fall under this default mode network to some degree.
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00:06:12 Anatomy of the brain Alright, now that we've covered our five senses,
let's talk a bit about value, motivation, and decision-making.
And we'll start with dopamine as a signal of value in the basal ganglia.
A ganglion is a cluster of neurons, and ganglia is the plural of ganglion.
The basal ganglia are several related ganglia that are at the base of the forebrain.
The forebrain is one of the three major divisions of the central nervous system based on the
embryonic origin of the different parts.
We can divide that into the forebrain, the midbrain, and the hindbrain.
The forebrain consists of the cerebral cortex, which, if you look at a picture of the brain,
is the wrinkly part of the brain that has all the different invaginations and folds.
And that is where much of our higher-order processing goes on.
In addition, we have what's called the cerebral nuclei.
These are closely related to the cortex and consist of the basal ganglia, the main part
that we're thinking about in this section, the amygdala, a major center of emotion, and
the basal forebrain, which is the major source of acetylcholine within the brain.
The forebrain also consists of the thalamus, which is very involved in communicating our
senses in partially processed form to get into the cortex for higher-order processing,
and also the hypothalamus, which sits just below the thalamus and is very involved in
homeostasis.
And then the retina, that we just talked about in vision, is also considered part of the
forebrain.
The midbrain is a small collection of nuclei in between the forebrain and hindbrain that
consists of the substantia nigra and the ventral tegmental area, or VTA, which are two areas
that are the main sources of dopamine, which is highly relevant to our discussion here,
as well as the superior and inferior colliculus.
The superior colliculus is very involved in controlling the motions of your eyes, as well
as changes in your head and even other body parts towards particular things that catch
your attention in visual space and may even have a role in shifting your attention to
different parts of visual space.
The inferior colliculus is involved in locating sounds in space.
And there are several other parts of the midbrain, as well, that I won't go into.
The hindbrain consists of the cerebellum, which may play roles in cognitive function
but is most well-established to control motor coordination and learning.
So, it's not the thing that makes you move, but it edits your movements, and it learns
about your movements to help you move more precisely and correctly.
And then the pons, which has several functions.
The pons connects the forebrain to the cerebellum.
The pons is involved in sleep, breathing, swallowing, controlling your bladder, hearing,
equilibrium, taste, eye movement, facial expressions, facial sensations, and posture.
And then the medulla oblongata, which controls breathing, heart rate, blood pressure, and
reflexes like vomiting, coughing, and sneezing.
The pons, and the medulla, and the cerebellum together make the hindbrain, and the hindbrain
and the midbrain together make the brainstem.
So, when we say that the basal ganglia are at the base of the forebrain, we're talking
about being right at the bottom of that wrinkly, forward projection that you look at when you
look at a picture of the brain.
I'm not a neurosurgeon, but my guess from looking at the pictures is that you would
find the basal ganglia if you went in roughly at eye level and sort of traced level back
to the middle of your head.
00:10:45 The role of the basal ganglia in suppressing the investment of energy in any
type of program until there is a worthwhile reason not to suppress it, and how dopamine
acts as a signal of value in the basal ganglia via disinhibition
Now, the chapter of this textbook about the basal ganglia is called "Modulation of Movement
by the Basal Ganglia."
Now, this makes sense because Parkinson's, which involves hypofunction of movement, and
Huntington's disease, which involves hyperfunction of movement, are basal ganglia disorders,
and they're most known for their effects on movement.
And so, it makes tremendous sense to think of the basal ganglia primarily by thinking
of movement.
But I'm not going to take that perspective.
I have done a lot of research on dopamine, and I consulted some other papers to make
this section, and I want to highlight something that they put in a sidebar at the very end
of the chapter.
They say, "Throughout this chapter, we have discussed the motor loop, which is how the
basal ganglia loops into the cortex to control movement.
But there is also a prefrontal loop involved in planning, short-term memory, which is the
memory that's occupying your attention right now, and attention.
And then there's also a limbic loop involved in emotion, motivation, and mood transitions."
So, I want in this section to integrate the chapter with some other papers that I've read
that I'll link to in the show notes to present the basal ganglia as having its primary role
to suppress the investment of energy in any type of program, whether it's motor for movement,
or it's attention, or it's mood switching, until there is a worthwhile reason not to
suppress it.
And dopamine is what provides that reason not to suppress it.
And what dopamine does is not activate a particular program.
Rather, the basal ganglia at default suppresses every investment of energy, and dopamine comes
along to represent that there is enough value to disinhibit one specific program under consideration.
And when you do that, it's still important that the basal ganglia is suppressing every
other alternative and is just lifting the embargo, so to speak, on one particular thing
that through dopamine, you subconsciously at the level of the basal ganglia have calculated
to be worth the investment of energy.
What dopamine does here is it signals value that is summed from information coming from
other areas.
There are sensory motor areas of the cortex that provide information about the value of
moving.
There are other areas of the cortex that provide information on subjective preference, information
on reward history, meaning not what you like but what you've benefitted the most from in
the past; that provide information about the cost-benefit analysis of switching, meaning
here it's not about the absolute value of your reward history but comparing that value
to what you know about the value of all the other alternatives.
There's also input from the amygdala that provide emotional tone to certain possibilities.
And then there's information from the hippocampus coming in about your memories, about all the
possibilities available to you, and that might not just be declarative memories that you
can describe but also nondeclarative memories that are things you've experienced that are
stored in your brain but that you don't necessarily have any conscious knowledge about.
The basal ganglia can be divided into two parts, called the striatum and the pallidum.
The striatum is the input zone where all this information is coming in.
The pallidum is the output zone where the output is mostly going to the thalamus in
order to process information that then goes to the cortex, or it's going directly to the
superior colliculus to control eye movements and maybe to some degree to control movements
of the head, arms, or even just your attention toward a specific target in visual space.
There are multiple subdivisions of these spaces that I'm not going to go into in this discussion
just because we don't have to get into that level of detail here.
The pallidum, the output of the basal ganglia, has a tonic, inhibitory GABAergic projection
to the thalamus and the superior colliculus.
That means that by default, these GABAergic neurons are inhibiting all of the possibilities
in the thalamus and the superior colliculus.
Meanwhile, the striatum has GABAergic projections from itself to the pallidum, and these are
inhibitory neurons that inhibit the inhibitory neurons of the pallidum.
In other words, what do you get if you inhibit an inhibition?
You in net get a stimulation.
But what we call it in technical language, because we're inhibiting an inhibitory process,
we say that's disinhibition rather than excitation.
So, what's mainly interesting to talk about is the very specific and dense connections
that striatal neurons make to parts of the pallidum that have very specific things under
their control.
There are also very diffuse connections of glutamatergic and GABAergic neurons in the
pallidum that regulate how inhibitory the pallidal inhibitory tone is.
But I'm going to put that point aside and just talk about the things under highly specific
control.
So, dopamine has its influence ultimately coming either from part of the brain called
the substantia nigra pars compacta or from the ventral tegmental area, or VTA.
And the substantia nigra pars compacta is more important in controlling movement.
The ventral tegmental area, or VTA, is more important in controlling cognitive processes,
and emotions, and motivation-related things.
But they're basically all doing the same kind of thing here.
So, dopamine will be released in the striatum to act on specific striatal neurons to enhance
their GABAergic inhibition of the pallidal GABAergic neurons and thereby disinhibit the
target in the thalamus or the superior colliculus and thereby allow whatever program would be
initiated in the thalamus or the superior colliculus to go on.
And what dopamine is basically saying is, there is enough value attached to this specific
program, whether it's moving your head to look at a specific thing, or it's changing
your mood state, or it's putting your attention somewhere, or it's making you move your leg
up, making you do a dance step, or whatever it is.
It's saying, there is enough value to allow this thing to occur.
00:19:00 Why we can view Parkinson's as fundamentally not a problem with movement
but as a problem with a perception of the value of investing energy in controlling movement
If you think about dopamine as a signal that there is enough value to invest energy in
something, then you could see the hypo-movement of Parkinson's through the value lens.
In other words, rather than saying, this is evidence that dopamine and the basal ganglia
play a role in movement, you could look at that and say, what's happening here is the
dopaminergic neurons that specifically connect to the parts of the striatum that signal the
value of motor movements are degenerating.
So, you have loss of the dopamine neurons concentrated in areas that have movement under
their control, but what you're losing is the subconscious calculation that any of those
movements or investments of energy in movement have value.
And you might look at that on the surface and say, well, that would explain the weakness,
that would explain the slowness, but what would explain the hand tremors, where it seems
like you have more movement during the tremor?
But it's not about, is it worth it to move, it's about, is it worth it to invest energy.
And controlling your movements is actually extremely energy-intensive.
The lowest energy state of a muscle is to be contracted, right?
What's the lowest energy state you could be in?
Dead.
And what happens when you die?
Rigor mortis.
Right?
The default low-energy state of a muscle is not relaxation.
Relaxing your muscle is extremely energy-intensive.
Contracting your muscle in a deliberate movement is also extremely energy-intensive.
So, your default state is not to squat heavy weight.
It's not to lift up a refrigerator.
But it is to have aimless contraction of the muscle.
You have to invest energy in the intentional control of your movements.
You have to invest energy in relaxing your muscles.
So even the tremors and aberrant contractions could be seen as a loss of the subconscious
calculation via dopamine that there is value in properly controlling your movements, that
there is value in relaxing your hand enough to not tremor.
At the same time, you need to invest energy in keeping your attention on something, and
you need to invest even more energy in switching your attention to something else.
It takes a lot of energy to transition from happiness to sadness, or from sadness to happiness.
So your ability to switch between mental states is also going to be controlled in the basal
ganglia by dopamine because you have inputs from the amygdala about your emotions, you
have inputs from the cortex about your subjective preferences of how you like to feel, and that's
all going to go into a calculation of whether it's worth it to invest energy in the program
of switching from happiness to sadness or from sadness to happiness.
00:22:26 Tonic and phasic dopamine and the importance of COMT-mediated methylation for
regulating the tonic level of dopamine So, how do we relate this to nutrition?
Well, I did a whole episode on this called "Methylate Your Way to Mental Health With
Dopamine," and the principal framework here is the idea that, just like tonic and phasic
norepinephrine like I talked about before, there is tonic and phasic dopamine that represent
two different pools that are under the control of different enzymes.
Tonic represents the ambient presence of dopamine that is continuous over time.
Phasic represents very fast bursts of dopamine that last fractions of a second.
The tonic dopamine downregulates dopamine receptors, kind of like acetylcholine downregulates
acetylcholine receptors in the muscles when you're poisoned with organophosphates, only
here, it's not poisoning, it's just a level of tuning.
So, the more tonic dopamine you have, the fewer dopamine receptors you make, and the
less sensitive you are to a phasic burst of dopamine.
A good analogy to use is imagine a wave rising above sea level.
When you judge how big a wave is, do you judge it by the height of the wave to the ocean
floor?
No, you judge it by how high the wave rises above the general body of water that you're
looking at.
So, you could think of your brain reading a phasic burst of dopamine like a wave against
the background of tonic dopamine, representing the body of water that it's rising above.
The higher the level of tonic dopamine, the smaller that wave of phasic dopamine looks
like to the brain.
The lower that level of tonic dopamine, the larger that wave of phasic dopamine looks
to the brain, and that's mediated by how sensitive are the cells to the phasic dopamine burst
based on their expression of dopamine receptors.
Well, the phasic dopamine burst, like every other neurotransmitter, you want to clear
it relatively rapidly, and you clear it with reuptake primarily.
And once it's in the cell at the synapse, you're primarily using monoamine oxidase,
which is a copper-dependent enzyme, to break down the dopamine.
But not all of the dopamine gets taken up very quickly.
A lot of it starts to diffuse out of the synaptic cleft and start to become part of the ambient
pool of dopamine.
And outside of the synapse, that level of dopamine is largely going to be dictated by
the expression of catechol-O-methyltransferase, or COMT, the enzyme that methylates that dopamine.
As a result, the tonic level of dopamine is reduced primarily by COMT, whereas the phasic
pulses of dopamine are regulated mainly by the dopamine transporters and are not influenced
as much by COMT.
So, if you improve your methylation status, you will have lower tonic dopamine, and the
phasic pulses of dopamine will look bigger.
The more your methylation of the tonic dopamine pool, the more that phasic dopamine will signal
that something has enough value to invest energy in, especially to invest energy over
a long period of time, and especially to invest energy in fundamentally changing your attention
to something new.
Now, that might sound a little bit contradictory about investing time in one thing versus changing
your attention to something.
But remember, dopamine is not the signal of something's value.
Dopamine is the signal that represents the calculation of all the value inputs.
So, you largely have glutamatergic neurons that are coming in from the cortex, the amygdala,
the hippocampus, communicating emotional value, memories, whether conscious or subconscious,
value preferences, reward history, comparison of rewards of different options.
And all these are getting calculated to how high is the stimulation of that relevant dopaminergic
neuron, how stimulated is it to be worth sending out a big pulse of dopamine in response to
that thing.
It's not methylation that's dictating your subjective preferences, or your reward history,
or your memories, or your emotions.
It's methylation that's dictating how high of a bar do you need to meet with all those
inputs to signal that that decision and that investment is worthwhile.
So, if you have very low dopamine across the board, you may not be very motivated to do
anything at all.
If you have extremely low tonic dopamine, you might not ever stick with anything.
But if your level of tonic dopamine is too high so that the phasic pulses in response
to things that you value are never read as being meaningful enough, then you may get
stuck on something that you don't want to be stuck on because you just can't convince
your subconscious brain that the next thing has the value that you think it has.
Because you do have your cortex telling your striatum about your preferences, saying you
really prefer it, and you do have your reward history suggesting that it would be beneficial,
and you do have your amygdala telling your striatum that it has positive emotional tone,
and you do have your hippocampus telling your striatum that there's all these memories that
underlie why that would be a positive thing, but if all of that input makes a phasic pulse
of dopamine that just doesn't get read as having much value because the dopamine receptors
are so downregulated by the high pool of tonic dopamine, then you are stuck in a rut, and
you just can't convince your subconscious brain to make you summon the energy to change
what you're thinking about, to change your mood, or to invest effort in something worthwhile.
So, the net effect here is, assuming that you have enough nutrients to synthesize the
dopamine, you want the proper balance of methylation so that you can maintain the tonic pool just
right.
High enough to stick to something and focus on it but low enough that if something really
high-value comes in that you should change your attention to, you are free to change
your attention to that thing and then stick and focus to that thing.
That means having the methyl donors folate, B12, and choline, and it means having enough
glycine as the buffer of overmethylation.
On top of this, vitamin A regulates dopamine receptors.
In vitamin A deficiency, you don't have enough expression of dopamine receptors.
So, you can have the right level of dopamine, and ultimately, it's not going to communicate
the value of that thing.
I would think that would mimic having too high a pool of tonic dopamine.
00:30:36 The importance of GABA in suppressing the programs that dopamine doesn't signal
has value in order to make the dopamine signal of value meaningful
I also think this is interesting to turn back to the discussion about how the GABA supplement,
800 milligrams, decreased reaction time on choice-switching tasks.
That suggests a better ability to make decisions under pressure because of better suppression
of the alternative choices.
Well, that sounds a lot like how the pallidum of the basal ganglia suppresses all of the
alternative options.
The ability of dopamine to attach high value to a particular thing is dependent on the
GABAergic suppression of all the alternatives.
So, if you don't have enough GABA, then you might not be able to put that dopamine to
use properly because the alternatives aren't actually being suppressed.
00:31:33 Overview of the autonomic nervous system; the sympathetic nervous system mediates
the fight-or-flight response, and the parasympathetic nervous system mediates the rest-and-digest
response.
Alright, let's move to their discussion of the autonomic nervous system, also known as
the visceral nervous system, which is controlling the involuntary actions of cardiac muscle,
smooth muscle, and your glands.
This is all under the control of the hypothalamus, and we have neurons from the CNS, the central
nervous system, that we call preganglionic, and lower motor neurons, meaning motor neurons
outside the central nervous system that are called postganglionic, that meet and interface
at the autonomic ganglia.
For the parasympathetic nervous system, which is often called the rest-and-digest nervous
system, the ganglia are near the target organ.
So, if you're controlling the pancreas, the ganglia is near the pancreas, et cetera.
For the sympathetic nervous system, the ganglia are all near the spinal cord.
Most parasympathetic functions are under the control of the cranial nerves that come from
the brainstem.
These are the ones that constrict your pupils, stimulate your saliva, constrict your airway,
decrease your heartbeat, increase the digestive actions of your stomach, decrease your blood
glucose by enhancing glucose uptake, enhancing glycogen storage, and suppressing gluconeogenesis,
and increase the digestive actions of your intestines.
A few of the parasympathetic functions are under the control of the sacral nerves, meaning
at the bottom of your spine, and these include increasing intestinal activity, contracting
your bladder, which helps you pee, and arousal of and erection of the penis and clitoris.
Most of the sympathetic functions are under control of nerves coming from the thoracic
spine.
These are the ones that dilate your pupils, decrease your saliva, constrict your blood
vessels, relax your airways, increase your heart rate, increase your sweat, decrease
your digestion, increase your blood glucose, mainly by releasing stored glycogen, and increased
adrenal hormones, epinephrine and norepinephrine.
Some of the sympathetic functions are under nerves that come from the lumbar spine, such
as decreasing the digestive actions of your intestine, relaxing your bladder, which helps
it fill, as opposed to contracting your bladder, which helps you pee, and stimulating orgasm.
I find it interesting that these different functions are just located at different parts
of the spine.
I would think, but I'm not sure, that if you have problems in your spine, that it could
spill over into some of these functions, and I would think that it would have a greater
impact on the sympathetic rather than parasympathetic, simply because the cell bodies in the ganglia
are actually very near your spine for the sympathetic nervous system and not for the
parasympathetic.
But the nerves are still coming out of the spine even for the parasympathetic, so who
knows.
And I find it interesting because I have a lot of tightness in my thoracic spine that
looks like it's right around the area that controls the heart rate, and my resting heart
rate has always been pretty high, even at my youngest and athletically fittest.
And so, I do wonder whether there's a connection there.
I suppose a lot of chiropractors, and craniosacral therapists, and other bodywork people would
probably agree that there is a connection.
I just don't know how much science there is on it.
00:35:16 The roles of acetylcholine and norepinephrine in the autonomic nervous system, and the importance
of nitric oxide to the sexual functions of the autonomic nervous system
For all aspects of the autonomic nervous system, acetylcholine is the neurotransmitter used
at the preganglionic points.
Postganglionic, the parasympathetic is mostly controlled by acetylcholine, except for the
sexual functions.
The sexual functions of the parasympathetic nervous system use nitric oxide.
In the sympathetic nervous system, most of the functions use norepinephrine except sweating.
Sweating uses acetylcholine.
Nitric oxide is the one of these neurotransmitters that I haven't connected to nutrition yet,
so I'll say a few things about that.
Nitric oxide is made from arginine, so you need enough arginine.
There are arginine supplements, and you can also use citrulline supplements as possibly
a better way to increase arginine levels.
Of course, there is enough arginine in the protein that you eat if you're eating adequate
protein.
The enzyme is nitric oxide synthase, and it has zinc-sulfur clusters that keep its proper
conformation.
If you have zinc deficiency, this conformation falls apart.
Maybe there's a form of sulfur deficiency where the same thing would happen.
And if you have oxidative stress, remember, that general wear and tear on the tissues
associated with aging, enhanced with metabolic problems, toxin exposure, and so on, that
will cause the zinc to fall out of the zinc-sulfur clusters that keep it together, and that will
also lose the function of the enzyme.
If you look at some of the literature out there, this is called eNOS uncoupling, and
that's because nitric oxide synthase in the endothelial form, which is the form in the
blood vessels, is abbreviated eNOS, and the reason it's called uncoupling is because the
basic structure has to have two units of eNOS bound together by this zinc-sulfur cluster.
So, to say it uncouples means that that pairing of the two parts falls apart.
And this is bad not only because you make less nitric oxide but also because the enzyme
starts dysfunctioning and worsens oxidative stress.
So, when you're thinking about nourishing nitric oxide, you're thinking about arginine
from protein, you're thinking about zinc, and you're thinking about antioxidant support.
And remember, that's needed for erections, both during male and female arousal.
Since overall, acetylcholine is more dominant in the parasympathetic than sympathetic nervous
system, perhaps you could make a case that choline supplementation might help you if
you seem to be stuck in the fight-or-flight mode and kind of never properly in the rest-and-digest
mode.
If you're in the opposite position, you want to focus on nutrients that support norepinephrine
production, like tyrosine—protein, but perhaps tyrosine supplementation, antioxidant support
for the BH4, copper, iron, maybe salt, vitamin B6, and vitamin C.
00:38:33 Sleep and circadian rhythms, the importance of vitamin A, morning sun exposure,
and avoiding blue light at night And now we come to their discussion of sleep.
Why do we sleep?
Sleep helps us, as I mentioned before, not mentioned in the book, make cholesterol for
our synapse production and our myelin.
As they do mention in the book, sleep helps restore brain glycogen content.
Remember, your brain uses 120 grams of carbohydrate a day, so to have some carbohydrate on hand
is very helpful.
It reduces the energy needed for heat and metabolism, and helps with the consolidation
of memory, and helps with the removal of wastes.
One thing that I thought was very interesting here was a discussion of how you can use sensory
experiences to enhance learning in your sleep.
So, if you're studying something or learning to do something and you are exposed to, say,
the smell of pine, then you can expose yourself to the smell of pine while you sleep, and
the sensory association with those things will enhance the consolidation of memories
around that thing that you were learning.
I've never tried that, but it sounds rather interesting.
So, they begin their discussion of sleep with a discussion of the circadian rhythm, and
as I mentioned when we were talking about the retina, vitamin A is part of the melanopsin
protein in the intrinsically photosensitive retinal ganglion cells, ipRGCs.
And that carries the signal of blue light to the suprachiasmatic nucleus of the hypothalamus,
which initiates a program in the brain associated with daytime, including shutting down melatonin
synthesis in the pineal gland, which is part of your nighttime program.
So, vitamin A, you need for your circadian rhythm, and that's primarily found in liver,
and egg yolks, cod liver oil, and butterfat, so large amounts in liver, small amounts in
butterfat.
That's in the form of retinol, which is the form that your body uses.
You can also convert carotenoids in red, orange, yellow, and green vegetables into retinol
for use in the body.
Some people are better converters than others, so I believe it's always good to have some
retinol from animal products in your diet.
I think the best way to get the signal in that it's daytime is to get at least a half
hour of exposure to open outside sunlight in the morning.
So, going for a morning walk or doing something you would otherwise do, reading the paper,
looking at your phone, whatever you do in the morning, exercises, if you do it outside
in the sunlight, I think that's the best way to get that.
It's really important that it be at the same time every day, or at least close to the same
time every day, especially if you don't feel like you have a working circadian rhythm,
and you're trying to establish one, then it's really important to be very consistent and
regular.
At night, you need to have the blue light shut off to tell your brain it's nighttime.
Best thing to do in terms of light is to practice blue blocking for two to four hours before
bed.
A simple way to do that is to not use screens, but if you do use screens, like your phone
or your computer, have iOS Night Shift, or f.lux on the computer, or some other program
that will warm the screen.
A more intense way to do that would be to have blue-blocking glasses, and to have ambient
low-blue lights for your apartment or house, and things like that.
But decrease your exposure to blue light at night for two to four hours before bed, and
that will start the synthesis of melatonin.
00:42:17 Melatonin synthesis, the importance of vitamin B6, BH4, oxidative stress, vitamin
B5, methylation, and tryptophan uptake into the brain
To make melatonin, ultimately this is coming from the same pathway as serotonin.
So, serotonin is an intermediate in the synthesis of melatonin from tryptophan.
So, if you recall from earlier when we talked about serotonin, we get tryptophan from dietary
protein, and then using BH4, which is inhibited by oxidative stress, and using vitamin B6,
we make serotonin.
But then in the pineal gland, we continue that process by first N-acetylating serotonin
to make N-acetylserotonin, which requires acetyl CoA, which is dependent on healthy
energy metabolism and particularly on vitamin B5, or pantothenic acid, which is literally
part of the coenzyme A molecule.
And then we take N-acetylserotonin, and darkness stimulates its methylation to melatonin.
So, all the nutrients involved in methylation, especially folate, B12, and choline, are all
going to be important here.
Now, it's important—I could have mentioned this for serotonin, as well—it's important
that this tryptophan get into the brain.
And one of the problems with that is when you eat dietary protein, there are other amino
acids, collectively known as the large non-polar amino acids, that inhibit the transport of
tryptophan into the brain.
If you eat carbohydrate to stimulate insulin, you take those other competing amino acids
into your muscle cells, and you increase the ratio of tryptophan to those competing amino
acids in the blood.
That helps get the tryptophan into the brain more effectively.
The timing doesn't matter because the serotonin needs to be in your brain anyway, and in fact,
in melatonin synthesis in the pineal gland, you basically store N-acetylserotonin and
wait for darkness to initiate its methylation to melatonin.
So, you could get this in at breakfast time, and that would be sufficient to have it there
at nighttime.
So, some bolus of carbohydrate and high-glycemic carbs—ironically everyone says high-glycemic
is bad and low-glycemic is good—but high-glycemic carbs, like white rice, are more effective
than low-glycemic carbs at stimulating the insulin that gets the tryptophan into the
brain.
On the other hand, if you're trying to eat a low-carb diet, I would recommend trying
some tryptophan on an empty stomach because if you're fasting, your amino acid levels
are going to be lower because you haven't eaten protein for a while.
Taking the tryptophan then, because it's alone, will help the tryptophan increase its ratio
to the competing amino acids and get into the brain.
So, either carbs with your protein at at least one of your meals in the day, or tryptophan
on an empty stomach, can get tryptophan into the brain.
00:45:16 Why you can't mimic your natural melatonin rhythm with melatonin supplements
Now, one of the things that impressed me in just flipping through this chapter on sleep
in the textbook is they have a graph of melatonin levels through the night.
The melatonin naturally peaks at 2:00-4:00 a.m., and it's a curve where it doesn't just
turn on and then go off when the light comes on.
It just naturally, slowly rises over the course of hours to peak at 2:00-4:00 a.m., and then
naturally, slowly decreases.
So, I don't see how you can possibly reproduce that with a supplement of melatonin.
I'm not against taking melatonin.
I, in fact, always have a bottle of melatonin on hand in case I need it.
Mainly I use it during traveling.
But I used to be addicted to melatonin—not addicted, but my insomnia was so bad, the
only way that I could fall asleep at night was to take time-release melatonin.
And I regard the success that I have had—I regard it as a sign of my success that I never
need melatonin to sleep anymore.
If your treatment for insomnia involves taking melatonin, you haven't fixed your insomnia
yet, I'm sorry, because fixing it means you make your own melatonin.
And making your own melatonin is the only way you're ever going to get that nice, slow
increase to a peak at 2:00-4:00 a.m. that then goes back down nice and slowly again.
There's just no way to have melatonin released into your system at a rate that reproduces
that curve.
And I don't know what the downsides are to not having that curve, but you're supposed
to have that curve, and so it's better for your physiology to work normally than for
it to be very badly hacked.
00:47:00 Antidiuretic hormone, the importance of light hygiene for preventing you from getting
up to pee in the middle of the night, and why salt might also help
At night, you also have an increase in antidiuretic hormone, or vasopressin, ADH, that rises to
suppress you from needing to pee at night.
So, several things strike me about this.
First of all, let's say you have this problem that you pee at night.
Probably the circadian regulation of your ADH isn't up to par.
Well, we could say a few things about that.
Number one, that's one of the neuropeptides that requires vitamin C, copper, zinc, and
glycine to produce the alpha-amide peptidylglycine residue that supports its biological activity,
so those nutrients are needed to help prevent you from peeing at night.
They shouldn't be needed at night.
They should just be needed as good status in general to prevent that problem.
Second thing is, if your ADH is regulated by your circadian rhythm, then that means
that you need a circadian rhythm.
I'm sorry, but just because you sleep eight hours a night doesn't mean you have a working
circadian rhythm.
Just because you fall asleep when it's dark and wake up when it's light does not mean
you have a working circadian rhythm.
If you have a working circadian rhythm, you get tired and ready for bed at a pretty similar
time every night, and you wake up without needing an alarm to do it—maybe you have
an alarm that you wake up to every day because you're giving yourself chronic sleep deprivation,
but let's say you decided not to give yourself chronic sleep deprivation by setting an alarm
every day, you would in that case wake up at a pretty similar time every day because
you have a working circadian rhythm.
I think a lot of us are walking around without working circadian rhythms, and if you wake
up at wildly different times of day on the weekend than on the weekdays, you probably
don't have a very strongly working circadian rhythm.
So, I'm not out there to preach morality about when to go to bed and when to wake up, but
if you have problems with waking up to pee in the middle of the night, and that's hurting
your sleep, if you have not done the work to entrain a working circadian rhythm, that's
definitely one of the things to do.
Then, one final thing I'd think is, salt stimulates ADH.
And it's not that when you eat salt, you want to not pee.
It's that when you eat salt, you want to concentrate the salt in your urine so you can get rid
of more salt than you do water to normalize the balance between salt and water in your
body.
So, it does make sense to eat salt not generally but specifically at night before bed.
That might help you boost ADH to suppress the desire to pee at night.
Now, that might backfire, too, because it might make you thirst to drink more water,
and if you drink more water, that's going to reverse those effects, and maybe that will
make you have to pee.
But if you can get away with getting salt without water into your system, that might
help.
00:50:51 Whether the timing of carbohydrate, protein, and choline supplements makes a difference
for your daytime wakefulness, your nighttime sleepiness, your deep sleep, and your REM
sleep Now, when you sleep, there's a balance between
cholinergic signaling, meaning using acetylcholine, and aminergic signaling, meaning using biogenic
amines, like histamine and the catecholamines.
And in sleep, the cholinergic dominates the aminergic.
While you're awake, the aminergic dominates the cholinergic.
When you're asleep, there are differences in the stages of sleep.
So, during non-REM, deep sleep, cholinergic signaling is very low, but aminergic signaling
is really low, like it always is during sleep.
So, although you have low cholinergic signaling, you still have dominant cholinergic signaling
over aminergic signaling.
During REM sleep, you actually have pretty high cholinergic signaling.
You still have low aminergic signaling, and that's why you're not awake.
When you're awake, you have the highest cholinergic signaling, but you also have really high aminergic
signaling.
Even though your acetylcholine levels are the highest, your levels of biogenic amines
are really ramped up, and they're dominating the level of cholinergic signaling.
Now, I think this makes the strongest argument for not eating protein before bed if you have
trouble sleeping.
I'm not making a blanket statement, don't eat protein before bed.
If you sleep fine, and your main goal is increasing your muscle mass, you should be eating protein
before bed.
But if you're not that concerned with gaining muscle, and you are very concerned about sleeping,
and you're not sleeping well, then eating a low-protein meal before bed is probably
a good idea.
A second thing I'm not too sure about is that it might help to have choline before bed.
The reason I'm not sure about it is that even though you want your cholinergic to dominate
your aminergic signaling, you want your cholinergic signaling to go down, and there's some evidence
that in Alzheimer's, where acetylcholinesterase inhibitors are used to help with Alzheimer's,
there's some evidence that if they're dosed in the morning and not at night, sleeping
is better.
So, you don't want high cholinergic signaling at night, but maybe if you have a low-protein—maybe
a couple egg yolks at night is a good thing.
Maybe if you're using alpha-GPC as a supplement to boost acetylcholine levels, taking one
at night is a good thing.
You'd have to try it out pretty cautiously, but I definitely think the idea of a low-protein
meal in the evening does make sense.
Now, when you are awake, there are a lot of different things that go into wakefulness.
Acetylcholine, norepinephrine, histamine, and serotonin are all contributing to the
wakefulness state.
The production of histamine is governed by orexin, also called hypocretin.
Although I know of no human dietary studies, in vitro, meaning in the lab, you make more
orexin in response to amino acids, and you make less in response to carbohydrate.
I think that's a rationale for eating less carbohydrate in the day, especially during
times where you get sleepy.
So, if you have a mid-lunch crash, eating less carbs at lunch might help with that.
And even on a low-carb diet, if you bias your carbs to the evening meal, that might help
you sleep better on the basis of suppressing the orexin and thereby suppressing the histamine
levels in your brain at night.
Interestingly, perhaps you could make the same rationale for modulating protein and
carbs if you have anxiety and panic disorder, since brain histamine probably plays a role
in that, as well, by being too high during the day.
00:54:49 The possibility that glycine and magnesium could help get rid of conditioned
fear responses A brief note on their section on fear.
Conditioned fear requires LTP-like processes in the amygdala, and perhaps magnesium, by
reducing inappropriate stimulation of NMDA receptors, could reduce inappropriate conditioned
fear.
Not that it's bad to fear.
If we had no fear, we'd all be dead.
But many of us walk around with too much conditioned fear.
Some of us might want to undo some of that.
Magnesium might help, and maybe perhaps glycine to help with long-term depression, meaning
removing those fear-based circuits.
00:55:35 Thoughts on consciousness; are we a ghost in the machine, or are we just a machine?
Alright, I'll end with a couple notes on consciousness.
So, one sentence that I found really interesting in this book is on page 662, where they say
that, "no defining neural signature of awareness has been discovered."
In other words, we know all kinds of things about what goes on in the brain to impact
what we are aware of and to impact our subconscious, the things that we're not aware of, but what
is it that makes us a self-aware person that perceives the things that we are aware of,
and that does not perceive the things that we are not aware of?
And neuroscience has not discovered anything about what produces that perception of a self.
At least, nothing that can be defined as the cause of that perception of self.
Are we really ghosts in a machine, so to speak?
Well, they also talk about evidence that there is no unitary consciousness, that this is
just an illusion.
And the example that they use is the same one that I read about years ago in Steven
Pinker's book The Blank Slate, where he basically makes the same argument against the concept
that we are a ghost in a machine.
And that is the example of split-brain patients.
So, these are cases where there are people with intractable epilepsy.
Nothing else works to stop their seizures, but cutting the corpus collosum, which is
the connection between the right and left hemispheres of the brain, does work.
And in these cases, the side effect of this is that there is just no communication between
the right and left side of the brain.
You can communicate to one side of the brain or the other by sending messages through one
or the other eye when the opposite eye is closed because the visual fields are wired
into—at least in parts of the brain, one visual field is wired into a specific half
of the brain.
So, I'll read from this about the example they give: "The perceptual consequences of
this surgery," meaning split-brain surgery, "first studied by Roger Sperry and Michael
Gazzaniga in the 1960s showed that the divided hemispheres in these patients functioned relatively
independently and that awareness generated by neural processing in one hemisphere is
largely unavailable to the other.
"For example, when simple written instructions, such as 'laugh' or 'walk,' are presented visually
to the left visual field and thus to the right brain of a split-brain patient, many subjects
have enough rudimentary verbal understanding in the right hemisphere to execute the commanded
action.
However, when asked to report why they laughed or walked, they typically confabulate a response
using the superior language skills in the left hemisphere, saying, for instance, that
something the experimenter said struck them as funny or that they were tired of sitting
and needed to walk a bit.
"Thus, the same individual would appear, under these circumstances, to harbor two relatively
independent domains of awareness.
This evidence raises the provocative question of whether awareness is really the unified
function we generally take it to be, as well as what the role of the corpus collosum is
in engendering such unity."
I think this definitely raises that provocative question, but I don't think it really disproves
the idea that we're some ghost in a machine.
I'm not saying a ghost in a machine is the best model for understanding us, but even
without split-brain patients, we already know that there are all kinds of things that influence
our behavior that go beneath the radar of our perception.
So, it's not really obvious to me that this is splitting our center of awareness in two
so much as it would be removing a portion of what would otherwise fall into our awareness
into our subconscious, into the things that influence our behavior that fall beneath our
awareness.
So, I think at this point, if you're wondering whether there's a ghost in the machine, whether
there's some kind of spiritually based soul that is occupying our body, or that is integrated
with our body, or that is an epiphenomenon of our body, these are all beliefs that still
are a matter of faith, and really science has nothing to say one or the other on, as
far as I can tell.
01:00:29 The default mode network is fundamentally about our inward, introverted-directed processes,
contrasted with the executive control network, which is fundamentally about our relationship
to the outside world and our extraverted functions.
Now, if you've been paying attention to Michael Pollan's work, you might be saying, "Hey,
wait a second, what about the default mode network?
Isn't that the sense of self?"
The last section of this chapter on cortical states, that discusses sleep, and wakefulness,
and awareness, and consciousness, is titled "The Default State of the Brain."
This default mode network is a network of different parts of the brain that all become
activated together to a greater degree when we're at rest.
In other words, if you have someone, and you're measuring what's going on in their brain,
and you say, "Don't think about anything.
Just sit there," then these things light up and become more active when that person seems
to not be—at least from your perspective as an experimenter when you told them not
to do anything, not to think about anything, that person should be quote, unquote "less
active" because you didn't give them a task.
And yet, this network of different brain parts that all kind of functionally network together
is lighting up and becoming more active.
They refer very, kind of, vaguely to an opposing network that they don't give a name to.
They say that the default mode network is, quote, "anti-correlated with activity in dorsal
parietal regions associated with the attentional control network and predicted lapses in attention
and the ability to switch from one task to another."
In other words, there is some network that is more active when you have attention to
the outside world and you're doing tasks, and when that network is more active, the
default mode network is less active, and vice versa.
I'll quote from the book again, "The obvious question is what purpose neural activity in
a default mode network serves.
That is, why should these regions be active if and when the brain is doing nothing in
particular?
Although the default mode network activity might be related to mental idling, another
possibility is that this network is activated when attention is inwardly focused, the standard
attentional control system being activated primarily when a person is focused on events
and stimuli in the external environment."
The default mode network is known to be abnormally less active in autism and more active in schizophrenia,
and it's decreased during the use of psychedelic drugs, and it can basically be shut off at
will by highly experienced meditators who are able to bring on a sense of the disillusion
of the self.
Although this section moves in the direction of referring to two opposing networks that
are inwardly and outwardly focused, I think it's not described as clearly in those terms
as a description that I found in a paper that I'll link to in the show notes, "A Neuroeconomic
Framework for Creative Cognition" by Lin and Vartanian.
So, let me read this paragraph describing what they cast as these two opposing inwardly
and outwardly directed networks of the brain: "The default mode network and the executive
control network are engaged by different types of tasks.
Specifically, the DMN is activated by tasks that involve internally directed processes,
such as self-generated thought, simulation of future events, and spontaneous thought,
and it exhibits decreased activation during tasks that involve attention to external stimuli.
In contrast, the executive-control network is part of a 'task positive' set of regions,
and the activation of these regions increases during tasks that require attention to external
stimuli.
The observation of their joint activation during creative cognition has led to the idea
that the two networks support different aspects of creativity: Whereas the default mode network
supports the generation of creative ideas, the executive control network modulates activity
in the DMN to ensure that task goals are met."
I think this description is way more interesting than trying to understand the default mode
network as this strange case of why the brain does something at rest.
01:04:54 How activities that had nothing to do with people skills but allowed me to flex
my extroverted muscles, like exploring the outside world on my own, helped me with my
people skills The reason I found this so interesting is
because my own personal experience in the last few months before I read this had been
leading me to believe that there are fundamentally introverted networks of the brain and fundamentally
extroverted networks of the brain that are very broad and are responsible for, on the
one hand, all introverted tasks and, on the other hand, all extroverted tasks.
And the reason was that I started studying personality type, and in particular, I had
been reading a lot about Myers-Briggs, which is based on Carl Jung's conceptions.
And in this idea, many of us are introverts, and many of us are extroverts, but what that
means is not that we just have introverted processes, but that we just have a tendency
to emphasize our introverted processes more or have a tendency to emphasize our extraverted
processes more.
But if we are an introvert, we must have an extraverted side, or we would have no relationship
to the outside world.
And if we're an extrovert, we must have an introverted side, or we would have no anchoring
to our inner sense of self, and our core convictions, and our beliefs and values.
So, in this concept, you have a primary driving function, and in my case, that's introverted
thinking.
That's, some people nickname—Personality Hacker nicknames that Accuracy.
It's the theory building.
It's the grand theories of cause and effect, as you can tell if you've followed my work.
But in the Myers-Briggs system, my secondary function is my main extraverted function,
and that's exploration.
It doesn't necessarily mean going out and traveling.
It means exploring to find insights and inspirations from new information and new experiences.
Certainly, you can explore by reading books, but the peak of exploration is really to do
things you have never done before in a place far away from home.
And one thing that really struck me when I got back from Greece this year was that my
social confidence in interacting with other people, which has never been a great skill
for me, was dramatically better when I got back from Greece, even though it was better
in ways that I hadn't been practicing at all.
So, the enormous time—although there was a part of my trip where I was meeting family
and spending a lot of time with family, other than that, the overwhelming bulk of my trip
was on my own as an introvert.
And yet I came back, and it was easier for me to be the life of the party, or to flirt,
or ask someone out on a date, just people skills that had nothing to do with my trip
to Greece.
And at that point, I started reading more about personality type, and I started realizing
the importance of exploration as my primary extraverted function.
Now, keep in mind that this is an extraverted function, but yours might not be exploration,
right?
Or in your case, maybe what you need if you're an extravert is to work on your primary introverted
function.
So, it could be different depending on what your type is.
But for me, everything I'm reading is about how if I don't exercise my main extraverted
function, which is exploration, or technically called extraverted intuition, then I will
become pathologically introverted.
In general, not just on that specific function, but just in general, I will become too much
of an introvert for my own good.
And so I thought, okay, I'll put this to the test.
I'll start exercising exploration in all kinds of different ways.
I will, as an example, I would go out to work in a coffee shop, I would always walk home
a way that I had never gone, even if it was more time-consuming and less efficient.
And just doing things like this that have no involvement with people skills at all would
dramatically increase my confidence and people skills far more than anything I'd ever done
to specifically improve my people skills, like reading books about the theory of people
skills and trying to implement them.
I'm not saying that's not helpful.
I'm just saying that my experience with this was much more like how engaging a muscle system
can spill over into strength in another muscle system.
For example, there's evidence that within certain contexts, not saying this is practically
relevant for an athlete, but you can get stronger in your left arm by exercising your right
arm because you're strengthening a general neural network that's responsible for strength
in both arms.
Well, in this case, I'm exercising my primary extraverted function, and that's giving exercise
to some fundamental network of my brain that is involved in all extraverted activity.
If I were an extrovert, maybe I would have my primary opportunity to grow by exercising
my main introverted function and thereby giving more exercise and more strength to a primary
neural network involved in all introverted function.
The default mode network responsible for inner-directed processes, and the executive control network
responsible for outward-directed processes.
01:10:53 Nutrition cannot replace the cognitive work necessary to have a healthy mindset and
life, but nutrition does make it easier to do the right thing for your mental health.
So, my final thought here then is although I'm focusing on how we can relate nutrition
to the science of what's going on in the brain, none of that will ever change the importance
of habits, and actually doing things, and changing how you think, mindset, practices.
The way that I think of it is that nutrition is impacting the physiological milieu that
is making the difference between it be ing an uphill battle or a downhill battle to do
self-improvement work that will help you think better, feel better, and act better.
So, it doesn't ever replace thinking better, feeling better, and acting better, but it
makes it easier or harder to do the right thing.
So, histamine in your brain is never going to give you a panic attack.
A high level of tonic dopamine in your brain is never going to be the thing that forces
you to always think about the bad things that everyone in the world has done to you.
But if your default state of your brain is to be hyper aroused in a panic-oriented direction,
it's
going to be harder for you to engage the cognitive processes that prevent
a panic attack.
And if your tonic level of dopamine from insufficient methylation is making your mental processes
more sticky, then
to the extent that what you need to do is escape from negative
thought patterns that are stuck in your brain, it's going to take more mental work, and it's
going to be harder to unstick yourself because your brain is
so sticky.
So, with nutrition you never replace the cognitive work that
it takes to have a healthy mindset and healthy life.
But it's an essential part to making doing the right thing for your mental health an
easier thing to do.
Alright, I hope you enjoyed this more-than-four hours of neuroscience.
Signing off, this is Chris Masterjohn of chrismasterjohnphd.com, and I'll see
you
in
the next episode.
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