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Nutrition in Neuroscience Part 4 | Mastering Nutrition #56

I’m Dr. Chris Masterjohn of, 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. If you want an ad-free version of this with
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up for the CMJ Masterpass at We’ll dig right into our discussion of nutrition
and cognitive function after this word from my sponsors. 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,
and I’ll see you in the next episode.

Randall Smitham



  1. Humza Iqbal Posted on February 1, 2019 at 1:46 pm

    What's your thoughts on Ancestral supplements beef brain?

  2. HaZZarD Posted on February 1, 2019 at 8:40 pm

    This is very useful info. I think maybe we need a "theory of everything" for human fluorishing that take in consideration different disciplines like psychology/philosophy/nutrition/hormones/lifestyle etc etc. Everything is important but nothing on his own can give us the big bicture. I think your work is helping in this regard.

  3. Philip Hernandez Posted on February 2, 2019 at 5:18 am

    That was dope.

  4. ThebirdmanTrainer Posted on February 2, 2019 at 9:21 am

    I like the way you think 🤔

  5. Ben Nguyen Posted on February 2, 2019 at 4:20 pm

    Enjoyed the Parkinson's discussion (16m)!

    Regarding the cerebellum, there was a great Stem Talk episode (#39) about the make-up of brain neurons, much it discovered by literally blending brains in a CleanBlend and making brain soup! Dr. Suzana Herculano-Houzel talks about how the number of neurons usually increases with the size of the brain, and how it determines the energy needs of the brain (Glial cells also increase with brain size, but its density is constant). Interestingly, a large animal like the elephant, has 3x more neurons than humans, but 98% of those neurons are in the cerebellum/movement, whereas in humans they are concentrated in the prefrontal/cerebral cortex.

    Apparently, the amount of neurons required for movement and basic function is relatively small (compared to 30% for vision), and so humans further capitalized the cerebral cortex advantage by inventing cooking!

    BTW, there was also a good Sam Harris episode with Geoffrey West (From Cells to Cities) that also talks about the economics of scaling as it relates to the life span and brain energy of any mammal.. for example, doubling the size only requires 3/4 more energy. He also mentions how the number of heartbeats, across all animals, is a constant 1 Billion, and is equal to the size of the animal * heartrate!

    Regarding sleep (45m), despite practicing all the proper sleep hygiene, and eating relatively low amounts of protein before bed (mostly glycine and creatine).. I wake too early and cannot fall back asleep. I'm having my Vitamin A serum levels tested, and I currently supplement with Mg, and Vitamin D3.. perhaps I should add Vit.C/Copper/Zinc? Do you know of any way of delaying the rise in cortisol?

  6. Chris Masterjohn, PhD Posted on February 15, 2019 at 3:31 pm

    00:39 Cliff Notes

    12:08 Anatomy of the brain

    16:41 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

    24:56 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

    28:23 Tonic and phasic dopamine and the importance of COMT-mediated methylation for regulating the tonic level of dopamine

    36:34 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

    37:28 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.

    41:11 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

    44:28 Sleep and circadian rhythms, the importance of vitamin A, morning sun exposure, and avoiding blue light at night

    48:12 Melatonin synthesis, the importance of vitamin B6, BH4, oxidative stress, vitamin B5, methylation, and tryptophan uptake into the brain

    51:10 Why you can’t mimic your natural melatonin rhythm with melatonin supplements

    52:55 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

    56:14 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

    01:00:44 The possibility that glycine and magnesium could help get rid of conditioned fear responses

    01:01:30 Thoughts on consciousness; are we a ghost in the machine, or are we just a machine?

    01:06:25 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.

    01:10:52 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

    01:16:48 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.

  7. Daniel Sundkvist Posted on February 28, 2019 at 4:25 pm

    Let's see if i got this straight.
    Do these increase the dopamine tone?

    Taq1a A1+ Allele
    rs6277 affinity mutation
    Low expressing MAO-A/B
    High expressing VMAT2

    Is the tonic/phasic model applicable in the fronto-striatal balance model? Meaning; that no matter what mutation you adress to decrease the tone, it still apply the benefits from increased phasic sensitivity? Seeing that COMT is the major synaptic clearance in the PFC but striatum got more regulatory systems.

  8. anon mouse Posted on May 8, 2019 at 7:34 am

    To make things clear at the time the New Testament was translated into English ghost meant soul and so holy ghost means holy soul. Which is related to the older Jewish idea of Shekina(sp?) and the even older Zorastrian idea of the Good Mind.
    Ghost in the Machine is an old English phrase meaning we have an eternal soul(ghost) which temporarily lives within a machine(body).