Huberman Lab - Perform with Dr. Andy Galpin: Nutrition to Support Brain Health & Offset Brain Injuries
Episode Date: August 14, 2024I'm honored to share Episode 10, the final episode of Season 1 of Perform with Dr. Andy Galpin. Dr. Andy Galpin is a tenured full professor at California State University, Fullerton, where he co-direc...ts the Center for Sport Performance and leads the Biochemistry and Molecular Exercise Physiology Laboratory. Andy is both a friend and a colleague, and I'm delighted to have assisted in the creation of this podcast. I'm certain you'll both enjoy and learn from it. Season 1 featured 10 episodes, where Dr. Galpin covered everything from building strength, the importance of strength for long-term health, the science of breathing, the benefits of sleep extension, genetic testing for personalized training, and nutrition for injury recovery. While we have Episode 10 of Perform with Dr. Andy Galpin here, please be sure to follow Perform with Dr. Andy Galpin on your preferred platform to listen to all the episodes from Season 1 and to get notified when Season 2 is released. Show notes for this episode can be found at performpodcast.com. Timestamps 00:00:00 Introduction from Dr. Andrew Huberman 00:01:08 Brain Health & Injury  00:05:06 Sponsors: LMNT & Continuum  00:08:16 Nutrition & Supplements for Brain Injury  00:12:44 Brain Injury Categories, Traumatic Brain Injury (TBI), Concussion  00:17:09 Brain Injury Pathophysiology  00:22:16 Burst Capillaries, Initial TBI Response  00:30:03 Delayed TBI Response, Neuroinflammation  00:34:19 Sponsors: Momentous & Maui Nui  00:36:52 Creatine Monohydrate; Second Impact Syndrome  00:41:52 Strength of Evidence Scale, Creatine  00:47:15 Creatine Doses, Frequency, Adverse Issues; Food Sources  00:53:22 Sponsors: AG1 & David Protein  00:56:05 Fish Oil, DHA, EPA  01:00:38 EPA & DHA Dosage, Timing, Adverse Issues; Food Sources; Omega-3 Index  01:04:46 Vitamin B2 (Riboflavin), Vitamin B  01:08:57 Riboflavin Dosages, Timing; Food Sources  01:11:25 Choline  01:18:37 Choline Supplements & Food Sources, Alpha GPC, Dosage  01:21:30 Branched-Chain Amino Acids (BCAAs), Sleep  01:25:04 BCAAs Dosage, Whole Food Sources  01:28:02 Magnesium  01:31:20 Magnesium Dosage, Timing, Supplements, Adverse Issue; Food Sources  01:33:09 Blueberry Anthocyanins  01:35:28 Anthocyanins Dosage; Food Sources  01:37:17 Caffeine & Brain Injury Recovery  01:38:50 Perform Episodes, Perform Newsletter, Acknowledgements  01:41:19 Zero-Cost Support, YouTube, Spotify & Apple Subscribe & Reviews, Sponsors, YouTube Feedback, Social Media  01:42:56 Conclusion by Andrew Huberman  Disclaimer
Transcript
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Welcome to the Huberman Lab Podcast,
where we discuss science
and science-based tools for everyday life.
I'm Andrew Huberman,
and I'm a professor of neurobiology and ophthalmology
at Stanford School of Medicine.
As some of you may know,
our Huberman Lab team recently launched a new podcast
called Perform with Dr. Andy Galpin.
Andy is a professor of kinesiology at Cal State Fullerton
and is a world expert in exercise physiology
and human performance.
This new podcast, Perform with Dr. Andy Galpin,
explores all aspects of human performance.
It shares the latest science and gives practical tools
on things such as how to improve cardiovascular health,
how to build strength and muscle mass,
how to maximize recovery with nutrition and supplementation, and much more. What follows is the final episode of season one of
perform with Dr. Andy Galpin. If you enjoy it, I encourage you to go and subscribe to it wherever
you're listening now and to listen to the other nine episodes of season one. I'm certain you'll
really enjoy this first season from Dr. Andy Galpin. And now episode 10 of Perform with Dr. Andy Galpin.
The science and practice of enhancing human performance
for sport, play and life.
Welcome to Perform.
For the final time this season, welcome back friends.
I'm Dr. Andy Galpin.
I'm a professor of kinesiology
in the Center for Sport Performance at Cal State Fullerton. So far in the first season of perform, we've talked about everything
from muscle to the immune system to liver and lungs, metabolism, genetics, sleep, blood work.
And so I thought we have to end this thing on what I hate giving credit to because I'm a muscle guy,
but probably deserves it. And that's the brain. There are obviously many factors that go into getting your brain to perform at its best.
But today, I want to focus specifically on what you can do from a nutrition perspective
to reduce your risk of as well as recover faster from brain injuries, concussions and TBIs.
I think it's worth reminding you, though, that if it's good for preventing
and returning faster from a brain injury, it's probably safe to assume it's also good for brain performance as well
as long-term health.
Now I'm particularly passionate about this subject, having dealt with it a lot personally.
I've had a concussion or two myself, and I've spent much of my career working with athletes
prone or at high risk of developing similar injuries. This includes football players, wrestlers, fighters,
boxers, and so forth.
That said, those are not the only people
at risk of a brain injury.
In fact, those things are quite common
and not only in athletes.
So I'm really excited about this topic
because brain injuries are really common.
They can be completely debilitating.
And there's actually a lot of evidence that nutrition and supplementation can have a big
effect in, again, both reducing your risk of getting one as well as coming back faster
once they've happened.
And so I really want to make sure everyone knows what their options are from a supplementation
as well as whole food perspective on getting back
and returning as fast as possible and minimizing the symptoms of brain injuries. Now as I was
saying, traumatic brain injuries or what we'll refer to as TBIs are really common. In fact,
a lot of people in the field refer to them as the invisible disease because they don't come with a
physical appearance. There's no cut, there's no bruise or joint sticking the wrong way, bone poking out of
the skin.
And so these things can happen and you don't necessarily know that an injury occurred.
Other problems include the fact that the symptoms that are associated with a TBI or concussion
are really similar to those generally associated with aging. So you talk about memory recall issues, mood, sleep, and other things that people don't
necessarily know are because of an injury they may think is just due to normal aging.
In fact, we'll get into this a lot as the episode progresses. But a lot of the research on brain
health with aging, Alzheimer's, dementia, and other related topics, come from the same
data sets that we work on for TBIs and concussions, and the inverse.
So there's a huge overlap or Venn diagram between the types of research, the study design,
the actual papers themselves, the interventions, the models, whether we're talking about data
from humans or animals and rats and ferrets
and things like that, there's a large overlap between these two bases. They're different,
of course, and we'll try to highlight those. But these are some of the reasons why I want
to get in today's episode, even if you're not an athlete, because many of you are still
at risk of getting a TBI. In fact, the vast majority of concussions and TBIs do not come
from sports. They come from accidental slips and falls
and other problems like that.
In addition, they're still gonna tell us
a lot of indirect information
about overall healthy brain aging.
So the goal here will be to reduce our risk, of course,
but if it does occur, to minimize the symptoms
and return back to a healthy brain as fast as possible.
Now before we go too much further, I'd like to take a quick break and thank our sponsors
because they make this show possible.
Not only are they on this list because they offer great products and services, but because
I actually personally love them and use them myself.
Today's episode is brought to you by Element.
Element is an electrolyte drink mix that has an ideal ratio of sodium, potassium and magnesium,
but has no sugar. electrolytes are critical to proper
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Today's episode is also brought to you by Continuum.
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Now, before we get started on the details, I want to highlight a couple of things.
First, remember, I have a PhD.
I am a scientist.
I've published in this area.
In fact, I have recently submitted a literature review as a co author, and we'll talk about
that later. But I'm not a medical doctor. If you think you have any risk of or potentially
have had or suffering consequences from any type of brain related injury, please see a
medical professional in this area. I wanna focus this episode on nutrition
and supplementation related to brain injury.
But I also don't want anyone to think
that I'm suggesting this is all you should do
for your brain injury.
I also don't want anyone to think
that I'm suggesting this is enough
to stop your chances of ever having a brain injury.
So that being said, the landscape of the research and many of the scientists in
this area are on the same page in the fact that there is emerging evidence
that several micronutrients and what we'll call biological compounds really do
have the ability to reduce the risk.
I hesitate to say prevent, but can help prevent and treat brain injuries, concussions, TBIs,
and related events.
Now, over the course of today's show, I'm going to walk you through a bunch of different
micronutrient and nutraceutical options you have.
We'll cover the evidence, how much to take, the protocols, and so on and so forth.
But before we do that, you have to actually understand a little bit of the terminology,
because depending on what type of brain injury you have,
you may want to take a different route with your nutrition.
So getting going with that point, what is a brain injury?
You've heard me now say concussion, TBI, brain health,
and a bunch of different terms like that.
What is actually the difference?
In fact, do you even know the difference between a TBI and a concussion?
It's been my experience that most people don't.
And so we'll maybe just start right there.
So a brain injury can mean a lot of different things.
Honest answer here, there's not that much research
in humans and randomized control trials
on what to do to prevent or reduce an injury.
In fact, if you think about research design,
that's really hard to do.
The only way to execute these kinds of studies in humans
is to set up an enrollment center, say at a hospital,
probably around an area that has a lot of kids
playing in sports, wait for people to show up with an injury,
ask them if you can enroll them in a study
and go on from that.
We can't go out and give humans head injuries
and concussions.
And so it's really challenging.
It's hard to get an adequate sample size.
And you're also relying upon those people
coming into the study, having the same type of brain injury.
And we know that that does not happen.
And so brain injuries themselves, there's a lot to learn
and there's lots of different types.
It would be foolish to think
that we know how to prevent all of them, or recover from all of them. Some types of injuries
we know more about, other types we know way less. And so there's not one type, which means there's
not one solution. And this is going to explain why almost always you will see mixed results. Easy example here.
We're gonna talk about one of the major problems
that are associated with brain injuries is sleep.
So supplements that help with sleep,
therefore are going to be helpful
for folks who are experiencing sleep related problems
with a brain injury.
However, if you have a brain injury
and are not suffering symptoms of sleep loss,
then a sleep aid may or may not actually work. However, if you have a brain injury and are not suffering symptoms of sleep loss, then
a sleep aid may or may not actually work.
If both those individuals, let's say we had two people, one having issues with sleep,
one not, both enrolled in the same study, you're going to see the magnitude of effect
of the supplement or the nutritional factor gets a little bit washed out.
So those are common themes you will see.
I won't bring this up again, because honestly I could do that
with just about every single study.
But it's something for you to really consider
in the back of your mind.
All right, now the goal then is to present to you
information that I think has a strength of evidence.
I'll explain to you what my criteria
for a strong evidence is a little bit later.
And things that I think kind of justify
what we'll call low risk and high potential reward. And we'll typically break those down into things
you can do before the injury, during or immediately after the injury, as well as long term post
recovery. So you can think about that as pre, peri or post, or simply preventative, and then
treatments post injury. So in terms of terminology, I'm going to try to be consistent with three basic phrases.
So a brain injury is often broken up into three categories based on the severity.
There's mild, which is the lowest, moderate, and severe.
Now fortunately, mild is by far the most common.
In fact, some papers will indicate that over 90 plus percent
of brain injuries are qualified as mild.
What that means typically is there is a 30 minute
or less change in state of consciousness.
So if you were unconscious for a couple of minutes,
you probably had a mild traumatic brain injury.
This is often associated with things like confusion
or post-traumatic impact amnesia.
So you forgot what happened immediately afterwards
or you had a little bit of a time travel
as I like to call it.
And this can occur for a couple of hours
or even up to one day is the general line
that we cross there.
The overwhelming majority of recreational and sport-related concussions fall into this category.
Therefore, almost always, though not always,
but almost always when you hear the word concussion,
you can generally translate that into a mild TBI.
Now, not all TBIs are concussions,
but all concussions are TBIs.
Okay, so one more time in case I lost you there.
Concussion is effectively a mild traumatic brain injury
based on those categories.
If you had worse effects, so you were unconscious for longer
or your amnesia will last longer,
then you may be actually be considered
to be in a moderate category.
So moderate technically is defined
as a loss of consciousness or amnesia
for somewhere between 30 minutes to up to 24 hours.
Symptoms associated with this are more severe.
It is headaches, confusion, dizziness,
nausea, vomiting, slurred speech, drowsiness,
difficulty concentrating, so on and so forth.
And so another kind of back of the envelope way to
differentiate between mild and moderate is mild. Again, not always, but rough guidelines here.
Mild is fairly acute. So in and immediately after the injury, you had symptoms, but then you're
usually back to normal. Moderate often comes with downstream problems, not the injury themself.
So this is when you have behavioral changes
because of the TBI, you've got again,
difficulty with memory that lasts a long time.
That's again, back of the envelope kind of distinction.
If it is worse than that, we call it severe.
That is technically a loss of consciousness or amnesia
for somewhere between 24 hours to up to
or more than seven days.
And moderate and severe also have similar dementia like symptoms.
Now I mentioned this earlier, but think about this.
Severe TBIs oftentimes come with memory and attention problems, decision making problems,
learning impairments, mood, big sleep disturbances.
And so you can imagine somebody who's in their 50s, 60s,
or 70s who start experiencing things like that.
They may personally just think,
oh, this is, I'm getting old.
Family members may think, oh, grandma's got,
you know, starting to show dementia signs.
Could be possible.
Could also be possible that grandma is simply suffering from a
severe TBI. And so this is what I was referring to earlier when I said there is actually a big
crossover here. It's a bit of a gray area. They can actually be the same thing. They can clearly
be different as well, but there is a large crossover between them. So hopefully that helps
you understand a little bit about what the difference between a concussion and a TBI is,
what a mild, moderate, and severe traumatic
pain injury are.
And I started sneaking in some of the physiology
about at least what's the symptoms.
What are the behavioral and actual consequences?
That is important to understand because now that'll tell us
what we do in terms of a treatment or prevention strategy
In order to finally connect that dot though
We got to walk through just a touch and I promise this will be just a touch of the physiology or pathophysiology
Of each one of these categories. So we understand what we're trying to do with the nutrition or the micronutrient
Why they solve those problems and then ultimately how that translates into reduction
or elimination of these symptoms.
So what's actually happening in the brain
when we experience any of these three levels
of a brain injury?
There's a couple of resources I want to give you.
If you want to learn more about this right now,
I based a lot of this episode heavily off of these papers,
so I want to give them their due credit. They will, of course, be linked and PDFs will be available in the show notes. You can find those
at performpodcast.com. But for those of you who want to write it down right now, a paper that I
found particularly helpful came out just last year in 2023, and that is titled Optimization of
Nutrition After Brain Injury, mechanistic and therapeutic considerations.
In addition to that, my friend and colleague, Dan Garner,
has a product available for purchase on Amazon
called the Brain Synergy Protocol,
and I will talk about that a little bit later.
And then finally, I honestly took the vast majority
of this episode off of a paper that I co-authored,
and that's depending on when you're listening to this,
either in review or potentially published by now,
called Mitigating Traumatic Brain Injury,
A Narrative Review of Supplementation
and Dietary Protocols.
This was led by Tommy Wood, the fantastic neuroscientist
at the University of Washington,
and was first authored by Federica Conti,
another tremendous neuroscientist in her own right. So they did the
bulk of the work here. We contribute on this paper together. And I thought it was honestly so perfect
for a show that I thought I'm just going to take this entire thing and make a whole episode out of
it. But nonetheless, let's get into the paper right now. So what's actually happening in your
brain when you experience injury? Typically, we've been told that when you have some sort of injury,
you have to go through this whiplash experience. So you have to say a sudden stop, your brain
inside your skull continues to travel and then smashes up against your skull and then
therefore has a bruise on the brain. While that certainly can happen, that's actually
probably pretty unlikely. Generally, what's going to happen if that occurred is you would
see the injury site being on the outside, right?
So you can imagine let's just say the front of your brain smashes into the front of your skull
You would expect the injury to be right on the front on the outside part of your brain
The reality of it is that's not where most
Concussions and TB eyes occur. It generally happens more towards the middle of the brain
Remember the outside of the brain is where your gray matter is.
That's mostly where your neurons are.
On the inside is the white matter that's made of mostly fat and it helps you conduct messages
more quickly throughout the brain.
See, what typically happens in brain injuries is you get more of what I call the accordion
effect.
And so you have so much fluid in your brain that if you were to slosh it around a little
bit, there's not much room to slosh.
And so it protects your brain from hitting the skull.
But what can happen though is an intense pressure inside the tissue because it squeezes together
and then gets expanded back out.
Picture the accordion here, me taking my two hands, putting them closer together, smashing
it, pulling it back apart.
And so you have this kind of egg looking oval of that that is supposed to your brain and
it gets smashed down into a vertical piece of paper and then extended way back out and
stretched and so on and so forth.
So it's not the actual connection or contact to the skull that is always the issue.
Sometimes it's that stretching and pulling in that pressure wave that causes the damage
on the interior or
various portions of the brain. And so the injuries are highly varied in the brain.
It can be everything from a capillary or blood flow supply that is damaged or torn. The axon themselves can be torn.
This then causes a host of issues that we'll get into step by step, but it's everything from temperature
problems, energy problems, metabolism problems, inflammation, and physical structural damage.
So many different options that can occur, but that's basically what happens
for most, but not all. This is obviously a complicated area. I don't mean to oversimplify it
depending on if you had a single event, say a car crash
or a single slip and fall, or numerous sub concussive events, think of blast injuries
and folks in the military, small impacts with combat athletes or other people in professions
that kind of bang their head a little bit, don't necessarily get huge symptoms, but they
have a lot of these stack over time. All of it results in different problems.
I'm just trying to highlight a small example of what it can look like as a quick overview.
That being said, there are some generalities and commonalities between different forms
of TBIs, and I'll just cover them broadly right now.
The top of our list here is what's called comprised excitotoxicity.
I'll explain
what that means later, but this is arguably one of the bigger problems you will experience.
There are ionic disturbances, so your positive and negative charges get all messed up. There
are blood flow to the brain that's called cerebral blood flow, edemas and swellings, oxidative stress,
inflammation, and then as I mentioned before, even damage or even death in the cells that are directly in the brain or related to the brain.
That can actually be going on acutely for weeks or even months to decades throughout life.
So I can't go over all of this. It would take me the entire show, if not many.
But I do want to cover a couple of very specific examples so you can start to grasp what this could look like.
The first one is just if you've had capillaries burst.
So remember, you have capillaries that surround all tissue in your body and that's where all
of your blood exchanges happen.
So you have this network and this bed of capillaries that surround your brain.
When those burst, you can't get nutrients and fuel in and you can't get waste products
out. And so in the most fundamental problem here is you don't get nutrients and fuel in and you can't get waste products out. And
so in the most fundamental problem here is you don't get oxygen to the brain. So we lose
cerebral blood flow. We lose energy production because we're not getting fuel in the brain
because we physically torn capillaries. This, if this was on your arm, like it is on mine
right now, you might have a purple and black arm. Thank you, Cam Haines. But in your brain, you wouldn't see that. This goes right back to the invisible
disease problem from earlier. More detailed example would be the following, though. Oftentimes
we'll break up TBIs into what we call the initial response and then the delayed or phase
two response. So let's say you had some sort of direct hit.
Again, pick your example.
It might look something like this.
Your initial response would be an over activation
of the neurons.
That's right.
The nerves that are associated with the injury area
become overly activated.
Now this initial response is caused in large part
by what's called over activation of neighboring neurons. So you remember all the nerves connected
one to one to one, they're not actually physically connected. There's a small space in between them.
And they communicate by releasing what's called neurotransmitters. So what happens
in this area is you have a damage to one, it over communicates to the next
one, and you get way too much neuron activity. That's called
over excitation, or excitotoxicity, because you get way too much neuron activity. That's called over excitation. Okay, or excitotoxicity,
because you're excited so much that it comes to the level of toxicity. And excited, meaning
the neurons being too active. Now this happens in large part because of a molecule called
glutamate. You'll see this all over the TP at TBI literature, supplementation, marketing,
very commonly talked about because it is very real and very
important. It's the main neurotransmitter that's
responsible for this excitatory activity. Okay. Now this gets
released in response to that. We have a whole downstream cascade
of problems. And this starts off as an initial response. And then
I'll show you how this turns into that delayed phase
response later.
So we have this over-excitation. Now, if you go back to our episode on muscle, you'll learn
more about how nerves and cells contract, why sodium and calcium and potassium and chloride
are responsible for action potentials and so on and so forth. For now, sodium and calcium
very specifically become overly activated.
In fact, you literally oftentimes have damage to the plasma membrane.
So the little thing that surrounds your cells gets damaged, it gets broken.
And so because of that, the things that are supposed to be in the cell and things that
are not supposed to come in the cell start leaking everywhere.
So sodium and calcium start coming in and out of the cell in inappropriate manners.
Now this causes things that are eventually going to be cell death and degradation
because of production of what's called ROS. ROS is R-O-S, a reactive oxygen species.
So remember, oxygen is very reactive. It is good and bad.
You have to have oxygen for fuel, allow you to create fuel rather.
It's a byproduct needed to make aerobic metabolism.
That's the same time.
Excessive amounts of it are going to be damaging.
This is how we break down tissue.
This is how we create and clean out dead and debris cells.
And so if we're generating way too much
of this reactive oxygen species,
this is almost
synonymous every time with oxidative stress.
These are kind of similar terms.
Not the exact same thing, but pretty close.
This also activates several enzymes that damage the cell structure.
These are everything from what we'll call proteases.
So an ACE is an enzyme that breaks down a protein to lipases.
These are enzymes that break down fats
Nitric oxide synthases and endonucleases and other things like that a whole cask of enzymes that start breaking the thing down
You don't know exactly what's happening here, but the cell thinks that there's problems
Because there are and so it just starts activating cell death. So we're having issues with that. Okay. In addition to that, that calcium specificity becomes a
problem because it alone harms mitochondrial health and
efficiency. And so the cells that do stay alive start
getting really damaged mitochondria. This is again,
because of a membrane damage issue that allows too much
permeability of things in and out. And that, of course,
eliminates or drastically reduces
mitochondria's ability to work, which means your ability
to make ATP. Remember, ATP is the cellular currency.
It's the only way any living cell can create energy.
And so mitochondria is not the only way we can make ATP.
Hold on to that. We're going to come back to that.
But it is a primary way and it is the
exclusive way in which we generate aerobic metabolism. So the way that we create fuel with
oxygen has to go from mitochondria. So damaged or ineffective mitochondria is going to directly lead
to reduced ATP production. Reduced ATP production simply means we have way more cellular energy in
our brain. This idea of brain fog or fatigue
or can't remember things recall executive decision. If you don't have energy, your brain
can't think. That's quite literally what's happening. And this is why some of the supplements
and micronutrients we're going to talk about later have such positive effect as they help
restore what's called that energy balance. The damage occurred,
you weren't able to get transportation of oxygen and things in. This allowed permeability of
calcium. This allowed too much excitation, which means we're burning too much energy.
At the same time, we don't create enough energy. And so we end up being in this really catabolic
or negative energy state. And now we can't think well, we're dealing with signs and symptoms.
And overall, more importantly,
our brain is actually physically unhealthy.
And so because your brain is measuring energy production
at all times, it knows this imbalance is occurring,
it's gonna try to alleviate it.
And the best way to do that is to ramp up energy production.
But since it can't do it aerobically,
it has to turn to anaerobic methods.
And specifically what we're talking about here
is anaerobic glycolysis.
One more time, go back to our previous episode,
I believe it was episode two on muscle,
and we talk about the physiology and bioenergetics
of how we use carbohydrates for fuel.
It's the same.
We're in the brain here, we're not in muscle,
but anaerobic glycolysis is still anaerobic glycolysis.
It's still the breakdown of carbohydrates
for the production of ATP.
So in this particular case,
since the ability to store glucose in the brain
is quite limited,
and the amount that we can get into the brain
through the blood-brain barrier is also somewhat limited,
if we're only or mostly relying upon anaerobic glycolysis,
you can quickly see we're not going to be able
to handle all the supply.
Because not only does the brain take
an enormous amount of energy,
it's in fact, depending on the situation, our most energy costly organ in the body,
and now it's injured and it has more energy demands to recover,
and it has less energy production,
we're going to be really running into problems with our energy deficit.
So to summarize all that, effectively what's happening here is you've got this disrupted cell homeostasis.
This leads to all kinds of problems like cell death or apoptosis, DNA fragmentation, necrosis,
cytoskeletal degradation, and a whole host of other things that are short and long term.
And that's just the phase one part.
That's the initial response.
From there, and once we've dealt with that,
we now have to handle step two,
or the delayed or second phase,
which is generally associated with neuroinflammation
and prolonged oxidative stress.
So what we're talking about here
is this pervasive inflammatory cascade
that is in combination with our metabolic changes
specifically to the blood brain barrier.
Now remember, that's the thing that keeps things
out of your brain and in your body
and kind of keeps the separation there.
If we've got a brain injury,
we potentially have damage to that membrane as well.
And so we've got excessive inflammation happening,
not even talking about the acute response.
Now it's staying there and persisting for days, weeks,
months, or potentially even longer.
This causes migration of what's called
peripheral immune cells into the brain
and releases a whole storm of cytokines.
These are communication tools that come out of your body
from one organ to the next.
They're not necessarily good or bad,
but in this case, it's so large and it's so extreme
that it
continues to exacerbate this inflammatory problem.
This also causes activation of things that are called residual neural cells.
There's a whole host of these things like astrocytes, complement proteins, and so on.
These things release reactive oxidative spreesies, they release that glutamate again, and they
release those cytokines.
And so you can see how this circle just sort of perpetuates itself.
It's not always a bad response, but in this particular case, since there's been so much
structural damage, one more time, the cycle just continues. This is going to really harm
the brain's healing. It's going to facilitate formation of what are called membrane attack
complexes. You could just hear from that term. That's probably not facilitate formation of what are called membrane attack complexes.
You could just hear from that term. That's probably not a good thing. Again, we're trying to clean out the damage, but it's going to come with a lot of problems. This is going to create
very specifically pores in the membranes of the target cells, which means those are going to
often die. Now, in the case of a skeletal muscle from exercise, this is okay.
It's pretty easy to repair. But when it's happening in your brain, it's a problem. So
overall we've got that oxidative stress response and that's going to start damaging fat, protein
and DNA. Remember, a big portion of your brain is made of fat. So while we're typically not
concerned about oxidative stress harming all the fat
in the rest of our body,
that represents a serious damage to our brain
and one that potentially is not reversible.
Now I know I got pretty technical there.
So if I lost any of you, don't worry about it.
Just think about it this way.
At the highest level, TBI is gonna involve
some likelihood of a physical injury or damage. This could be your capillaries or
any of your vessels, your blood brain barrier, your membranes
of your cells, your astrocytes, your neurons are actually
physically torn. If you were a house, this would mean your
windows are smashed, your doors broken, they got a hole in a
wall. It's not a functionality issue as it is an actual structure is broken and has to be repaired.
Now in addition to that, we're going to be dealing with a secondary problem, which is
now because we don't have the physical structure to get in nutrients and get waste out, we
can't make energy.
So problem number two is a massive energy deficit.
Your brain's gonna try to get around it. It's gonna start ramping up our less
effective methods of producing energy, but it's never going to catch up. And so
physical damage number one, energy deficit number two. Number three in
response to number one and two is this prolonged inflammatory response. And so we're sending
in molecules that let the inflammation continue and they exacerbate it and they start breaking
down and killing and getting rid of actual tissue. So the ones that maybe were not injured
initially will be injured or removed entirely in the weeks to months because of this inflammatory
response. So effectively those are our three big problems which means now we
can talk about what nutrition options we have to solve or mitigate or at least
attenuate slightly reduce some of those issues. I'd like to take a quick break
and thank our sponsors. Today's episode is brought to you by Momentous.
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Let's jump right into it with our very first nutrient compound,
and that's creatine monohydrate.
You're probably sick of hearing me talk about it,
because I've been doing it for so many years, but it's for good reason.
There's so much data on it, it is by far the most widely studied support supplement,
and it's not even close.
It's been studied in every population, healthy, diseased, young, old, men, women, kids, so
on and so forth, and there's really very limited side effects, if any, that have been reported.
Now creatine itself is a naturally occurring
derivative of three very specific amino acids, methionine, glycine, and arginine. These are
really, really common. Creatine itself, I typically have talked about how it's stored in muscle
and used as a great fuel source. But many people don't realize it's actually also stored in your
liver, testes, and brain. The last one, of course, is where we're going to pay our attention to today.
Now it's stored in the brain so that it can be used as a very quick fuel source.
Your gear should be turning at this point.
Remember, one of the primary issues we have with the TBI is that energy demand problem.
And so it made a ton of sense to scientists very early on to say, okay, we know that we
have energy issues.
We know that the fastest way any of our tissues
can make energy is through creatine monohydrate.
And we know it's in store in the brain already.
It makes sense to try that to both prevent
or reduce the risk of and then treat brain injuries.
So it's no surprise when we look at the research here
on both TBI as well as aging and normal brain health research, to find that
creatine monohydrate often improves cognitive function in both brain injury and normal healthy
aging folks. Now, it's not the world's most powerful nootropic, but it is effective and
been shown again in many models and many studies across many laboratories. So because it's so
effective at giving energy, especially in low
oxygen situations, you'll see evidence across injury and TBI papers, but also just normal
cognitive function and healthy individuals to see benefit, right? So creatine is effective in
all of those populations and the physiology, biochemistry make total sense. Now, specifically
regarding TBIs and concussions,
one of the things you want to pay attention to a lot as what's called the second impact
syndrome. Many people have not heard of this, but this is a basic idea of repeated head
blows cause more damage as time goes on. And so one of the things that's been shown with
creatine is it is really effective for that second impact syndrome. More specifically, it's been shown that the repeated head blows cause more damage
if the creatine is depleted prior to the additional impacts. Okay, so imagine you had one single
impact, the more creatine depletion you have, the worst damage you get if you have a secondary impact.
depletion you have, the worst damage you get if you have a secondary impact. This is any athlete that's going to be in
sparring or competitions where we're getting a lot of impacts.
This is military or special forces or anything like that,
that is again, it's getting low impact repeated exposures or
blasts. Okay, the more creatine depletion that happens, the
worst the damage in your
brain that occurs after the second or repeated impact. So right there, we can see that if
you've had an injury, making sure your creaking stores are replenished as quickly as possible
is really important. If we're going to continue in that exposure. Now that's important, because
many people don't recognize or realize the first injury happened to begin with.
Okay, most of them are unreported.
Most don't realize it hard to diagnose.
And so prophylactically, it just maybe makes some sense to make sure that you're taking
care of business, not necessarily just when you have an injury, but if you even think
you're at risk or in high risk situations or prior to high risk exposure or competitions.
Right?
Good example of this, there's a pretty famous study, I think it was in high school, football risk situations or prior to high risk exposure or competitions. Right?
Good example of this, there's a pretty famous study, I think it was in high school, football
players, high school or college, but nonetheless, football players, American football that is,
that did indicate the creatine stores in their brain, and that makes specifically in the
motor and prefrontal cortex, reduced over the course of the season.
Now, this is not a perfect study design, but
you can see what this is alluding to. If you're in a situation again with repeated head impacts
over the course of the season, the number of impacts, in fact, maybe I'll back up quickly.
In this particular study, what they did is they filmed the games. And so what they measured
is for each individual player, how many head contacts they had.
But there was an association between those players
that had more head impacts,
not even necessarily injuries,
and the level of creatine reduction in the brain
over the course of the season.
So again, we're making some assumptions here,
but I think it's fair to at least say it's plausible.
The more impacts on your brain,
the more creatine is reduced, potentially the higher risk you are for second impact syndrome injuries. Now, before we go any
further with the creatine research, I need to do a quick
pause and explain to you what I mean when I say strong evidence
or weak evidence. There's no perfect way to do that. But an easy way to roughly understand is called the
strength of evidence scale. Okay, so I will abbreviate that
and the rest of today's episode by just calling it the SOE, the
strength of evidence. Okay, this takes into account research
design, the quality of the relevant studies, the
applicability to patient care, and a number of other factors.
It's up to you ultimately, to decide what is an actionable level of evidence or not.
Some people that are maybe suffering from a brain injury consider a study in animals to be enough,
and others want to see a randomized control trial in humans. That's not for me to decide,
that's up to you. But I do want to share with you where the level of evidence is,
and you can make your choice from there. So the S O E is on a scale of one to five, a score of one
is the best. That is the highest score possible. This means we see consistent results across
multiple studies. We've seen it in both randomized control trials as well as systematic reviews,
and so on and so forth. A score of, say, four or five would be the opposite.
That would be our lowest score.
Maybe there's evidence there, but it's from case studies
or case control studies.
Maybe it's mechanism only or some other model that's close,
maybe research from aging or dementia.
Not the same as brain injury, but it shares some mechanisms.
You get the idea here
So for example the SOE for creatine monohydrate is a 2
My opinion personally, that's pretty good
Summarizing the collective evidence here. There's been a lot of research on everything from kids to rugby players to mountain bikers and
Collectively you're gonna see it supports cognitive health.
It's been shown actually in psychiatric disorders. There's, I believe, two randomized control trials
that I'm aware of that have found five grams of creatine per day added in addition to antidepressant treatments, improve depressive symptoms. All right. So take that for what you
will. And regarding TBIs and brain injuries. There's an argument we can make
here for preventative use, specifically for neuronal damage
and injury. There's been shown to reduce cortical damage
following a TBI by anywhere between 35 to 50%. That'd be five
zero. Pretty substantial amount there should catch your
attention. They don't know exactly how it works. But it's thought to prevent some of that mitochondrial dysfunction I
was talking about a few minutes ago. Helps maintain the membrane health.
Certainly has a role in fending off that downstream reactive oxygen species ATP
calcium so a lot of those things we just got done covering that's why we covered
them. Creatine probably has a role,
again, we need more information here,
but likely has a role in either eliminating
or at least drastically reducing some of those issues.
And finally then, what you care more about
is the downstream TBI effects have also been documented.
What I mean here is sleep, cognition,
and actual mood seem to be enhanced with the creatine.
Furthermore, there's actually some studies that have specifically been done on kids.
There's one I'm thinking of in detail here that was everything from 1 to 18 year olds
that had severe TBIs. In this particular paper they gave them 0.4 grams per kilogram of body
weight. If you do the math there that that ends up being a pretty standard dose.
But appropriately, it was done based on body size.
You have two year olds and 18 year olds.
We can't give them all just five grams.
So a relative dose was given to them within four hours
post injury and done so for six months.
In that particular study, they found improvements in everything from amnesia to the length of stay in the ICU,
improvements in communication, locomotion,
and social skills.
And more importantly, one of the things I loved most
about this was the researchers were clear in the fact
that the treatment provided costs significantly less
than the standard treatment protocol.
And this is something I thought was really important because I know supplements are not cheap,
and many of you can't afford any cost whatsoever. But if you can, while creatine, I know, I know,
I hear this all the time, has gotten more expensive in recent years, it's still likely far cheaper
than a standard hospital protocol. So if you can possibly afford it,
seems to be a pretty good option.
Another thing I want to point out here,
because it comes up all the time as well,
in this study, again, remember, kids,
six months of creatine, there were no signs
of any kidney, liver, or heart side effects.
So overall, we would deem creatine
as a pretty strong chance of success
in both the physiology, as well as actual symptoms,
with a very low likelihood of injury or adverse effects.
For me personally, I wouldn't hesitate
to give this to one of my kids.
If they have it, it's entirely up to you
to make your choice.
I'm not advocating you do anything
that you don't wanna do or uncomfortable with. Just Just letting you know for me, when I look at the
research as a parent myself of two young kids, I would not hesitate at all to use this in my
children. So how do you actually use creatine? Well, you have a couple of options. One, you can
try to get this from Whole Foods and I'll present to you exactly what that would mean in amounts.
Or you can use the supplementation route.
I guess a third option would be to use a combination of both.
So most of the data on creatine monohydrate for brain injuries,
they're typically using dosages of about 20 grams per day.
Now that's four times the typical dose you'll see for performance benefits.
So this is one of our major things we have to pay attention to.
This is not a dosage, that's just your standard,
five grams, five grams, five grams.
It is much higher for the brain health benefits.
Now, oftentimes that's a little bit challenging.
And so you'll see typical protocols
instead of taking 20 grams at once,
are things like five grams administered four times per day.
All right, so the benefits are typically thought of
as both acute and chronic.
I know I've said many, many, many years now
that a creatine is not an acute thing.
It's not caffeine.
You don't take creatine right now
and feel this big stimulation effects.
It takes weeks or months to build up.
However, one paper that came out recently
kind of shook everyone's world, a 2024 paper.
Just one paper here, so temper a little bit.
I'm tempering my own expectations.
But a recent paper suggested that a very high dose, I think it was 0.35 grams per kilogram
of body weight, was enough to attenuate the drop in cognitive performance after sleep
deprivation. So you take people through sleep deprivation, the next day you give them this
giant bolus of creatine and those that took the creatine had less of a cognitive drop from sleep
deprivation. I actually think the benefits started at about three and a half hours and lasted up to
nine hours. So potentially say something bad happened and you didn't
get a great night of sleep, and you could take this maybe 20 gram dose in the morning
and by noon or so or for the rest of the day, you might have some improvements in cognitive
function. That's the first paper I've ever seen that I'm aware of to show an acute effect
of creatine. But since that was so dramatic,
I wanted to make sure I drew it to your attention.
So to me, you have an option there for brain health.
And now if we consider this
in context of the episode of today,
even getting this creatine in immediately
potentially has a brain impact.
And that's why I wanted to bring that study up
as it relates to the current topic.
Other studies have found that that 20 grams per day
for seven days enhances cognitive function.
This is specific to the mountain biker study I'm referring to.
And so generally, me personally,
this is not the studies, this is me personally
based on the work that I've read.
I think five to 10 grams per day
is probably plenty for most people as a prophylactic.
So kind of an ongoing option to be at that number. That said, and again candidly, this is what I do
for my athletes, seven days or so prior to a high risk situation, a competition, something like that,
a race or an event, we're going to opt that dose to 20 to 30 grams for that seven
days.
All right.
Again, one more time.
When I do that, it is hard to choke down 20 grams at once.
That's a handful of scoops.
And so we'll often try to get five to 10 grams in the morning, five to 10 grams at night
and split up the dosages throughout the day simply from my practical perspective.
Now one of my favorite sayings is there are no free passes in physiology. Creatine is not perfect.
It's not a panacea, and there are some potential risks.
The biggest one is GI distress.
Some people have a gas or bloating or stomach cramps
at even five grams a day.
So taking them to 20 or 30 may cause some serious issues.
It's not that frequently reported.
I've never experienced it.
I can't think of a situation
where I've ever had an athlete or client reported,
but it is a real thing.
It is pretty uncommon, but it is reported.
And so you will want to pay attention to that.
Outside of that, there isn't really any documented problems
associated even with high dosages,
20 plus grams a day, for years. There
have been studies in kids, elderly, various we'll call risky or unhealthy populations for many, many
years. You can look all across all basic all those studies and you just won't find really
any other adverse events outside of the possible mild or moderate GI distress.
Now, if the supplement does give you GI distress
or you can't afford it, don't have access to it,
or for any other reason, just don't like supplements,
you can theoretically get here with food,
but it is admittedly very challenging,
especially for those vegans and vegetarians,
because the primary source of creatine from food
comes from muscle or meat.
The most common places of creatine and meat
are going to be things like beef, chicken, salmon, tuna, cod,
and they mostly have somewhere between 400 to 600 milligrams
of creatine per 100 grams of meat.
Now, I know in America you're thinking,
what the hell is 100 grams?
The rest of the world knows exactly what that means. But 100 grams is about three and a half
ounces. Okay. A typical serving size at a restaurant is, you know, seven ounces or so. And so you can
kind of double it. In other words, beef specifically has 600 milligrams of creatine per 100 grams.
But a typical serving is 200 grams, so you'd be getting 1200 milligrams.
1200 milligrams is also 1.2 grams.
Okay?
Now, the average American at least eats about 350 grams or 12 ounces of meat per day. So if you did some basic math there,
which would mean you're at about 2000 milligrams or two grams of creatine per day. So while it
is possible theoretically to get all your creatine from food, it's honestly quite challenging.
So supplementation just might be the better option in this case.
I'd like to take a quick break and thank our sponsors. Today's episode is brought to you by AG1.
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Now, AG1 is not a replacement for eating whole foods, but it is a great way to fill in the
gaps and it's been a big help pushing some of my clients just in the right direction
for eating more high-quality foods because it helps them with cravings, digestion, and
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those ingredients are of the best sourcing. If you'd like to try AG1, you can go to drinkag1.com
slash perform to receive five free travel packs plus a year's supply of vitamin D3 plus K2. Again, that's
drinkag1.com slash perform to receive five free travel packs plus a year supply of vitamin
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Again, that's davidprotein.com slash perform to purchase if possible, or be notified when
they are available. Our next topic is
fish oil. More specifically, what I mean here is DHA and EPA.
DHA is accumulated in the brain. In fact, it's about 10% of your
brain or so. So makes a lot of sense that this one's gonna be
pretty important. It's critical for everything from neurological
function to injury risk, metabolic rate, prevention of neurodegeneration,
aging and brain health and Alzheimer's,
dementia and so on and so forth.
Incredibly important to actual structure.
EPA is a little bit different.
It's mainly involved in vascular function, inflammation,
oxygen delivery, nutrient delivery to the brain
and so on and so forth, right?
So these are typically tied together,
so I'm not going to really differentiate them as
most omega-3s come with both EPA and DHA.
Now while I said earlier that creatine is by far the most studied support supplement,
because it is, omega-3s are by far the most studied regarding traumatic brain injury.
There are dozens and dozens of studies, systematic reviews,
randomized control trials on omega threes and brain related injuries and various head
traumas. However, you might be surprised to know I'm not aware of any direct evidence
of omega threes and TB eyes. So this is a great example of me saying, Hey, look, there's
still a lot of good tangential or indirect
evidence here so much, I feel like it's overwhelming, but not necessarily that much directly on
TBIs. For the reasons we described earlier, they're just hard studies to carry out. In
general, what you're going to see is, frankly, they work. They work for both pre and post
impacts. The SOE is technically three here,
and you generally see main effects
and benefits from cerebral perfusion.
So this is getting that blood and oxygen
and flow of nutrients in and out of the brain.
Remember, the primary cause of injury there
is that structural, that tissue and that axon shearing,
that kind of ripping apart.
And so what that does is cause that cascade of secondary insults
that mismatch the blood flow and the metabolic demand.
We talked about that earlier.
Omega-3s land right on that problem for solutions.
And the reason is it helps dramatically with what's called arterial
pliability and compliance.
And so when we're having issues getting blood in, the arteries can either be broke or damaged or stiff,
and omega-3s really help it become more pliable
and open and closed more effectively
is one way to think about it.
It's also why you see so much evidence
and research on omega-3s for heart health and blood pressure
and so on and so forth,
has the same effect essentially essentially, in the brain.
Other thing it does that's a huge benefit outside of that cerebral perfusion is it modulates
inflammation post-injury by regulating that Ross reactive oxygen species.
It interacts with all kinds of cytokines like interleukin-1 and TNF-alpha, if you're familiar
with those.
If not, don't worry about it.
Even actually, there's one in particular called NFKB,
that brain folks will know exactly
what I'm talking about here.
This actually functionally, it affects a gene expression
of a bunch of inflammatory things.
So it kind of cuts off inflammation at the genetic level.
So lots of ways that it has an impact.
To give you a couple of specific examples,
one of the most common issues associated with TBI,
long-term is called atrophy of the hippocampus. Now that's associated in one of the most common issues associated with TBI long-term is called atrophy of the hippocampus.
Now, that's associated in one of the areas that's mainly responsible for learning and
memory, and we know that those are problems.
We know that higher omega-3 intake is associated with a bigger hippocampal volume.
So we have cross-sectional studies here, longitudinal ones that suggest that people that consume
more tend to have a larger hippocampus.
And we also see a significant increase in these areas
at the dosage of about 2.2 grams per day.
2.2 grams of fish oil per day
associated with a bigger hippocampus,
therefore potential to improve or enhance
our learning and memory.
Similar things have been done with memory specifically.
In fact, one study looked at, I think it was a combination of 900 milligrams of EPA
plus 260 milligrams of DHA.
And that resulted in greater accuracy and speed of recall tasks.
So mental recall memory.
EPA in general is often really associated with cognitive function,
and the DHA is associated with axonal injuries. It works on a thing called neurofilament light or
NFL and that's actually been specifically shown in college football
players I believe again at that two grams per day dosage of DHA. And so in
general to get to the end here the dosage for brain related injuries is
somewhere between two to four grams per day,
though there's really little risk. The only adverse issue you're going to typically have
here is potentially some loose stool. Again, there's not that much evidence of it. But if
you have a, you consume a bunch of oil that can kind of run through you a little bit,
probably not going to see much happen there very often. The timing of it doesn't matter that much.
You would certainly want to be taking it before the injury as well as after the injury.
And the timing of the day is honestly totally irrelevant.
And so pretty easy, pretty fast one to go through, very effective.
I personally will be totally honest, I take a lot more than four grams for other benefits,
but very fairly, the available evidence on not necessarily directly TBI RCTs,
but the other associated areas of brain health and injury and damage pretty consistently show
the effect happens at about two or so grams. And studies that have looked at higher doses
don't see any additional benefit. So I think it's very fair to say two grams a day or so
is the effective dose. And more than that may not give any additional benefit. So I think it's very fair to say two grams a day or so is the effective dose and more than that
may not give you additional benefit.
What's that look like from food?
Another example where vegans and vegetarians
really should honestly strongly consider
supplementation here.
We're gonna get fish oil from fish, pretty obviously, right?
Salmon, herring, sardines, mackerel, trout
are generally the most highest concentration ones.
Salmon being the most obvious example,
that's got about two grams of fish oil
per hundred grams of cooked meat.
Again, that'd be three and a half ounces or so,
which is not an outrageous dosage at all.
Unfortunately, the standard American diet
is typically about a hundred milligrams of omega-3s per day.
And we need to get to two, right?
So you're gonna have to up your ante.
It's totally possible,
but most people just don't do enough of it.
This is a really important one to go after.
I know I just covered information,
but I wanna also highlight the fact that you can check.
What I mean by that is,
unlike creatine where it's going to be really hard
to measure your creatine monohydrate,
especially in your brain levels,
you as a preventative strategy
should look at your omega-3 index
and identify whether you have problems,
because there's a lot of evidence to suggest
if you go into a brain injury with a better omega three, the brain
injury will be less significant. So our starting place here is
to actually not go into the injury with a problem. I
mentioned this, but I'll be more clear. The omega three index is
not a perfect way to measure it. But it is an effective blood
test you can get done. And what that's gonna effectively tell
you is the percentage of EPA and And what that's gonna effectively tell you
is the percentage of EPA and DHA
that's in the membrane of your red blood cells.
And there's been a handful of studies on this
that are quite impressive, in my opinion.
Studies on football players and even basketball players
have found that the mass majority of them
have an omega-3 index of less than 5%.
Optimal is like eight to 10, maybe even 12. The overwhelming majority
of these athletes are less than 5%. In fact, I think the studies I'm thinking of right
now, the two kind of combined, basically none of the athletes had higher than 7%. Again,
8 to 12 is what we're looking for. In fact, the reason we're doing that is because there's
been known and shown documented cognitive benefits at 10% plus, even as low as 8% plus.
So in these studies, no athletes are there.
In fact, most of the, over 50% of the athletes
in these studies had an omega-3 index of less than 4%.
So it is really, really, really common in our athletes
to see omega-3 status being really insufficient.
And the same thing has happened in the general population.
So you can 100% achieve enough for brain health
through food if you'd like.
You just need to make a concerted effort for it.
And you can see and go back to hear the dosages.
Or you can use supplements or a combination,
but you absolutely wanna make sure
that you're doing this prophylactically,
as well as if you do experience an injury,
getting right on the supplementation as quickly as
you can. Next up is what's called vitamin B2 or riboflavin.
We're going into riboflavin next because it is a requirement
for proper DHA utilization. Here's what I mean. There's some
really nice studies showing that if you give people DHA, but they
have insufficient B2, B6, B9, B12 and choline,
they won't integrate that DHA into their brain. So it's
really, really hard, technically to get the DHA to
integrate into the phospholipid membrane without these B
vitamins. And so part and parcel to our appropriate omega-3
status is making sure we're not vitamin B deficient. And
specifically in this case, we're talking about riboflavin. So it is a coenzyme for ATP production. It's a part of
many of our energy production cycles. It's also highly responsible for glutathione.
You'll hear me bring this up again, but glutathione is our chief endogenous antioxidant.
It's the big whopper. Okay. So going back to our problems associated with injury, riboflavin is going to
play a role in two of those ones, energy production, as well
as inflammation or antioxidant capacity. So really helpful from
that regard. Right? Since we know TBI has metabolic problems,
it makes sense that these B2 and other B vitamins are going to
probably play an important role.
The SOE on riboflavin is a three.
Now personally, that's enough for me to take action.
You're welcome to choose your own level of action on our score here, but I have utilized
and will probably continue to utilize riboflavin for head related injuries.
There's great data in rat studies that have shown riboflavin helps with some of the behavioral
modification issues associated
with downstream TBI problems.
Humans, there's not that much research, candidly.
Again, that's why it has an SOE score of three,
not two or one.
And what we do know is there's kind of two studies
in particular that are classic,
and they both used about 400 milligrams per day.
One of them is a bit older, 1998, I think it was published,
and it was actually in migraines.
And what it showed is that it was safe and well tolerated.
Now, interestingly, this was followed up in 2023,
and they gave again 400 milligrams,
I think they actually did it twice per day,
instead of once per day, starting 24 hours after injury.
I think they had 50 plus people in the study
and they're all about 20 years old.
Now in that they found a significant reduction
in the number of days of recovery by about half.
So the group that did not get the supplement,
the typical recovery day was 22 days long.
The supplement group, it was cut down to 10.
So this was a very, very, very impressive result.
And so it seems to
be a somewhat high reward low risk option. Additionally, the other B vitamins like B6 and B12
have probably more limited research, but they're really plausible. They're also really safe.
They've been studied a lot and a lot of unhealthy or risky populations and they just don't really have
that many negative side effects. So sounds logical to try these ones. There is a little
bit of work here, particularly when I'm thinking of as some rat studies in cases of things
like folate deficiency. When that happens, a little bit of a background there. When you
are deficient in folate, you have higher levels of what's called homocysteine.
And homocysteine is highly associated with additional oxidative stress and a whole host
of other negative health cascades.
So really high homocysteine is bad news.
Right?
Homocysteine is often also elevated when B vitamins are too low in general.
That alone is associated with neuropathy of TBIs, brain atrophy, cognitive decline with aging, and
so on and so forth.
And so the clinical trials that have been done in this area where they combine these
B vitamins and omega-3s have been shown to reduce homocysteine, and that has then also
been associated with a reduction in cognitive decline.
So if you can't pay attention to all those B vitamins, try to get them as high as reasonable or at least not in those danger areas.
Take a look at homocysteine and pay attention to that.
And if you do that, that will give those omega 3s a better chance to work more effectively.
And you should be in a better spot.
So what's riboflavin look like in terms of supplementation and food?
One more time, the dosages that have been studied for migraines and headaches and brain
health and things like that are 400 milligrams per day. One of the studies did that dosage once
per day, another did it twice per day. But those are really, really common. Now you can look all
over the internet and you will generally find every multivitamin has riboflavin, but it's not
very much. So multivitamins are not going to be the place you can go to to get enough
B12 or B2 rather for this issue. You're going to have to go to companies that make B2 specifically.
Okay. In terms of timing, again, you want to take this after your brain injuries, certainly,
but the better option is just to make sure your B status is high enough prior to going in. Okay.
But if you didn't do that or don't know, you'd want to take this post-injury. Time of day doesn't matter at all. Some people
will feel a little bit of an energetic effect. So perhaps earlier in the morning, others
don't, but you might want to consider that. I'm not aware of any risks associated with
it. Obviously, everything has some risk of some dosage in some people, but for the most
part, there's very little harm here. B vitamins typically don't have many issues if you over consume
them outside of perhaps wasting your money, I guess, if you want to think about it that
way. But there's really very little consequences at reasonable dosages. So it should be okay
there. If you want to get this from whole food sources, this is where things like liver
come in handy or fortified cereals. Whey protein
actually has a decent amount. Beef liver specifically has 3.4 milligrams of riboflavin per hundred
grams. Whey protein is about half that. I think it's about two actually. So it's not
a terrible source. So you can run the math very similar to how we just did it before.
I won't drag you through it again, but if we have to eat something like 15 times ish, the amount of
the serving size I just listed to get to that 400 milligrams per day, that's going to be
a pound, a pound and a half, sorry, a kilo or a kilo and a half of beef liver per day.
So again, theoretically possible, but just pretty unlikely
or pretty unrealistic for most people to get these at this dosage through just food. Now remember,
these are not daily amounts you have to take. We're talking about the dosages specifically for a
brain injury. And so it's actually not that crazy to think you're taking it. If you've experienced
something like this, it's not something that you need to do every day your entire life
Next on our list is choline now. This has a handful of functions first. It's helpful in preserving that blood-brain barrier
Because it wards off membrane breakdown. It's critical to that cell membrane So it has a handful of effects there
The second big thing it does is it is the primary precursor to the neurotransmitter acetylcholine
The second big thing it does is it is the primary precursor to the neurotransmitter acetylcholine.
You may remember that acetylcholine is the primary neurotransmitter.
That's the signal, the molecular signal that goes from one neuron to the next that activates
it.
We talked about this in a little more detail in a previous episode on muscle.
So you can go back to that to learn more.
But the third thing it does, it is a precursor to that important antioxidant glutathione.
So a handful of functions here,
both structural damage, cellular communication,
and activation, as well as antioxidant.
We also know from a lot of research
in the area of brain aging,
dementia, Alzheimer's, and so forth,
that higher dietary intake of choline
is strongly associated with decreases in several biomarkers
that are associated with that Alzheimer's, dementia, and other risk factors.
So from a dietary perspective, from a molecular and mechanistic perspective, it's starting
to line up as a pretty important molecule for both TBI as well as long-term brain health.
To summarize the collective evidence, it is well tolerated and safe.
It's plausibly helpful, like I just described.
And there's even some minor benefits
in both physiological and cognitive domains
following head trauma.
The most common form of choline in the research
is what's called Cetocholine or CDP choline,
as you'll see it sometimes.
And it's been tested in multiple TBI randomized
controlled trials.
In fact, a recent meta-analysis indicated that
there's about a 20% likelihood of success or effectiveness
with acetylcholine for TBI treatment.
So it's not perfect, but 20% is pretty good in my opinion.
Getting into the research just a little bit further,
there's a handful of animal and human
studies that are worth talking about at a very high level.
The animal research looked at 100 milligrams per kilogram of body weight per day, and I'm
bringing up those numbers intentionally.
I want to put some context behind that, honestly, because I've just heard people misinterpret
this paper a lot.
So 100 milligrams per kilogram per day, immediately
after an injury, which resulted in significant improvements in what's called spatial memory
performance. Now, you can't simply equate body weight here to humans, you'll get an
absurd number that won't make sense. It doesn't actually work that way for details we don't
want to talk about now. But what this would equate to is something
like 60 to 70 milligrams per kilogram in humans. And that is high. And it's about three to five
times the dosages used in human research. But it's not impossible either. So I do want to
acknowledge that those numbers are, again, high, but it's not completely crazy either.
numbers are again high, but it's not completely crazy either. In fact, some of the studies at 250 milligrams helped with the blood brain barrier breakdown
and edema were largely reduced in those trials and also had benefits in hippocampal neuronal
death for the seven days following injury.
So pretty good mechanisms from the rat studies.
In terms of the human, you will see that the studies are mixed, okay, one gram per day for 30 days has been found to in least mild TBI to produce statistically significant improvements and recognition memory, which is obviously an important downstream behavioral problem that's associated with TBI. And that study was actually repeated about 20 years
after the initial one.
And they used a pretty similar protocol design
and found actually no difference in TPI symptoms.
I think it was headaches, sleepiness, dizziness,
and concentration and things like that.
However, what's really important to note here is
in this study, the majority of the participants
had really minor TBIs,
meaning their colon edger pathways were probably not affected. This is a classic case of something
I warned out the beginning or earlier in our conversation. If you're not actually giving a
supplement or taking a food, that the mechanism of effect is not the mechanism of injury, then you
shouldn't expect a benefit.
So I think this is really a case of that.
I actually do feel like the strength of the evidence for calling is okay and reasonable,
but that 2023 follow-up study to me is not an indication that the original study was
flawed or didn't work, but simply you had mild injuries that didn't result in damage
to that pathway.
So the supplement provided very limited or mixed benefits.
In addition, I know of two meta-analyses that reported generally positive benefits here,
regardless of TBI severity.
So that's some more information on positive benefit.
And the probably landmark study in this area came out fairly recently.
It was called the COBRIT study.
I think it stands for like Cytocoline Brain Injury Treatment Trial.
You know how scientists always like to make these acronyms for our big studies.
Again, honestly, I feel like this is being misinterpreted in my opinion.
And so want to touch on this just really briefly.
But in that they found no evidence of benefit
for cognitive function or cognitive status
90 days post-injury with two grams a day of citricoline.
Now, a lot of people have used that to say,
we told you it doesn't work, it doesn't work,
and that's fine, people can interpret how they will.
My personal opinion on this study though,
is that it's highly flawed.
And I'm saying that because in it,
they considered adherence to be 75%,
meaning if the people in the study took their Cetalcholine,
75% of the time, they were considered to be adherent.
Only 44% of their participants met that 75% mark.
40% were considered to be non-adherent.
So that means they took it less than 75%.
And the rest, they don't even know.
So for me, it's hard to suggest that it didn't work
when the vast majority of people didn't actually take it
most of the time,
and those that did was still only 75% of the time.
So cool study, helped add a lot of information,
in my opinion, to the database,
but I don't think it should be interpreted
as saying that choline then therefore doesn't work
or it's a myth or any of those other
more extreme interpretations of these data.
More directly for the context of our show today,
been done on football players where brain choline,
specifically in the primary motor cortex,
is known to diminish across the season,
similar to what we saw earlier with creatine.
Probably as a result of those continuous head impacts,
so it couldn't be inferred directly from this study,
but pretty easy to make a guess that's likely scenario.
And this actually may contribute
to that second impact syndrome and accumulation of damage.
So similar idea here as creatine, to me, pretty strong case.
So based on the different study designs, mixed results, and other limitations, the SOE for
choline lands at a three.
So what are we looking at in terms of food and supplements?
Well, first of all, you're not going to find choline supplements on their own very commonly, it's almost always
going to be in the form of what's called alpha GPC or in
the more direct version of phosphatidylcholine. Now, alpha
GPC is immediately metabolized into phosphatidylcholine or PC
once you orally ingest it. So you can think of these as
similar products. Many companies make either PC straight or Alpha GPC,
or have a little bit built into oftentimes like B complexes.
Dosages are usually a little bit lower, 20 to 30 milligrams.
If you're getting the Alpha GPC directly,
Momentous, of course, the sponsor for the show,
as well as other companies generally will will make dosages 300 to 400 milligrams
per serving, so you need to take three or so of those
to get to this dosage level.
But you will find that fairly commonly.
Okay, now, in terms of timing,
you're probably wanting to take something like 500 milligrams
per day as a daily dosage prophylactically.
However, if you've had a direct head injury, this might be the time to ramp up to one to
two grams. These generally do have a nootropic effect. And so you would want to take these
earlier in the day. So you certainly don't have any problems cognitively or with sleep
later on.
In terms of food, if you need to get up to that one to two grams after an acute injury,
you're probably going to want to use supplementation. But it's quite easy to get to that 500,
that baseline prophylactic usage, straight out of food, a couple of eggs and some turkey,
you'll almost always get you right there. The most common places to get choline in food are meat,
poultry, fish, eggs, dairy, beans, cruciferous vegetables, beef liver, for
example, has around 400 milligrams per 100 grams of
liver, eggs, it's about 150 milligrams per egg. And so you
can actually see all right, three or four eggs in a day gets
you really close to that 500 number. Most people, a couple
of eggs, a little bit of serving meat, you're going to be right there throughout the day, which again will put you in a pretty good
spot. The average person though, doesn't get enough choline. Typical numbers in men is
around 400 milligrams women. It's about 300 or so, which is well below the AI or adequate
intake, which is 550 for men and 420 or so for women.
So you would have to probably do something
in the neighborhood of like 12 eggs
to get you to that two grams of choline per day.
So like I said, totally fine to get this from food
as your normal baseline health strategy.
But if you did want to get those upper dosage
with an acute injury,
you probably gonna have an easier time getting a little bit of supplementation rather than
trying to eat 14 or 15 eggs in a day. All right, moving on to our next one, we're looking
at branched chain amino acids. To clarify, when I say BCAs, I'm almost always talking
about three amino acids in particular, isoleucine, leucine and valine. Now leucine is the primary driver of muscle growth or muscle protein
synthesis, which is why there's so much steam behind BCAAs for muscle growth. We'll talk about
those details later. But in general, if you get enough protein, BCAAs are not really needed for
muscle growth. That said, does something different in the brain. The human data do suggest that the severity of your TBI symptoms correlate well with the degree of BCAA suppression in the brain. Bigger drop in BCAAs,
more symptoms. The BCAAs have two big effects. One of them is the fact that they are what's called
a nitrogen donor. And the other is that they help transportation interference across the blood brain
barrier. So let me let me walk you through what those mean really quickly, as it's important to understand
why they actually work in this case, but perhaps are not so important for muscle growth.
Now when I say nitrogen donor, what I mean is they are specifically used as in broken
down to give off nitrogen, which can be used for glutamate and GABA.
I already talked about glutamate earlier
and how that is a primary problem
with extreme excitotoxicity.
So getting too excited, turning too many neurons on.
Now both GABA and glutamate are heavily involved
in TBI pathology, like we just talked about.
From the transporter perspective,
when you eat protein, the amount or just as food or
supplement the amount of BCAs in your blood goes up.
Makes sense.
But a bunch of proteins in your stomach, they get broken down into amino acids, amino acids
in your blood go up.
If you ate a complete protein that will come with a bunch of BCAs, the amount of those
go up in your blood.
Now, as the BCA concentration goes up, two molecules called tryptophan and tyrosine,
they happen to share the same transporters to get through the blood brain barrier.
So if you have this big rise in BCAAs in your blood, the BCAAs will block up those transporters,
which means the uptake of tyrosine and tryptophan are blocked.
So they're not going to get across the blood brain barrier,
not gonna get in the brain.
So the amount actually in your brain of TNT,
tyrosine and tryptophan, go down.
What that does is cause problems with things like serotonin
because TNT act as precursors for serotonin,
which of course is in a precursor for melatonin and various
catecholamines.
Right?
So this could be contributing to the TBI induced sleep problems.
And so you can see the basic logic there.
The current evidence does suggest that actually sleep is not compromised with BCAAs, but actually
even potentially improved.
I know of actually a study coming to mind right now that looked at 30 grams of BCAAs administered twice per day
found it actually improved insomnia and other latency
related issues. This study I think was in veterans with
chronic TBI. And so we know some about the mechanisms that I
just outlined has a potential to be influencing some of our
sleep related problems and it seems to be causing
a positive and beneficial effect for sleep, which is a huge concern and one of the biggest symptoms
associated with a brain injury. The SOE on BCAAs is surprisingly a two. Remember, one is best,
five is worst on the scoring. So the data are actually pretty strong here. It is pretty clear
that it works as much as we can define work. There is extensive evidence in post-impact for both mild and severe TBIs.
The benefits range from cognitive deficits, so reductions in cognitive deficits, to what
I just described, some of these sleep-wake abnormalities, with the main effects probably
being correction of that excitotoxicity issue and some of the GABA and other glutamate problems
that we have just described.
Probably the most famous study in this area
is called the HITHEADS trial.
I believe this came out in 2024 actually, so pretty recent.
It was a pilot randomized controlled trial.
They had, I think like 10 to 35 year olds in there,
so teens, pre-teens, all the way up to normal age.
And they followed them for three weeks
or 21 days post-injury.
And this was really cool.
They had, I think five arms in this study.
So some of the participants just got a placebo
and then they broke up the rest
of the intervention by dosage.
So they got 15 grams a day, 30 grams, 45 or even 54.
I'm not sure why it's only 55. But they wanted to see, is there effect at all compared to placebo? 15 grams a day, 30 grams, 45, or even 54.
I'm not sure why it's only 55. But they wanted to see, is there effect at all
compared to placebo?
And if there is, what's the optimal dosage?
And they gave them five different dosages
from low dose to more moderate to pretty high
and scaled all the way up.
And one of the things that they found
was a pretty clear dose response,
such that the most improvements were found
in that 54 grams per day, decreased
symptoms of concussions, faster and better return to baseline.
There were not benefits actually in what was called processing speed.
So that had been shown in some of the earlier studies we talked about, but they didn't find
that here for whatever reason.
But they had all those other benefits.
One more time, highlights the fact that not every supplement, not every food, not
every nutrient fixes every problem. Okay, so benefits here in the concussion symptoms, but
not necessarily the processing speed. But the effects one more time were dose dependent and one
more time like we keep bringing up, there was no adverse effects reported. The data that we currently
have suggests up to 55 or 54 grams per day, more specifically is a dosage.
You would want to make sure you're at that higher dosage
past injury.
You can be at a much smaller one,
just honestly make sure your protein intake is high enough.
You can use whatever number you like.
We've talked many times though,
I personally like one gram of protein
per pound of body weight.
If you're at that,
you're probably getting enough BCAAs at baseline.
And then we would go to only this higher dose
post-brain injury.
To break this down food wise, BCAAs, it's protein.
It's dairy products, it's meat and poultry.
Most meat's gonna be three to four grams of BCAAs
per hundred grams of serving.
And so similar math that we've done before, okay?
This is gonna result in you having to have like 40 or 50
ounces of meat per day.
Not something you need baseline, but in these small cases,
again, I don't want you to feel like I'm pushing you
to supplements, but it is just significantly easier here
for small times and for specific scenarios
of a brain injury to go to supplementation here.
Our next micronutrient is magnesium.
Oh my goodness, could I go on and on and on about the physiological benefits of magnesium.
It is involved in well over 600 reactions in your body from cell signaling, vascular
function, ATP production, protein synthesis, neuroplasticity, learning, memory, and I could basically think of anything that happens
in your body and magnesium's central to that.
I don't have to draw this out then.
It's pretty easy for you to assume
this is gonna be an important role in your brain
pre and post injury.
We also have very strong data.
If you are deficient in magnesium,
you have associations with a host of comorbidities, health conditions,
type 2 diabetes, metabolic syndrome, hypertension, headaches is another common one, migraines,
heart disease, so on and so forth.
We know that it probably inhibits receptors that are directly targets of antidepressants
as well, and is a strong contributor to that brain excitotoxicity after injury. So you do not want to be deficient in magnesium.
You can listen to read almost anything in the sports performance realm and you
will see magnesium as a top-tier supplementation. It is really robust and
a strong line of evidence and recommended by, again, many people in this field.
But surprisingly, the SOEs only three here.
There's a well-documented drop in magnesium, especially in your central neurons after a TBI.
And the extent of that drop is associated with the severity of the injury
and the level of behavioral disturbances.
So not only the injury, but your symptoms as well. Animal and human research here from the
animals, it's associated with edema, brain and blood
concentrations, calcium problems, like we talked about
earlier, these are going to result in those behavioral
modifications, memory, cognitive function, spatial and working
memory, and so on and so forth. From the actual human stuff, a
couple of studies that are worth
drawing attention to here.
One looked at acute TBIs in kids
and saw a significant reduction
in post-concussion severity scores
48 hours after the injury,
when they used 400 milligrams of magnesium twice per day.
Now another study was, used a similar design and didn't find a benefit,
but this was actually using magnesium from an IV for five days. Now no one really actually knows
why this one trial worked and the other one didn't. The obvious thought is maybe there's
something that happens when you adjust it through your stomach that aids in digestion or makes it
more bioavailable. But when you took them in the IV, it didn't.
To me, that's honestly not a great answer,
but I don't have any other reason
to think that that happened.
So really honestly, to summarize here,
it is very, very safe.
It's very little harm.
It has so many other health
and performance related benefits.
There's so many health consequences
that are associated with magnesium deficiency.
It helps with symptoms and behaviors that are hallmarks of TBI like we've talked about.
So I know the SOE is technically three, but personally it's about as high in the list as I could think one supplement could be.
The dosages we described one more time, 400 milligrams per day.
The timing doesn't matter.
You'll want to have some in there pre as well as post-injury, and you can take it at any point in
the day. Now, depending on the type or form that you use, you might want to take it later in the
evening. Some people report and depending on the type, magnesium helps you fall asleep. I personally
feel no effect at all, but most people do. I still then take my magnesium at night,
just because, just in case.
There's all kinds of forms.
You've heard of magnesium 3-enate at this point,
bisglycinate, malate, and right now,
I don't know of any compelling evidence
to suggest one of those forms is any better than another.
Obviously, magnesium 3-en 8 has become more popular recently.
And that may turn out to be more effective.
It may not, I'm not sure.
There's just not enough data for us to have
really an answer at this point.
And so you can take whatever form sits best with you.
The obvious risks associated with magnesium
are the GI distress.
Biscu lysinate, malate, 3 and 8
are generally pretty well handled.
And so you shouldn't have too many issues with it.
If you want to get it strictly from food, you're looking now at things like pumpkin seeds, chia seeds, almonds and spinach.
Typically, I think pumpkin seeds are about the highest.
You'll find they've got around 200 milligrams of magnesium per 100 grams roasted. And again, you can do some math there and realize, all right, that's at least 200 grams
of roasted pumpkin seeds I'd have to get
to get to my 400 milligrams,
which is honestly quite a lot, not impossible.
Some people eat tons of almonds and spinach
and things like that, especially vegetarians and vegans,
but it is quite a bit, given how cheap, effective
and easy to handle and how many other things are benefited
with magnesium as a supplement,
we use it pretty commonly.
Our final food item to discuss
is what's called anthocyanins.
Now these come almost always from blueberries,
so henceforward I'll call these blueberry anthos,
that's how I refer to it.
Now these are phytochemicals in the flavonoid family.
There's over 700 known antho molecules.
And we're honestly basically just learning about this stuff.
So we have a ton of improvements needed,
a ton more analysis and understanding of mechanisms
and so on and so forth.
But there's enough here to go on at this point.
We know that anthos are involved in cardiovascular disease,
metabolic syndrome, type two diabetes, cancers,
vision, skin health, inflammation, neurodegenerative disorders, and probably 50 more things.
Really ubiquitous, really robust, and critical to a bunch of human functions.
TBI specifically, animal research here, blueberry supplements or blueberry extracts post-injury
have been shown to improve what's called brain derived
neurotropic factor or what you may have heard of as BDNF,
which is inversely correlated with indirect markers of memory
performance and cognition.
Now a similar study has found that blueberries also protect
against oxidative stress, which makes a ton of sense.
You've all probably heard about the antioxidant properties
associated with blueberries and blueberry extracts.
So this is no surprise for most people.
The SOE for anthos is a three.
And in terms of human data,
I don't think there's a single RCT,
randomized controlled trial,
that exists for blueberries and TBI at this point.
That said, there have been studies, many RCTs,
some of the fact that range from developmental to aging
to clinical populations on brain health.
And so this is a classic example of where we can infer
some things from general brain health over to TBI
at a pretty low risk, high reward possibility.
The collective evidence indicates that it does help
with attention, memory, executive function.
There's a lot of evidence, specifically,
we use a handful of papers that haven't done
looking at blueberries prior to golf
and enhancing brain performance in sport context.
So there's a lot out there.
We know it works, but we also know we're missing
a lot of the details because of what I
just described earlier. It's pretty new. A couple of examples.
One study in kids in particular looked at 15 or 30 grams of
freeze dried wild blueberries, and saw significant improvements
in cognitive function in a dose dependent fashion. More blueberries
the better. Other work has been done in an older adults looking
at things like 100 milligrams blueberry extracts
and seeing a better episodic memory performance,
reduced cardiovascular disease, and so on and so forth.
So what this would look like from a whole food source,
you know, to get something like 500 milligrams
of the anthos, you'd need 100 grams of blueberries,
which is, I think a cup has 150.
So I'll translate that for you a little bit.
You have a couple of blueberries
and you're probably hitting your numbers.
It's really that easy.
I would actually say that of all the things
we've discussed so far today,
this is the easiest one to get out of straight food.
You will be hard pressed to find a program
that ever comes out of myself,
our rapid health and performance company,
or any other one that I'm associated with,
that doesn't have a couple blueberries in it.
And it's for these reasons that many more.
So it's a pretty easy number to hit,
pretty consistent and has a lot of benefits, right?
I will also tell you,
people love to give blueberry olives a credit here,
but it's not the only food item
that's got the anthos in it.
Strawberries, cranberries, they have it too.
There's not as much data.
I don't know if you know if there's any data,
but I imagine if they did those studies,
you'd probably find the same benefit.
So I'm actually not as particular on this one.
I don't have evidence to support myself,
but I don't think it's that big of a stretch
to think the same chemicals,
in this case that are in blueberries,
probably also exist in raspberries and strawberries
and other similar forms.
So we will spread our berries out,
but if you want to stick to giving all the love
to blueberries, you're not gonna hurt my feelings.
As far as I understand it,
that represents all the evidence on food-related items
one can take for brain health TBIs and concussions.
The only thing I'm aware of that's actually detrimental
for brain healing is caffeine.
And there's enough evidence here
that this is probably pretty bad news
when trying to heal from a brain injury.
It causes neurovascular constriction.
It leads to less blood flow.
We know that caffeine consumers are more susceptible
to diminished emotional health, bad sleep quality,
depression, and somatic symptoms with brain injuries.
And so what my recommendation here would be
over consumption is the problem.
Do not over consume caffeine
if you've experienced a brain injury.
I don't think there's any reason to think caffeine consumption is gonna give you more risk to experienced a brain injury. I don't think there's any reason to think
caffeine consumption is gonna give you more risk
to have a brain injury, but if you have one,
you wanna make sure you're really careful.
Ask your doctor, check in there,
but that's the only one on my list
that we have reason to think that you should avoid.
That concludes today's episode on nutrition
for brain injury, TBIs, and concussion.
I think it's worth reminding you though
that if it's good for preventing and returning faster from a brain injury, TBIs, and concussion. I think it's worth reminding you though, that if it's good for preventing and returning faster
from a brain injury, it's probably safe to assume
it's also good for brain performance
as well as long-term health.
My goal of today, as always, was to provide you
with a ton of information so that you can be excited,
you can learn, you have some things to try,
but to also be fair with the state of the data,
and you can make your decision about what you wanna do
or not do based upon that.
Given this was episode 10,
not only are we done with today's discussion,
we are done with season one of
Perform with Dr. Andy Galpin.
I can't thank you all for the support.
I seriously was overwhelmed with comments
from people I know, don't know.
It was blew past my expectations.
And so I really just cannot thank you all enough.
If you're a new listener, this is maybe your first episode, you can go back and check out
all previous nine episodes on performpodcast.com.
You can check out the notes, you can go to YouTube and you can see the exact sections
of a particular video if you're
interested in that.
And we've made it as easy as possible, hopefully, for you to go straight to the information
you're looking for and not spend time on things you are not.
I can also share with you another fun announcement, and that is that season two is officially
been confirmed.
It's going to be coming out pretty soon.
If you want to know more about when that does hit the radio waves, you can stay tuned of course on my
social media, but also I would recommend signing up for our newsletter. Finishing
this off here, I cannot conclude this season without some very specific
thank-yous. First of all to all the sponsors, it was overwhelming your
support. The people jumped on board quickly and were really really helpful, so this show would not have existed without them.
So I know ad reads are a thing, but please do me a solid.
If you enjoyed any part of any of the episodes of the season,
go check out the sponsors. They really are phenomenal products.
I got to thank my special man, Vindog. You know who you are,
helped me a ton in preparing for this.
He's not the front of the camera kind of guy,
so appreciate it, Vince.
Natasha, of course, my wife, super, super supportive,
and all the time it's spent to come up here
and get this stuff done.
My students, former and past and current,
could not have done any of the stuff
that allowed me to be up here without all of your support
and truly doing all the work in the lab.
Same thing for all of my colleagues and fellow scientists, whom helped me directly with this show or indirectly.
And that I stole your research or read it at least and was able to have information to share with people.
So science is not easy.
And a lot of times people don't get the credit for it.
And I thank you all for your contribution.
All of my teammates and colleagues at my company's rapid health and performance
biomolecular athlete, absolute rest and vitality.
Again, tons and tons of support for everyone.
So I appreciate that.
And then finally, of course, my man here, my boys here at Psycomm.
And of course, Dr. Andrew Huberman. Love you all.
Super appreciative of it.
Thank you all so much for joining on this ride and I'll see you next season.
Thank you for joining for today's episode.
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Thank you for listening.
And never forget in the famous words of Bill Bowerman,
if you have a body, you're an athlete.
I hope you enjoyed this episode of Perform
with Dr. Andy Galpin.
I encourage you to listen to the other episodes
of season one, wherever you're listening now.
And last but certainly not least,
thank you for your interest in science.