Dr. Rhonda Patrick and Joe Rogan debunk myths like alkaline diets and sugar fueling cancer, clarifying blood pH regulation and cancer cell metabolism. They highlight cruciferous vegetables’ anti-cancer glucosinolates, noting raw consumption maximizes benefits, while oxalate risks from juicing are rare. Patrick explains dietary gaps for vitamin D (10,000 IU/day toxicity threshold) and omega-3s (EPA/DHA vs. ALA), recommending supplements like microalgae oil or krill oil for bioavailability. Stem cell research and personalized nutrition via Wellness FX emerge as key preventative health tools, underscoring science over pseudoscience. [Automatically generated summary]
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Cue the music, young Jamie.
Dr. Rhonda Patrick is here.
unidentified
We're going to find some shit out about health.
Joe Rogan podcast.
Check it out.
The Joe Rogan experience.
Train my day, Joe Rogan podcast by night, all day.
Yeah, actually, I could have gone a little more detail, but I was like, please do.
Yeah.
You know, so that feeling of anxiety, you know, that like you get before you get on stage.
I mean, you're a comedian.
I'm sure you're really familiar with that.
You actually are expressing a chemical called dinorphan.
And it's an endogenous chemo in your brain, and it binds to something called a kappa opioid receptor.
It's kind of like the counter of the endorphin, which binds to the mu opioid receptor.
So the endorphins are the feel-good.
Well, its nemesis is the dinorphin, which is that anxiety-like feeling.
So, but here's the interesting part.
That anxiety-like feeling that you feel before you're, you know, going to do something like you're, you know, really, that you care about or that's kind of anxiety-provoking.
For me, public speaking does it.
I get it right before I'm going to do it, you know, give a talk or something or do a podcast in front of, you know, 500,000 people.
So that dinorphin binding to the kappa opioid receptor, what it does is it upregulates the mu opioid receptor so that after you get that anxiety feeling, you have a better endorphin rush because you upregulate the mu opioid receptors, which bind to the endorphins, the feel-good ones, and you actually become sensitized to them.
So there's a biological mechanism by which having that anxiety actually does you good.
So it's kind of like a stress at first, but then later on, you feel better and you're more relaxed.
You know, that's interesting because one of the best feelings ever is after you compete.
Like when you fight, one of the things that people get addicted to is you get addicted to the rush, for sure, the adrenaline rush, and you get addicted to just the challenge of competition being life magnified on such an incredible scale that everything else seems kind of pale in comparison.
But the big addiction, I think, is to the feeling that you get after you compete, especially if you win.
There's just amazing feeling like life is incredible.
You just, you, like, the ground feels better under your feet.
Yeah, no, I totally know what you're talking about, and there's a biological mechanism for that.
And it's interesting because it's also the same mechanism that occurs when you are working out really hard.
I mean, it's painful while you're doing it.
But the more pain you experience, the better the rush.
It's the endorphin high people talk about.
It's actually that that mechanism is anxiety-inducing, stress-inducing, is an important factor in that because of this mechanism I talked about where you upregulate those receptors that bind to the endorphins and you become and you're sensitizing them so they become more sensitized to them.
So it's heat does the same thing, heat stress.
So, you know, exercise capsaicin, so eating spicy food, it's painful while you're eating it.
But what happens is you're upregulating those mu opioid receptors and you're sensitizing them to the endorphins, which is why you feel really good after eating spicy food.
I'm sure there's dope immune responses and all that stuff involved.
I mean, there's complex mechanisms and things going on in your brain, but when you're eating or when you pleasure, when you enjoy a certain taste of a food, but this particular mechanism where you've got this dinorphan and endorphin, you know, connection, it's really interesting.
And I think it's something I discussed in a recent article that I wrote about the sauna.
So I hope people find it interesting because I think it's interesting.
So hormesis, what it really refers to is having a little bit of stress, something that's a little toxic for you, something that's a little stressful on your body.
I mean, exercise for sure is that heat is a little stressful.
Things in some of the foods we eat, like the EGCGs in green tea or polyphenols in some of the fruits and also in red wine, these things are actually a little bit toxic to our body.
And what happens is that this induces stress response mechanisms in our body, the activation of a whole host of genes, like antioxidant genes, glutathione peroxidase, things like heat shock factors, which do a variety of different things.
So a little bit of stress activates this whole stress response mechanism in our body.
And then what happens is now we can deal with stress better.
So it's kind of like interesting to think about adding a little bit of something that's toxic to get a better response.
I'm like, well, actually, maybe it makes sense that in a small dose, I mean, obviously you don't want something that's like very toxic and going to kill your brain cells or anything like that.
But things in small doses, and I was assuming that maybe mycotoxins could possibly have a little slight hormetic effect.
You know, like I said, that was just me theorizing.
Isn't it fascinating, though, that that is sort of the way, like, especially when it comes to exercise, that you need to experience this like intense hardship in order to get this wonderful feeling of accomplishment, this endorphin rush.
I feel so good after I work out.
Like, I make all my best decisions after I have a really good workout.
It's just like my body has a perspective.
I have a better perspective.
If I haven't worked out in a couple of days and I'm stressed and then I have to make a decision, oftentimes I don't trust my judgment.
I'm absolutely addicted to the feeling and the physiological changes that occur with exercise.
And there are a lot of them that are occurring in the brain and elsewhere.
But it's the same.
What's really kind of fascinating recently, you know about inducing neurogenesis when you work out.
That's kind of well known, where exercise induces the growth of new brain cells.
BDNF is one way, IGF-1, these things can, you know, you grow new brain cells.
And so growing new brain cells has always been associated with learning and memory.
It's like, oh, you grow new brain cells.
And they've shown that that neurogenesis in adults at least is associated with new learning and new memory.
But what they found recently, and I found this really interesting because it kind of changed the way I think of it, is that when you grow those new brain cells, like when you're exercising, heat stress does the same thing, actually.
So getting in the sauna, when you're exercising, you're heat stress in your body.
I mean, your core body temperature is elevated.
It's very similar.
So what happens is you grow new brain cells and these new brain cells have to make new connections with other neurons.
And so what ends up happening is that other connections that you made with the connections you make between neurons, these synapses that you form, memories, it's things that you can remember, right?
I mean, you form these synapses and that's like a piece of information remembered or in some cases it's an experience that you had that you remember.
Well, you actually change those synapses and some of them go away.
So you kind of forget to make room for a new neuron to make a new.
So it really is interesting how also you have this connection, but it's a balance where you're forgetting things.
Like you're totally disconnecting some connections between old neurons that you had previously made for whatever thing you had learned or and you're making room for this new neuron that just was born to make a new connection and make learn something new.
So you have that balance.
Again, it's just, you know, it seems like a very important biological mechanism, this yin and yang, where it's like there's stress and then there's the response to the stress, which is good.
And, you know, there's things like forgetting things, but so that you can learn new things.
I mean, it's kind of important.
Can you imagine if you remembered everything you've ever you'd go insane?
I have a real problem with having too much information in my head and then forgetting things that other people remember.
And they'll remember it like it was this big important thing.
And I'm like, what?
Did we really do that?
I don't remember that.
And it's just because I've had too many experiences.
Like, there's too much stuff where if you go back to talk to someone you went to high school with, people that don't leave, that are stuck in that town, and they can remember, remember when we were 17 and we did that crazy thing?
You're like, no, I don't fucking remember that.
Like, how do you remember that?
Like, you got to get out of this town, man.
You got to make some new connections in your brain, son.
Yeah, I think, I mean, there's a lot of different things.
Serotonin release happens through a variety of different factors, but one could actually be very potent, something that's very potent that you're experiencing.
Do you know?
Does that make sense?
Where it's like it's not just your everyday stuff that you kind of block at, like it's just routine, but it's something just novel and would that be like the day you find out that Kennedy got shot or the day 9-11 happened or the day like extreme events.
Well, that's the thing with people who do MDMA, with people who party too much and do ecstasy, is the crush afterwards is their serotonin being depleted, right?
So some things that happen when you release a lot of serotonin, you know, into your synapses is that your body, because it's too much, there's more than it's supposed to have, you'll start to down-regulate other receptors.
And there seems to be like a negative feedback.
So what would happen then is the next day, you're not going to be as responsive to that serotonin.
And that's something that's a big problem with some SSRI drugs and things like that, where you're basically preventing the serotonin from being re-metabolized, taken back up.
And so it sits around in these synapses for a lot longer than it's supposed to.
And they've shown that the consequence to that is you actually down-regulate serotonin receptors, which is what serotonin receptor response to the serotonin that you're releasing.
So you can't respond to it, then what's the point?
So there's a lot of these feedback mechanisms that occur, and I don't even know all of them.
You have to be really careful when you're combining multiple drugs that are affecting like serotonin, for example, or that pathway, because then you can end up getting something called, I think they call it serotonin syndrome, where it's like people that are taking SSRIs have to be really careful and not take a bunch of tryptophan or, you know, because then you can induce like a toxicity that's that's pretty dangerous.
And I forget what all the, you know, you know, what all the actual effects of serotonin syndrome are, but they're they're not good.
It was published the last time I was on this podcast.
Actually, my paper, I didn't know it came out in press the day that I was on this podcast.
But so there's two different genes that convert tryptophan into 5-HTP.
Okay.
That's the rate-limiting step, where you convert tryptophan into 5-hydroxytryptophan.
And that's called tryptophan hydroxylase.
And there's one enzyme called tryptophan hydroxylase 1 that's local, it's localized or located outside of the blood-brain barrier.
And it's predominantly found in the gut, but it's also found in the pineal gland, which is actually separated by the blood-brain barrier.
It's close to the brain, but it's actually separated.
And it's also found in some of your T cells and placenta tissue.
And then there's tryptophan hydroxylase II, which is the brain form.
And that's found in the dorsal raphe part, the mid part of your brain.
And there's also some expression.
So your gut has neurons in it as well, enteric neurons.
That enzyme, that's the neuron one, there's some of that also in your gut, but mostly it's the other enzyme.
So there's tryptophan hydroxylase I, tryptophan hydroxylase II.
They both make serotonin.
So serotonin made in your gut actually causes GI inflammation.
And they've shown this in like mouse models because what happens is serotonin made in the gut activates T cells.
And T cells have a receptor to it on their cell surface.
And when they respond to serotonin, they proliferate and grow more.
And so if you're making, if you have a bunch of serotonin in your gut, you can get GI inflammation.
And I think this has also been documented with people that take too much 5-HTP, as well as people with colitis and such.
They've done mouse models where they knock out that enzyme, tryptophan hydroxylase 1, that makes serotonin in the gut, and it completely ameliorates the inflammatory symptoms in those mouse models.
So the other enzyme in your brain, so this is where my paper comes in.
It's a theoretical paper, but I found a mechanism.
So a theoretical paper means I didn't actually do any experiments on mice.
I didn't actually do a clinical trial.
I just, I found an underlying mechanism and I explained it all and found all this stuff that was buried in the literature and put it all together.
It's actually my first theoretical paper that I've ever written and published.
Yeah, thanks.
So what I found was that these two enzymes for tryptophan hydroxylase both have what's called a vitamin D response element in it, which is a telltale sequence that vitamin D, when vitamin D binds to a vitamin D receptor, it recognizes that and it can turn on a gene or it turns off a gene.
And when it turns on, the gene does what it's supposed to do and turns it off.
It's almost like it's not there.
What I found with it is that, so the sequence itself of this vitamin D element can determine whether or not it's going to turn it on or off.
And I found these two different enzymes of tryptophan hydroxylase had different response elements.
One was an on signal and one was an off signal.
The one in the brain was an on signal and the one in the gut was an off signal, suggesting that vitamin D was regulating the production of serotonin in opposite directions in different tissues.
So you needed it to make it in your brain.
But if you had enough vitamin D, it would shut off the gut one, not completely, but it turns it down so that you're not making as much serotonin.
You don't have as much GI inflammation.
And then I related this to autism because I know I'm getting way out there, but it's pretty cool.
So autism has been on the rise.
Like right now, the most recent CDC report that came out said that one in 68 children have autism.
I mean, it's risen like 600% since the 1970s.
Like it's astronomical, like how much it's risen.
So they can't really, they haven't identified a genetic cause.
Like over 70% of autism cases have not been linked to a genetic mutation, which means to me, something in the environment seems to be going on.
There's something, something that is, you know, interacting with possible genetic mechanisms that's causing this autism rise.
And, you know, vitamin D is one thing that's been, people getting adequate vitamin D has been on the decrease the same time that autism rises, autism's been rising.
And so I came up with this theory that low vitamin D during pregnancy and also during neonate when you're a young child can lead to serotonin deficiency in the brain.
And what happens is during the brain, during fetal brain development, serotonin is critical to guide neurons to where they're supposed to go, to make them proliferate.
It's an important differentiation factor to help them make the kind of neurons they're supposed to make.
It plays a very, very important role in regulating brain structure and morphology.
So vitamin D3, the way it works is you can make vitamin D in your skin.
So you can convert it into D3.
Yeah, so UVB radiation, you need UVB light.
And it converts something in your skin called 7-Dehydrocholesterol into vitamin D3.
And then this gets released into the bloodstream, goes to your liver, where then it's converted to 25-hydroxy vitamin D, which is what people, that's a major circulating form of vitamin D. And that's what you get measured when you go, you know, get your vitamin D levels measured.
And then it goes into your kidneys and gets activated to an active steroid hormone.
And it's called 125-hydroxy vitamin D. So vitamin D gets converted into an active steroid hormone.
And once it's converted into that active steroid hormone in your kidneys, what then it does is it binds to a vitamin D receptor in different tissues in your body, including your brain, and it does this thing where it turns on or turns off over a thousand different genes in your body.
So it's regulating a lot of different processes.
One of them, the serotonin.
So I basically came up with this theory that women were not getting enough vitamin D, and the child's brain was then becoming serotonin deficiency.
It was changing the structure of the way the brain was developing.
And they've seen now that autism actually seems to be occurring in utero.
And they're finding now they've been doing these studies where they're finding now there seems to be a good, strong environmental component, and they haven't figured out what it is.
So I'm hoping that people will start.
I'm not an autism researcher and I'm not a neuroscientist.
I mean, I know a little bit about it.
But what I did was I kind of just took a step back and started putting all these things together and came up with this hypothesis.
And I also found things like estrogen can activate that same gene in tryptophan hydroxylase.
So estrogen can protect you.
If you have low vitamin D, you can still make that serotonin from tryptophan because estrogen activates that same gene also.
And then the whole gut inflammation thing, autistics have this, and I think that they're, you know, they have high gut inflammation because they have too much, they have too much serotonin going on in the gut.
So that's another thing where it's like 5-HTP, the first thing it does is it hits the gut and you've got that enzyme in there that can, well, in the gut, so 5-HTP actually bypasses the tryptophan hydroxylase part.
It's now the next step, which is to be decarboxylated into serotonin.
So you can actually convert it.
If you take too much of it, you'll convert it into serotonin in your gut before it gets to your brain.
So it's something to keep in mind.
Serotonin does not cross the blood-brain barrier.
5-HTP does.
Wow.
So if you're converting the serotonin immediately in your gut, then it's not going to get to your brain.
I don't think that getting tired after eating it is a myth.
I think it's a myth that it's due to tryptophan because actually, so the pineal gland, so the pineal gland converts serotonin into melatonin, okay?
And the pineal gland is not, it's not part of the, it's separated by the blood-brain barrier.
So that competition, you know, for the branched-chain amino acids getting into the pineal gland is, we're talking about something different.
So, you know, you probably are getting a little bit of tryptophan being converted to melatonin, or serotonin and then melatonin when you're eating turkey.
But turkey, turkey has a lot of branched-chain amino acids as well.
We have a supplement that we sell that is, hold on, I'll grab it.
It's in this box right here.
That's 5-HTP, L-tryptophan, and a couple other things.
It's called New Mood.
Oh, you got one right here?
Yeah.
That's a 5-HTP supplement that was originally created.
It was originally, when we first came up with it, allegedly, my friend and partner allegedly likes to do ecstasy, allegedly.
And he came up with this.
They called it roll-off.
And the idea would be when you came off of, you know, when people do MDMA, they call it rolling.
And when you're off the MDMA, you know, you're like, oh, well, that was the nutritional boost that you needed to get your brain to produce more 5-HTP or to produce more serotonin, rather.
Actually, what's really interesting as I look at this is that you have vitamin D3 in it.
Yes.
Which really surprises me because whoever made this connection for putting the vitamin D in with L-tryptophan, I'm pretty impressed because that, until my paper was published in February, no one had known that vitamin D can regulate.
I mean, I'm sure, I don't know whoever made that connection.
That's an interesting, that's interesting that you were able to figure out to put vitamin D with L-tryptophan because I haven't seen any supplement on the market that's done that.
I mean, I don't know if whoever did this knew, but because tryptophan, you know, you need vitamin D to convert tryptophan into serotonin.
The fact that that is what creates so many different elements that regulate mood.
Also, now, I don't know if you're familiar with this.
There's always been this thing about dimethyltryptamine, which is the psychedelic drug that's produced by the brain.
It's also produced by the liver and the lungs.
Well, they've found recently, like within the last year, evidence that it's produced by the pineal gland.
It's always been like this big sort of, there was anecdotal evidence, but there was never real hard evidence until they actually showed that in live mice, the pineal gland is producing dimethyltryptamine.
Well, it's producing it during different periods of stress, during REM sleep.
But it's hard to get a brain, hard to get a mouse to sleep while you've got a fucking big saw mark on its brain or an opening in its brain and you're testing its pineal gland.
So the amount of evidence they have about humans, about when and where, is kind of limited.
But now they're making these correlating, they're making a correlation based on the mammal, based on the mice.
But they're trying to do more studies on human beings, more accurate studies.
And trying to come up with more accurate ways of testing, especially during different stages.
Because the hypothesis is, the theory is that when during heavy REM sleep and during periods of extreme stress when your body believes that it's going to die, like if you're under extreme physical trauma.
Like people that have had extreme physical trauma, you know, and they have that go-to-the-light moment.
The idea is that that's a dimethyltryptamine rush and that the reason why they have these intense afterlife experiences and they came.
I came back and it was amazing.
I got to see my mother and I went to this place and God was there.
You can get there if you take psychedelic drugs.
I mean you can get there right now.
A healthy person can have almost the exact same type of experience with psychedelic drugs and it's just a crazy psychedelic drug because your own brain makes it.
I mean, they tried to, like, okay, this is the, when you look at any of the studies that they've done on the human mind and the studies that they've done connecting various hormones and things like whether it's dimethyltryptamine or melatonin or tryptophan.
I think it's probably pretty safe to say that it's kind of, I mean, we know a lot about that stuff or they know a lot about that stuff, but they're not entirely certain about all the different effects that these regulating hormones have on the brain.
Well, the only guy that I know that's had grants to study it and has been allowed to study it by the Food and Drug Administration or who regulates who I guess it would be the FDA that would regulate that.
Jaguars in the Amazon find these DMT-rich plants and they chew them and eat them and have psychedelic experiences.
And they have a different, apparently they have a different way of processing things in their stomachs than we do because they're primarily carnivores.
So they don't have the same gut enzymes and things.
Like here's the jaguar.
I'll play this for you, then we'll discuss it.
But it's so crazy because this jaguar, like they do it actively.
It's like something they do on a regular basis.
And they've observed them many times.
They'll eat these grasses and these plants, rather.
And then they just trip their balls out.
unidentified
Large cats like jaguars eat leaves.
when regurgitated they cleanse their digestive system but like catnip some plants induce other effects
this jaguar is first one of the commonest rainforest vines it seems to cause playful kittenish behavior yeah But could something deeper be happening?
The human gut produces monoamine oxidase, which makes dimethyltryptamine, it doesn't, it kills it in the gut so that if you consume grass that has DMT in it, you don't have a psychedelic trip.
But I don't know if a cat has the same gut enzyme.
But it's just so the whole thing about the human mind is so fascinating where someone like you who is just sort of putting together all these different things that you found in different books and you go, well, hey, look at this combination of things that's going on and the vitamin D and vitamin D depletion.
And then here we have this issue with autism and autism has to do with inflammation and the gut and vitamin D. I put together a lot of stuff and I explained the male dominance and all this.
And really my goal was, look, maybe I'm right on, you know, maybe I'm wrong on some of these things, but I'm definitely right about some of these things.
Here, I'm interjecting it into the world, the scientific world for all you people that actually do research on autism and do research on serotonin and all this, because I don't.
I mean, that's not what I do.
And I think that that's, it's good to have theoretical papers like that sometimes where it's like you get someone who can make all these connections where there's tons of stuff buried in the literature.
And I had a mechanism.
I had a specific mechanism that explained it.
And you kind of just say, here, now, if you think this is interesting, follow up on it.
And actually, we started collaborating with a group that does do research on one of these, you know, looks at serotonin and does vitamin D research.
And they were just jumping out of their chairs.
They were so excited.
And so now they're doing experiments and have already found positive data, which is really nice and reinforcing.
But so that's, you know, that was, that was my goal is to kind of just make these connections, big picture, you know, find a mechanism.
Finding a mechanism by which vitamin D regulated serotonin was amazing and putting it out in literature.
I mean, but the whole vitamin D thing, vitamin D3, is important.
And I think it's something that most people are.
70% of the population is not getting an adequate, you know.
Actually, we have someone reach out to me on Twitter after the last podcast, an artist, and he was like, look, I really like what you're doing.
And I've been wanting to make a cool infographic, just basically summarizing everything I ever talk about with vitamin D. It's like all in one graphic.
And he did it for me.
And if you want to pull it up, it's on foundmyfitness.com.
And then it goes on, and this is like your tag cloud where it's like all the things that like go wrong when you don't have enough vitamin D. That's incredible.
Isn't that awesome?
So, and it's like learning impairments, you know, reduced serotonin, increased cancer risk.
Oh, I mean, nine, over a thousand different genes in the body.
So then you scroll down more and it shows a telomere because it actually DNA repair enzymes are regulated by vitamin D as well.
So if you're not getting enough vitamin D, you're going to have, you can see that break in your DNA.
You're going to get damaged to your DNA.
And then as you keep going, it shows you, oh, all the factors that regulate your vitamin D, like how sunscreen blocks UVB, so you can't make it with sunscreen.
Melanin, which is an adaptation to prevent UVB rays from burning you, actually also blocks your ability to make vitamin D. And body fat regulates it.
So all these different body fat regulates the bioavailability of it.
So it has to be released into the bloodstream to get converted into active hormone.
Age.
Age regulates it.
70-year-old makes four times less vitamin D from their skin than their former 20-year-old self.
All these things.
Living in the northern latitudes, another thing.
People that live in like, I think it says above 37 degrees nor with the exception of the summer, they cannot make any vitamin D from the sun.
Wow.
So the solution is vitamin D supplement.
And we, you know, this is just a really awesome way to put all this great information, you know, show it with graphics.
People like that, and it's hard, easier for people to understand.
And I go into, you know, what your level should be and all that.
But I was really stoked because I've been wanting to do this for a really long time.
And I have no artistic capabilities.
So someone just reaching out to me and wanting to help was like, you know, it was really cool.
unidentified
So where is it on your website if you were looking for it?
The reason why I wanted to get to that is because I had emailed you about this supplement that I had read about called TA65.
And I had read about it because my friend Bobby, he emailed me about it.
And his dad was taking it.
That's bad, Bobby for folks on the message board.
B-A-A-D-B-O-B-B-Y.
His dad was taking it and his dad started experiencing vision improvement.
And I was like, that's fucking crazy.
So like, what is this TA65 stuff?
So I go on to Google and I Google TA65.
And there's all these crazy claims and a lot of people are selling it.
And, you know, there's a lawsuit against it because there was a guy who was working for the company, a former executive, who is suing them because he says that it might have caused him to get cancer.
And I mean, the idea is what they're saying, this is the company that sells it.
This is the correlation between cellular aging and telomere length is rooted in solid research.
Telomeres become shorter every time a cell divides, and when they are lost, cells can no longer reproduce.
The enzyme telomeres, telomerase, how do you say it?
To lack functional telomerase showed brain degeneration and shrunken testes, but those effects were reversed when the enzyme was reactivated.
And such findings have sparked a lot of hype and encourage a cottage industry of companies that assess a person's biological age on the basis of their telomere length.
But TA Sciences has taken the buzz further and they sell a pill called TA65, which it says can shorten, can lengthen, excuse me, short telomeres.
This is, I mean, so complicated, but I think I can shed some light.
Okay.
So this is all right.
You know, telomeres, you know, every cell in your body has 46 chromosomes, with the exception of your, you know, gametes, which have 23.
But these chromosomes have your DNA.
Okay.
They're wound up with these histone proteins, and that's where your DNA is.
And at the end of these chromosomes are your telomeres.
The problem is, is that these telomeres have a funny structure where their DNA, it's a repeat of TTAGG.
And there's like this structural defect in the DNA of the telomere where there's a big overhang and like one of your strands of DNA is longer than the other one.
And so when your cell, when the cell divides and it's got to copy its entire genome with all those 46 chromosomes to make a new cell with all that same DNA, there's a little gap there at the end because it's like, oh my God, I don't have anything here.
How do I make the new DNA?
And so what happens is the next cell then has a little bit shorter telomere because there was that little gap that didn't get filled.
And this is happening successfully over multiple generations year after year after year after year.
Each time it gets a little shorter, each time it gets a little shorter.
And that becomes a problem because these telomeres are actually protecting your DNA from damage, you know, oxidative damage from unwinding and also from your chromosomes when your cell divides, they protect your chromosomes from fusing together and like getting all these funny abnormal translocations, which lead to cancer and other problems.
So you don't want that to happen.
And the problem is, is that most of our cells, with the exception of our stem cells and our lymphocytes, don't express this enzyme called telomerase, which is able to actually rebuild the telomeres.
It's actually able to rebuild the end where that telomere little gap where we can't make it.
So it's really cool.
It's like, well, here's this great enzyme that can rebuild it, but why is it only in our stem cells and why isn't it in all of our cells?
The gene is there, but it's just not activated.
It's silenced.
And the answer for that is, well, if you express too much telomerase in all these other cells, what happens is you can make a cell immortal.
And cancer cells have actually developed, they're so smart, cancer cells are like the smartest thing ever.
They've developed this capability to reactivate that enzyme to become immortal.
But the really ironic thing is, is that it's the critically short telomeres.
When your telomeres get to a really, really, really short stage, they go into this crisis where it's like, oh my God, what do I do?
What do I do?
And they either die or they go into this senescent state where they don't divide, or they somehow can reactivate this telomerase.
And at that point, if they reactivate this telomerase, if this is a damaged cell that already has mutations and stuff, you're like, boom, okay, we're going to keep you going now.
So it's kind of paradoxical that the short telomere length is what actually can reactivate the telomerase to make it become immortal.
Yeah, well, if you already have mutations, yeah, if it's already like an abnormal cell because you've already gotten damage and stuff to it.
Yes, exactly.
You can take a precancerous cell and say, here, keep going, grow more.
So this is the telomerase is in stem cells because your stem cells aren't dividing that much.
They're usually just sitting around waiting to they have to come out and divide and make more of a certain cell type and then they go back into just waiting around.
So they're not constantly dividing, meaning they're not constantly at risk for more damage.
And I can explain that later.
But anyway, so the telomerase and the mice, this is kind of cool.
So you talked about these telomerase deficient mice.
Well, mice actually, it's really weird.
They express telomerase in all their cells.
Their telomeres don't get shorter, and yet they only live two years on average.
And so in order to try to understand the biological mechanisms by which telomeres shortening, what those effects are, you have to genetically engineer them to not express that telomerase.
And what happens is over multiple generations, it takes like three, three or four, when you get to generation four, you know, then you start to see progeria types of effects where now these mice, they're born.
If this is the fourth generation of not having this enzyme, it takes like that long to actually get the telomeres to a really short level where it starts to have proger effects and they start to prematurely age.
Their tissues start to break down and they have all these sorts of aging effects.
And so what they've shown is they can reactivate telomerase at that point after four generations and it reverses those biological effects.
So the tissues become younger.
The stem cells are active and replenishing populations like they're supposed to.
So it's kind of cool.
It's like here you have this pro-aging mouse.
You reactivate the enzyme and it literally reversed the aging in these mice.
So in that case, it'd be interesting to see if having telomerase could help rebuild the telomeres.
But like I said, because of the potential danger of allowing a precancerous cell to become immortal, I think there's been a lot of, there's a lot of, people are careful about that.
And that's why it's not like on the market right now where you're just.
So the thing with reactivating telomerase is if you are, if you generally are healthy, you don't have a lot of, you know, your C-reactive protein is low, you don't have a lot of inflammation, a lot of damaged cells, then a lot of precancer cells, your immune system's getting rid of them.
You know, reactivating telomerase in a normal cell is not really a bad thing.
It's not going to make it a cancer cell.
It's going to make it immortal.
It's going to help it not have critically short telomeres.
The problem is reactivating it in a cell that has a bunch of damage in it.
And so to me, looking at how much damage is in your cell, like we can do that.
I do that right now in people.
I take their blood cells and I look at DNA damage.
And then I take the blood and I centrifuge it through this gradient where I can then isolate just the peripheral blood mononuclear cells, which are like mostly B and T lymphocytes.
That's in some monocytes.
So I don't have any red blood cells or platelets or any of those neutrophils.
I don't want those or macrophages or things like that.
So I take those peripheral blood mononuclear cells and I look at the amount of double-stranded breaks in the DNA.
So I can actually measure that.
I can quantify that.
And not only do I look at those double-stranded breaks in the DNA, so the double-stranded breaks, I think we talked about this a little bit last time.
So just normal living.
It's just, it's so, it's a like, here's aging for you in a nutshell.
Just normal living.
Your metabolism, your mitochondria are generating oxygen radicals, which, you know, get to your DNA and you get enough of these oxygen radicals.
It causes a strand break.
And then you get them in parallel.
You have two strand breaks.
UV radiation does the same thing, but let's just forget about all the outside stuff.
Like forget about carcinogens, UV, smoking, all that.
Just normal, you know, living does this.
And this happens every single day, you know.
And so your body has to repair that damage.
And I talked about those enzymes that are magnesium dependent and how magnesium is important for DNA repair enzymes.
And 45% of the population doesn't have enough of that.
Well, I'm looking at people that are obese.
And those people usually don't have a really good diet.
And they're most often magnesium deficient.
I don't want to say deficient because it's not like a clinical acute deficiency.
It's like they're inadequate.
They have inadequate levels of magnesium.
They're not taking in enough magnesium, which is 400 or so milligrams a day.
So I look at their DNA, their strand breaks.
And then I have this, because I think that they're not getting enough magnesium.
I'm not actually measuring their magnesium.
Someone else that I work with can do that, but I haven't found it necessary to do that yet.
Then what I'm doing is I'm measuring the capacity that their body has to repair a known amount of damage that I induce.
So I look at their baseline damage, see how much damage is there, and then I induce damage with an irradiator.
And then I measure over time the ability of their own enzymes to repair that damage.
And what I'm finding is that if I look at someone who's lean or obese based on BMI, then I'm seeing there's differences.
I'm seeing that people that are obese, like have a BMI of 30 or so, they have a lot more of this damage in their blood cells.
And not only do they have a lot more of this damage, their capacity to repair this damage is impaired.
So, and it makes sense to me.
You know, you're looking, you're talking about people that are eating poor diets.
They're eating very macronutrient-rich diets.
You know, they're eating a lot of processed foods and junk food, and they're not getting their micronutrients.
Their essential vitamin zinc, magnesium, these are required for like 300 different enzymes to work in the body.
And so I'm measuring one of those, and that's DNA repair, which is important to prevent cancer.
And there's other points of it we can get back to later in the conversation.
But so TA65 is, I was actually really impressed because I read a couple of the studies.
So TA65 astragalis root, some Chinese herb or something.
That's what it's from, I believe, from what I read.
And I think I'm saying it right, the astragalus root.
So it has the capacity to activate telomerase.
And there's two different papers that were pretty good.
One paper was a clinical paper where they looked, they gave people varying doses of TA65, and I don't remember the exact doses, but they did a dose response.
And they looked at a couple of things.
A, they looked at the activation of that enzyme telomerase.
And B, they looked at telomere length.
So they started the trial baseline, measured telomere length and telomerase activity.
And then they gave people these TA65 various doses of it.
And what they found is that in a dose-dependent manner, the TA65 increased the telomerase activity.
And not only did it increase telomerase activity in the very high doses in a subset of people, it actually increased the length of their telomere over baseline.
I've never seen this before.
Usually when you're doing, you know, a lot of other things that affect telomere length, vitamin D is one of them.
Vitamin D, the way vitamin D affects telomere length is totally different than the way TA65 does because vitamin D is preventing DNA damage, inflammation, things that accelerate telomere shortening.
TA65 is literally rebuilding the end of your telomeres.
So it's possible to actually start and end up with a longer telomere as opposed to other nutritional factors that regulate just delaying the attrition of it.
Does that make sense?
So that over baseline, they had like a 40%, I believe from reading that paper a while ago, a 40% increase in telomere length.
So then I went and read the other study, which was the mouse study.
And actually the woman, the lead investigator on that, I'm very familiar with her work.
I was really close to doing a postdoc in telomere in a telomere lab because I've been very interested in telomeres for quite some time.
So I had been familiar with her papers, like her publications.
And I was like, when I saw that she was, it was from her lab, I was like, oh, it's, I know, I'm familiar with her work.
You know, she's pretty good, pretty thorough.
And so her paper, what she did, was she took that same mouse model that I was talking about, where they, over successive generations, they knock out that telomerase enzyme and they, over, you know, three or four or five generations, they start to get these mice that have really short telomeres that are aging, their tissues are aging quicker.
And they gave those mice, like third or fourth generation mice, TA65.
And what they found was that giving those mice the TA65 was able to rejuvenate their tissue.
You know, the tissue started to look younger, very similar to telomerase reactivation, not as robust, which isn't surprising.
I mean, you're talking about reactivating the entire enzyme versus something that's just able to activate it.
But the mice didn't get cancer.
They didn't get any types of cancer.
So, but like I said, now if you were to take a mouse model, knock out their telomerase enzyme, inoculate them with cancer cells.
So give them cancer cells and then react, then give them the TA65.
They're probably going to do that experiment.
I mean, that's the logical thing to do next, just to make sure to really prove that it's pretty safe.
So bottom line is I was impressed with TA65, actually surprisingly so.
And, you know, personally, I think there's always that risk.
It's like, well, if you have a lot of precancerous cells, there's no telling.
Obviously, if it was a big issue, more people would be coming down with cancer.
I've read some folks online on a message board that I go to that say they started taking it, but I don't know enough of how many are taking it either.
That would be my one concern, though, is that having a bunch of precancerous cells, reactivating telomerase in those cells, then pushing them, giving them the fuel they need to then make more cancer cells.
The people that own the company, the whole thing is really, really odd.
I don't know exactly what happened because apparently there was like some sort of a physical altercation with the guy who's suing them, and they're suing him because they're saying that they lost $2 million in sales because he said that he got cancer.
Which is and they're also saying that if he had cancer, he had it before he started taking TA65.
If you have cancer before taking it, I'm not saying this is going to happen.
I'm saying theoretically, reactivating telomerase could push those cancer cells to full-blown, precancerous cells to full-blown cancer because now they're immortalizing them and letting them survive and propagate and proliferate.
Well, you can go alkaline cancer, and one of the first things that pops up is myth.
The acid alkaline myth.
What I've read that's counteracting this is that if you did alter the alkaline of your body, like the variables are so small that if you alter it in any sort of a shocking way, your body just is fucked.
I mean, I think with the exception of the gut, where you're trying to actually make a little more, you want these different gut bacteria to make more acidic, you know, to be more acidic and make more acidic type of environment to get rid of the bad bacteria, which can't grow in that type of environment.
But all the other stuff, I think, yeah, there's slight changes in pH.
And I mean, you're talking about activating these things.
The immune system's sensitive to this sort of stuff.
I mean, it's like all of a sudden you start activating your neutrophils and they don't know why they're activated, but when they're activated, it's just like fire, fire, fire, fire, fire.
And they're firing all kinds of crap, cytokines, which are making reactive nitrogen species, which are damaging your DNA and your lipids and your proteins.
So it's like, you know, there's things like that going on.
Well, this critique of it was saying that foods don't influence the blood pH.
And they were saying, this is, I'll just read what it says here on this guy's website.
It's a proponents of the alkaline diet have put forth a few different theories about how acidic diet harms our health.
The most ridiculous claim, more ridiculous claim, is that we can change the pH of our blood by changing the foods we eat and that the acidic blood causes disease while alkaline blood prevents it.
This is not true.
The body type is all referenced to, I'll give the guy's website.
It's Chris Cresser, C-H-R-I-S-K-R-E-S-S-E-R dot com.
This is not true.
The body tightly regulates the pH of our blood and extracellular fluid, and we cannot influence our blood pH by changing our diet with references.
High doses of sodium bicarbonate can temporarily increase blood pH, but not without causing uncomfortable GI syndromes, symptoms, rather.
And there are certainly circumstances in which blood is more acidic than it should be, and this does have serious health consequences.
However, this state of acidosis is caused by pathological conditions such as chronic renal insufficiency, not by whether or not you choose to eat a salad or a burger.
In other words, regardless of what you eat or what your urine pH is, you can be pretty confident that your blood pH is hovering around a comfortable 7.4.
You know, I just don't know enough about that stuff, honestly, to say definitively if it's, you know, I really don't.
I know that things in vitro, you know, when you're looking at cancer, if you're talking about growing cancer cells in a dish and changing that, you know, environment is one thing, but I don't know.
Well, I mean, you're obviously when you're eating sugar, you're inducing an insulin response, which then you take the sugar up into your cells, so that regulates the blood sugar levels.
Unless you're type 2 diabetic or something that's not working, then you can't regulate your blood sugar levels normally, and that's not good.
You know, the thing is, is that cancer cells do acquire this capability to become glycolytic, where they're, instead of using glucose to convert it into pyruvate and go into the mitochondria and use this whole mitochondrial metabolism,
oxidative phosphorylation, to generate energy, they become, they use this whole pathway that's called glycolysis, which is a, it's a much shorter pathway, and they're using it to generate, you know, that's how they're using it to generate their energy.
So I think that probably plays a role in people coming up with all these different theories and things that manipulating the glucose and all that, what it can do.
I know that, you know, I did a lot of work manipulating cancer nutrients in cancer cells in grad school.
And, you know, getting, if I had, this is in vitro, first of all, if I do it in vitro, if I take a cancer cell and I take away their glucose, but they still have all these glutamine, they have, you know, these other amino acids, and they were fine.
They'd grow slower, but they wouldn't die.
If I took away their glutamine, they would die within like 24 hours.
And it's, you know, for me to think about cancer cells, well, not only do they need energy, ACP, they need nitrogen source to make new nucleotides for new DNA and also new amino acids.
They need molecules like to build lipids for lipid or your lipid membrane.
So there's a lot of, you know, just taking away the glucose is one thing, but there's a lot of other macromolecules that are really required for cancer proliferation that are also important.
So taking some of the stuff that we're learning in science and immediately applying it, I think in some cases, can be a little dangerous, just because we don't exactly understand how all these mechanisms are working together.
So I'm a little cautious about taking something that we're learning in science and immediately applying it to yourself, especially if you have cancer.
I mean, if you think about like the last time I was here, I was talking about the folic acid and how that's a perfect example where folic acid is great for you if you don't have cancer because you can build new DNA.
But if you have cancer, taking a lot of it is not great for you because you build new DNA and that's what cancer cells are doing when they're dividing.
So that's, and there's another example of that with another micronutrient, one of the vitamin E's.
So actually, this would be a transition into some of the Off-It stuff because he was talking about that specifically.
So just to let everybody know, it seems, you know, if you're not interested in doing any of the research, it seems that almost everyone who's done any research on this alkaline diet thing says it's horseshit.
But they do say that these foods that they're suggesting that you eat to keep an alkaline rich diet are very healthy for you.
So in that sense, it's good for you because it's going to provide your body with the nutrients that it needs, especially if you're nutrient deficient.
You're much more likely to be unhealthy.
If you're much more likely to be unhealthy, your immune system is going to have a harder time dealing with any host of different diseases.
But that this alkaline thing of your body, your body basically hovers between 7.35 and 7.45.
Your stomach is very acidic with a pH of 3.5 or below, so it can break down food.
And your urine changes depending on what you eat.
And that's how your body keeps the level in your body steady.
But this idea that you're going to regulate the alkaline of your body with food and that you're going to keep your body in an alkaline state, horseshit.
Well, there's a lot of those sort of like myths going on.
In fact, recently, I think I saw on your Twitter, you posted something, I don't know, a couple days ago about kale.
And it's really kind of, these people are doing more harm in the sense in some cases.
So, you know, kale, kale in the cruciferous family, like broccoli, cabbage, Brussels sprouts, these things, they have something in them called glucosinolates.
Okay, and glucosinolates can get, they get cleaved by an enzyme called myrosinase, which is in the plant.
And it forms something called isothiocyanates.
And isothiocyanates are very, they've been shown to be very potent anti-cancer agents.
So they activate, it's actually a part of that hormesis I was talking about because these are generated in the plant as a natural defense mechanism.
It's one of their natural defense mechanism against bugs.
It's like a natural pesticide in a sense.
They produce it to keep bugs away.
Isothiocyanates are, for us, activate a variety of different genes that are involved in stress resistance, including tumor suppressor genes, which actually kill tumor cells.
And so, and they've shown this, they've shown this, you know, quite a few times, that if you give mice, like, you know, mice that have cancer, isothiocyanates, they will kill the cancer cells.
And the whole isothiocyanates thing also competitively binds to the iodine transporter in the thyroid.
So here comes this whole, oh my God, you can't eat kale, Bika, or cruciferous because it will screw up your thyroid and cause hypothyroidism, right?
So the thing is, though, is these isothiocyanates, they appear to competitively bind to the same transporter that iodine does to get into the thyroid.
Now, I was looking for the paper where they showed that, and it's like 1948, because what I wanted to see was a dose-dependent manner of giving them, you know, these isothiocyanates or kale and show how much of it competes with iodine and how much doesn't.
Well, I couldn't get access to that paper.
But what I did find is that when you give these mice isothiocyanates, a lot of them, that kills cancer cells, but it doesn't cause any thyroid problems, which leads me to believe is that the isothiocyanate is probably very, very, very small degree of competitive inhibition of getting iodine into your thyroid,
which if you don't, if you aren't low in iodine, wouldn't be a problem because you're not, you know, so if it's just a very small amount of it competing with it to get it to get iodine into the thyroid, it's not going to be a problem unless you're really, really deficient in iodine and then any small amount you need.
So in my opinion, and for me, I love getting isothiocyanates from these cruciferous.
And by the way, the enzyme myrosinase that converts that the glucosinolates into isothiocyanates is heat sensitive.
So if you heat it, it will generally inactivate it, not completely, but it does inactivate it for the most part.
And so you're not getting as many of those isothiocyanates, which is probably why people started to say, oh, boil your kale.
I personally want the isothiocyanates because the data is so strong showing that these things kill cancer cells.
I mean, to me, you know, hormesis, okay, it depends on what you're defining as bad for you or saying hormesis, it's activating a bunch of genes that are tumor suppressor genes that kill cancer cells.
I mean, it's good for you.
These isothiocyanates are good for you if you don't, if you're not like completely deficient in iodine, which most people aren't.
I mean, I think there's some problem with women in their 20s or 40s.
It kind of irks me because I'm like, I see all this stuff and it's like, no, you know, don't not, you know, don't eat your raw kale because you want to get things like isothiocyanates.
There's chemicals in these plants that are, yes, they're, you know, they're slightly toxic, but they're inducing stress response mechanisms in our body that are good for us.
They're fighting off all the bad stuff that we're making in our body every day.
You know, it's a good thing.
Precancerous cells are always happening.
You want tumor suppressor genes are genes that when there's something's wrong, like you have, you get that DNA damage I was talking about, something happens or a mutation happens in a cell, it senses it, you know, and it activates this whole response pathway where it's like die and it kills the cell.
So having something that activates those pathways in your body, like isothiocyanates, is a good thing.
It's, you know, and personally, I want more of them.
So the thing is, when you look at the, when you look in the literature, if you're trying to look at the effects of isothiocyanates on thyroid function, there's not a whole huge literature on it.
Like I said, I was looking for the experiment to prove to me, I wanted to see how much competitive inhibition there was.
I think they're also called IC3s, IC3s on the iodine transporter in the thyroid.
I couldn't find it.
I'd saw review articles where they referred to it.
I looked at the reference, go to the reference.
It's some other review.
It's just, there's no, I wanted to see the data and I had to dig, like dig until I got to 1948 where they did this competitive binding assay.
And then I found other papers talking about, oh, it's only an effect if you have low iodine, which made me think, well, I can't see the data, but what I think makes sense is that only if it's such a low competitive binding that it's not, you know, it's not like if you eat this, you're going to not get iodine.
It's that if you already are at that point where you don't have it, any little bit you don't get makes a difference.
And I know, and I know this because the mouse models where they're not even looking at thyroid function, they're looking at the effects of isothyocyanates on killing cancer cells.
Those mice have no problems with becoming hypothyroid, and they're giving them large doses.
So to me, I'm like, okay, well, that would have been a side effect they would have noticed.
And what people are saying on the internet from what I could see on this whole echo chamber thing that happens is that you need to boil your spinach, I guess, or in some people they're saying kale, because then you're going to inactivate this oxalic acid, and now it's not going to bind up minerals like magnesium and calcium.
And they're saying that this is a problem if you don't do this because then you're going to get kidney stones.
Right.
So I was looking in the literature and I found a really cool experiment done by this Japanese group where they took spinach, raw spinach, they boiled it, they fried it, they frizzled it.
I mean, so they did, you know, various different temperatures.
And they, you know, then you make it into a powder to give to these mice that are magnesium deficient.
They put them on a magnesium deficient diet and they fed them either the raw spinach, the boiled, the frizzled, fried.
And they measured magnesium levels in their blood, in their bone, and they measured calcium levels in their blood and bone and also in their kidneys.
And what they found was that there was no difference in the magnesium and calcium levels in the bone and also in the serum.
Whether or not you boiled raw, fried, whatever, frizzled.
However, sorry, no, the calcium levels, there was a difference from frying it or frizzling it, but the raw and the boiling were the same.
And basically the conclusions were it doesn't affect absorption, boiling or raw, it's the same.
You're going to absorb the same amount of magnesium, calcium.
There were magnesium and calcium in the kidney.
They did have them in the kidney, and it was a little bit higher concentrated versus the control, but it wasn't causing kidney stones and things like that, and there was no difference between boiling or not.
So if you're going to make the claim that having oxalic acid causes, you know, kidney stones and you need to boil it, well, maybe you need to say don't eat it.
This is based on the little bit of reading that I've done on those.
The isothiocyanates, I'm definitely convinced that, you know, the oxalic acid, you know, because it does bind minerals, it's a chelator, you know, there may be some cases where kidney, you know, can accumulate in the kidney.
But I think that from what from my reading, that's a really, really large dose.
And I haven't convinced myself yet.
I'm not saying it's not possible, but I haven't convinced myself that I need to worry about it.
But it's activating stress response pathways that are ultimately, it's like, okay, a little bit of bad for you, activating a pathway really, really good for you.
Because now you're turning on hundreds of genes that are involved in DNA repair, that are involved in glutathione peroxidase, getting rid of oxidation that are involved in making sure cancer cells die.
So to me, you are getting a little bit of these toxins from these plants.
So the point being that the incorrect correlation that people have made between the very low toxicity between these plants, kale, broccoli, whatever, and them being something that you should avoid consuming unless you boil them, that's just not.
So I think people can take something little and it becomes sensational and they're like, oh, it's very sensational because what's good for you is bad for you.
But if you do this little thing, it becomes good for you again.
And I think that it's a good marketing tactic in some respects.
There's a study that you could find on a PubMed site about oxalic oxalate nephropathy due to juicing.
And this patient with oxalate-induced acute renal failure that was attributable to a consumption of oxalate-rich fruit and vegetable juices obtained from juicing.
We described the case and also reviewed the clinical presentation of 65 patients seen at the Mayo Clinic in Rochester, Minnesota from 1985 through 2010 with renal failure and biopsy-proven renal calcium oxalate crystals.
The cause of renal oxalosis was identified for all patients, a single cause for 36 patients and at least two causes for 29 patients.
Three patients, including our index patient, had presumed diet-induced oxalate nephro.
In the context of chronic kidney disease, identification of calcium oxalate crystals in a kidney biopsy should prompt an evaluation for causes of renal oxalosis.
So to me, it sounds like, like I said, you know, you're, there's always going to be cases where you can't, you can't, you can probably cause that to happen because it does bind and chelate these ions.
Because if you juice, like think about like what a like a 16 ounce glass of juice, how many vegetables have to go into that juice or to liquefy it down to I make smoothies for the most part.
I don't juice.
Occasionally I buy cold press juices, but most of what I do, I just bind.
But it sounds to me like there can be cases where you're getting a really concentrated amount of this and you're doing it every day because there's people out there that go extreme and no matter what they do, they go like to the extreme.
And because you can, you know, the oxalic acid or oxal, the anion of it, the oxalate, can bind, does bind to these metal ions, it chelates them, then, you know, it absolutely could accumulate in your kidney.
It's really interesting that some now, I don't know how much of a degree this is dose dependent, but there's bacteria in your gut called putrefication bacteria.
And I call that because they're the bacteria that make that really nasty smelling fart.
It's like hydrogen sulfide.
It smells like pure hydrogen sulfide.
And those bacteria, the putrefication bacteria, they actually use like sulfate and nitrate as their source of energy.
And they convert it into like, for example, hydrogen sulfide.
But they need, so it's basically what we do with oxygen.
They do that with these sulfate and they make it into hydrogen sulfide.
It's like us converting oxygen to water.
That's how we make ATP.
They do this by converting sulfate into hydrogen sulfide and that's their energy, this putrefication bacteria.
Well, they need these, I guess, cofactors to do this, and that's heme.
Heme is in red meat.
And so some people that eat really, really large doses of red meat, like what happens is you're giving those bacteria heme and they start to make hydrogen sulfide.
And the thing with hydrogen sulfide, so you'll make, first of all, you get putrefaction of bacteria.
So you'll have nasty smelling farts like hydrogen sulfide farts.
And also hydrogen sulfide competitively binds to enzymes in our gut cells that make energy.
So they actually, so it goes, hydrogen sulfide goes and binds to these electron transport chain enzymes that make ATP in our gut cells and competitively inhibits them from actually being able to reduce oxygen to water to make ATP.
So then your gut cells start to like starve down there and starts to break down the gut mucus barrier.
And he listened to this guy and without debunking it online at all.
And I did it real quick.
I did a real quick debunking of it and found a bunch of people who called bullshit on all of his claims.
I mean while these studies were from 1942 and it's just like so so much of what this guy had said was horseshit.
One of them off it claimed that a study, what this guy was basically saying was that taking vitamins and taking antioxidants can actually cause cancer.
And, you know, Callan, of course, never wants to be wrong.
So he's telling me, no, no, no, no, no, all studies confirm this.
I'm like, the fuck they do, man.
So I sent him all this, this, you know, I barraged him with all these debunking sites and he backed off finally.
But for fucking days, his Twitter was all about don't take antioxidant.
Because I think that's what's going on with a lot of these fuckheads.
These contrarians, with these people that make these articles, I don't know how many of them are just idiots.
I don't know how many of them are like Brian Dunning, where they just sort of, they're mentally deficient.
There's something wrong with the way they're thinking where.
And I discovered that in communicating with Brian over three hours.
I'm like, oh, there's something wrong here.
And I don't know what it is.
And I don't want to know what it is, but you're not normal.
You're not healthy.
Your correlations are not healthy.
Justin discussing buildings falling.
His way of looking at things is unhealthy.
It's not correct.
I don't know if that's what this guy's doing.
I don't know if a lot of these people are doing things.
I think they're just trying to get attention.
They're like, kale's going to kill you.
Fucking kale's going to kill me.
Everybody knows that people are loving kale these days.
People are finding all these health benefit scales.
I talk freely and openly about how I drink kale salads or kale shakes rather on a regular basis and how I feel great when I take them.
So and then, you know, people will send me these fucking things.
So I retweet some of them and then I'll find contradictory articles.
I retweet those.
So this off it fucking thing just drove me up a wall because I started reading all the people that call bullshit on this guy and all these people that say that he's kind of dangerous, that the things he's saying are kind of dangerous because they're easily refutable, but he's trying to sell them.
So I didn't read his book, but I listened to the podcast and I took notes on what he said.
And I'm ready.
Let's go through some of this because I think it's really important.
First of all, this guy makes huge overgeneralizations, doesn't understand mechanism.
It's clear to me.
So the first thing he says is that we should have, if we're going to look at the effects of supplements, we need to do randomized controlled trials.
We need to hold all drugs to the same standard.
We need to do randomized controlled trials.
So randomized controlled trials are like the poster child for pharmacological interventions, drug interventions.
And what they are is you basically, you get a population of people, you split them into two groups, and you're going to have either your drug, blah, blah, blah.
Or placebo.
And you're going to give whichever group one, drug, blah, blah, blah, blah, blah, the other group, placebo.
And you don't know who's getting what.
They don't know who's getting what.
And then you're going to look at some clinical endpoint like heart attack or mitochondrial infarction or something like that.
And it's really a great design for that sort of thing because, you know, when you start off at baseline, everyone in the trial has same levels of drug, blah, blah, blah in their blood.
Guess what?
Zero because we don't make drugs.
We don't eat drugs.
You know, it's not something that we're eating on a daily basis.
This is a pharmacological drug that's been designed with a certain mechanism of action to act on a certain thing to do a certain thing, right?
Like, you know, statins, for example.
So, you know, you can do that where you have this randomized control trial for a certain X amount of time and you look at the effect on heart attacks and you don't have to measure anything, you know.
The problem is, is that you can't apply that same thinking for nutrition research because everyone has different levels of vitamins and minerals in their body.
People eat different diets.
I mean, you have people that are, you know, have inadequate levels of things, are deficient in certain things, have optimal levels of certain things.
And so if you just take this random group of people, put them into two groups, and then give them a vitamin supplement and then try to look at some clinical endpoint like heart attack.
Well, guess what?
You're going to have people that were severely deficient and whatever you gave them, they're still severely deficient.
Or you're going to have people that have total adequate levels and you're giving them a vitamin, they already have adequate levels of, and you're trying to look at some clinical endpoint.
You can't do nutrition research with the same mind frame whereas we're looking at, we're going to do the same type of trial that we do for drugs.
You know, that's just, you can't do that.
You can't do that.
You have to think about the way you control and design a clinical trial.
And when you're doing nutrition research, where you're looking at the effects of vitamins and minerals, first of all, there's two very different things going on.
When you have a pharmacological drug, you're giving it to someone because they're already falling apart.
Okay, they're already falling apart and you're trying to help them not fall apart as fast by giving them something that blocks X or Y or Z, like cholesterol synthesis for one statins.
With vitamins and minerals, these are things that are important for preventing you from falling apart.
These are things that we require.
These enzymes we need, you know, cofactors for enzymes that we need to do like hundreds of different physiological functions, thousands of different physiological functions, you know.
So we're talking about a different start point, right?
It's not like you give people vitamins when they're falling apart.
No, they need to be getting their vitamins to make sure they don't fall apart, you know?
And so the whole randomized control trial using that, that's so he kept saying this, like we need to hold vitamins to the same standard as drugs.
We need to have randomized controlled trials.
And that's how we determine whether or not they're effective or their efficacy, basically.
But like I said, you can't do that.
You have to measure people's vitamin and mineral levels.
Let's say you're looking at vitamin D at baseline to see how deficient they are.
For one, this is going to determine the dose that you give them.
If someone's like 12 nanograms per milliliter and you give them 400 IUs a day, they've even shown in that annals of internal medicine paper that doesn't work.
They're still going to be deficient at the end of the trial because 400 IUUs a day raises your blood levels by like five nanograms per milliliter.
So you can't, that is not the way to do nutrition research.
The difference being that giving someone something that's completely alien to the body but could be beneficial like a drug or giving them something that is absolutely essential to the body that is necessary and is a part of normal everyday diet, that you can't look at the two of them the same way.
That the drug may help people, but the reality is you're introducing something that's completely alien to the person's system in order to benefit them.
Whereas with vitamins, you are just regulating or measuring what is essential to the human body.
And pretty much has been established that vitamin B, vitamin D, vitamin C, all these different things, various aspects of nutrition are essential to human health.
And also, like I said, people already start off with varying levels of these vitamins.
So when you're randomizing them into two different populations, you don't know.
Some of these people could be very deficient.
Some have plenty of vitamin K or whatever you're looking at.
So you need to measure them at baseline.
So you'd have to get a deficient population.
You need to get a population that's low because the whole point of giving someone a vitamin supplement is to bring them up to an adequate level.
It's not to have some effect on top.
It's not like a drug where you're blocking some receptor and having some response.
No, you're taking vitamins and mineral supplements because you're not getting everything you need from your food and you want to get yourself up to an adequate level.
And so what you need to do is start off.
You need to measure people's levels at baseline.
Start off with the population that's inadequate, give them a vitamin mineral supplement to get them to an adequate level, and then you can measure something.
So it's really important, and I think I even talked about this last time, is quantifying these levels.
Well, this is the reason why.
You can't, you know, starting off with a population of people that has enough vitamin D and you're trying to look at the effects of vitamin D on cancer incidence.
Well, guess what?
You know, they already have enough vitamin D. They're already in this adequate range.
Or conversely, if they're really, really, really deficient and you're looking at the effects of vitamin D and cancer incidence and you give them a dose that still makes them, they're still deficient, well, guess what?
We don't know how vitamin D is affecting cancer incidents from that one study because they're still deficient at the end of the trial.
So the conclusion is, oh, my dose was inefficient, was inadequate to bring them to an adequate level of vitamin D. That should be the conclusion, not, oh, vitamin D doesn't affect cancer incidents, which is what people tend to do.
You have to sell your story to get it published.
You do years and years work of research and you find this negative data.
It's like, well, you got to sell it somehow.
So you're not going to sell it by saying, oh, well, didn't give them an adequate dose and they're still not up to adequate levels.
So that's really the one first thing about Offit and so many others, including the people that wrote this whole enough is enough editorial.
They're the same, they were looking at randomized control trials.
Most of the time, they started off with people, didn't measure anything at all at start or throughout the follow-ups.
And it's like, well, well, the enough is enough was even worse because the enough is enough, they were studying, two of the things they were studying were heart attacks in people over 65 and dementia, delaying the onset of dementia in people who are over 65.
Like, Jesus fucking Christ, you're talking about people who are dying.
Vitamins and minerals are important to prevent disease.
They are important to prevent disease.
You know, it's not like if you're already falling apart and you've already been deficient for years and years and years and years and years, guess what?
It's much harder to patch things up.
Much more difficult.
You've already acquired so much damage.
You've acquired so many different things that are going wrong that trying to patch it up later is really difficult.
And so, you know, in those studies, also, they did things where they were giving it to cancer patients.
And like I said, or smokers.
They were looking at the effects of beta-carotene or vitamin A in smokers.
And the thing is, is that smokers are a different breed because, I mean, they're taking in poison every day.
And what happens is their lungs have a very oxidative environment.
So when they take beta-carotene, which is part of the vitamin A family, this beta-carotene gets cleaved because they have oxidative stress and stuff going on.
It gets cleaved into some of these cleavage products, which actually damage DNA more and can accelerate cancer.
But the thing is, is that that's specific to smokers.
If you give the same dose of beta-carotene to a non-smoker, guess what?
That doesn't happen.
They don't get those cleavage products and it doesn't start to damage their DNA more and it doesn't accelerate cancer.
So, you know, you have to really, the context is so important.
Like, you know, you can't just say, oh, vitamin A is bad for you.
No.
Well, if you're a smoker, it's a, you know, this is a certain context where, you know, there can be problems with taking high doses of beta-carotene for that reason, where you've got all these oxidative, you know, stress things going on.
And so they cleave the beta-carotene to certain cleavage products that normal people don't get.
You know, so context is very important.
And this is something that so many people so often ignore, including Offit.
You know, another, he's basically states that, and he says, clear, it's clear and consistent that antioxidant supplements are bad for you and can give you cancer.
And he gives two examples.
The one example, he says, is the prostate cancer study.
And the second example, he says, is because you need pro-oxidants around in your body to prevent cancer cells.
It kills cancer cells, right?
Okay, so it's kind of like, well, that it's kind of a big overgeneralization.
And it really shows me his lack of understanding, his lack of understanding of mechanism, either because it's too much work to look into it because it's a lot of work, or just because he doesn't care.
So let's start off with the first part.
He says, you know, vitamin E can cause prostate cancer.
This is huge.
This is actually, there was a huge, huge study called the Select trial, where they took the selenium and vitamin E cancer prevention trial.
Selenium is also important.
It's a cofactor for about 25 or so different proteins that are, one of them being glutathione peroxidase and synthase and all these different antioxidant genes.
And it's been shown to selenium, high selenium was correlated with low cancer incidence.
So they thought that would play a role in prostate cancer.
So they did this big trial where they got like something like 30,000 men is pretty big.
And they gave them supplements.
They gave them either vitamin E. So vitamin E is actually, there's a whole family of vitamin E's.
It's not just one vitamin.
There's actually eight different forms of it.
And alpha, beta, gamma, delta.
And there's the present as either tacopherols or ticotrinols, trienols.
And the major forms are alpha and gamma tacopherol.
Okay.
And these two different forms of vitamin E, the alpha and gamma tacopherol, they're antioxidants, but they actually have separate functions.
So the alpha tacopherol is a very potent antioxidant.
So it's very good at getting oxygen, reactive oxygen radicals that's generated by like normal metabolism.
These things damage your DNA, but they also damage your lipid like bilayer of your membrane, cell membranes.
What happens is vitamin E is fat-soluble, so it gets in those lipid bilayers and it prevents that oxygen radical from damaging it.
And what happens is if you don't have that happening, your lipid membranes get stiffer and stiffer over time.
And this is part of aging, where they become rigid and it's hard to transport metabolites into your cells.
It's hard to transport proteins in and out.
It just, it screws up stuff.
So it's important to have something like alpha-tacopherol preventing that from happening.
It also prevents your proteins from being oxidized, which causes problems.
So that's really important to have, and you actually need to get it from your diet.
Vitamin E's, you have to get from your diet, from plants.
We don't make it ourselves.
The gamma form actually is also an antioxidant, but it's an anti-nitration one.
So nitration is formed from your immune system.
Just normal immune function, like fighting off things, creates reactive nitrogen species.
So these nitrogen species also do the same thing as oxygen species.
They damage your DNA, they damage your lipid membranes, they damage proteins in your body.
So having both alpha-tacopherol and the gamma-tacopherol, they're doing two independent functions, is important because they're making sure you're not getting those oxygen or nitrogen reactive species damaging crap in your body, basically.
And that's important to prevent cancer, to prevent a lot of diseases of aging.
So proteins that become oxidized or get nitrated aggregate and they can form things and plaques in your brain.
They can cause neurodegenerative diseases.
So it's important to have these antioxidant mechanisms in play to prevent that from happening as we age.
So with that said, the alpha tacophorol, and you can see how complex this is, the alpha-tacopherol is the major form in your tissues and in your bloodstream.
But the problem is, is that when you take really high levels of it, so the RDA is like 22.4 IUs.
When you take really high, like 10 times that, like 400 IUs, what happens is it depletes your gamma levels.
And this has been well known for like over a decade.
Multiple labs have shown this, including the lab I work in.
They showed it many years ago before I even joined their lab.
So taking high, high levels of alpha can be bad because it depletes the gamma.
And the gamma has a separate function from the alpha.
It prevents that nitration.
It also is an anti-inflammatory and inhibits Cox enzymes, which are involved in generating prostaglandins.
So what they did was they gave men either alpha to copherol, 400 IUs, so 10 times the RDA, maybe even more than 10 times, and selenium.
Okay, so they gave them either alpha-tacopherol, selenium only, or both, alpha-tacopherol and selenium, or the placebo.
And then they looked, they followed up, they did a couple of follow-ups to look at prostate cancer incidents, okay?
So the first study was about a five and a half year follow-up.
And this was published in like 2009.
And what it found was there's no effect.
Taking vitamin E had no effect on cancer incidents.
Taking selenium had no effect.
But what you can see if you look at the data is they measured their alpha and gamma levels at baseline.
And then at five and a half years, what happened was those men taking 400 IUs depleted their gamma tocopherol by like 45% at the end of the follow-up, which is like crazy.
That's not good.
And then the second follow-up, what it found is seven and a half years later, they found that, oh my goodness, the men taking, you know, 400 IUs of alpha tacophorol had a 17% increased risk of prostate cancer.
And then they went on to say, oh my goodness, you know, 400 IUs of vitamin E a day can cause prostate cancer.
However, the men taking the selenium with the vitamin E didn't get it.
So the men taking that alpha to copherol by itself, but took ones that took with the selenium with it didn't get it.
So the selenium protected and they didn't know why.
So another study then recently came out from the same, this is all the same big cohort of people, found that only the men that were severely deficient in selenium to start the trial that took the alpha tacopherol were the ones that had the increased cancer incidence.
So I started thinking about this.
Well, why is that?
Selenium also is important, like I said, it's important for like 25 or so proteins.
One of them is important for preventing nitration, reactive nitration products.
So I was like, wow, well, this makes sense.
You're taking high levels of alpha-tacopherol, depleting your gamma levels, which is important to get rid of nitration damage, right?
Which damages DNA, causes cancer, things like that.
And yet you can give someone the selenium or if they're not deficient in the selenium, that doesn't happen.
And one of these selenium proteins also does that.
So the bottom line is, does taking normal levels of alpha tacopherol, like 22 or 30 IUs a day, deplete your gamma levels?
No.
Is it good for you?
Like, is it going to prevent your lipid membranes from oxidizing and your DNA from getting oxidized?
Yes.
You know, is it going to give you cancer?
No.
It's actually the opposite.
It prevents cancer.
Is taking high, high levels of alpha-tacopherol dangerous?
Well, it can be, yes, because it depletes your gamma.
So, you know, taking high levels of alpha-tacopherol is not a good thing because it can deplete your gamma.
But that's only if you're also selenium deficient.
It's very, very complicated.
It is not simple.
And it's not as simple as taking vitamin E is going to give you cancer.
No, there's a whole host of complex mechanisms that are at play here.
And the reality is, you know, if you want to, 60% of the population doesn't have enough alpha-tacopherol, okay?
60%.
So if you want to supplement with it, just don't be dumb.
Take a lower level of it and supplement with the mix.
So vitamin E supplementation, in your opinion, you should probably just get it from diet to make sure that your levels are normal, healthy levels, and that it's the balance of the different types of vitamin A's.
So in a sense, he oversimplified things, but there is a danger of taking too many vitamins when you're taking vitamins like a vitamin E that could potentially, if you're taking one form of it, that could potentially deplete your absorption of the other form.
And he said that it's clear and consistent that supplemental antioxidants cause cancer.
Well, there's also other studies showing that these people profit in the case of prostate cancer, if you look at their blood levels of alpha, tacophorol, and gamma, those with the highest levels of alpha and gamma have the least prostate cancer incidence.
So there's inconsistencies in terms of what exactly is going on.
And we're still really understanding all the mechanism, trying to understand all the mechanisms at play.
But he also made the overgeneralization that taking supplemental antioxidants is bad because you need pro-oxidants to kill cancer cells.
And that was like the second part of his why supplemental antioxidants are bad.
And this is another example of context.
So if you don't have enough of the alpha, gamma, tocopherols, then you're going to have increased DNA damage.
You're going to have things that cause mutations.
And what happens is you're going to accumulate that over time and that's going to lead to cancer.
So not having enough of this vitamin E is not good.
And like I said, 60% of the population doesn't have enough.
But the flip side is that if you already have cancer, then taking supplemental vitamin E, what happens is because it prevents that oxidation, then there's mechanisms in your body that induce cell death.
When you have oxidation, when you have this damage to your DNA, tumor suppressor genes get activated and they kill the cell.
So what they've shown is that in mice, if you take mice that already, if you give them cancer and you give them supplemental vitamin E, you can attenuate that whole pathway that activates the death of these cancer cells.
But that's not the case if you take a mouse that doesn't have cancer and you give them vitamin E, it actually prevents the DNA damage.
So this is a case where you're looking at context.
So someone that doesn't have, you know, that is not, doesn't have cancer on their body, you want to make sure they're not causing DNA damage, which is happening, you know, every second, by making sure they have enough of these antioxidants.
But on the flip side of that, you know, if you already have cancer, taking a bunch of supplemental vitamin E is not a good thing because you can attenuate that pathway that is important to kill cancer cells.
So it's another thing where it's like context is so important.
You need to differentiate between people that are normal, healthy, and people that are trying to prevent themselves from getting cancer by preventing these things that cause cancer, which vitamin E can help prevent, versus talking about someone that already has cancer.
In my opinion, it's a big, big overgeneralization.
And it's probably, you know, because diving deep into this stuff is it takes time and it's complex and you need to understand how some of these things are interacting and working.
You know, so it's much easier to be like, oh, you read, you read the study, the conclusions, and oh, yep, that's it.
You know, the whole alpha to coferol and gamma to coferol, it's something I think is important for people to understand.
You know, it is alpha to coverol is the major supplemental form.
And the last study I saw said something about like 11% of the population takes high levels of alpha to coferol.
So, you know, you have a certain percent of the population that's going overboard, and they probably don't know about the effects that's going on, you know, the depletion of their gamma and how that can be bad.
So I think it is important for those people to realize that.
But on the flip side, you know, someone like Offit, his solution to that is he wants to have high-dose vitamins, FDA regulated, so that people like him, who have an MD, can prescribe them.
And so that's his solution to, you know, high-dose vitamins.
And yeah, it's, if you think about it, first of all, you know, who's going to define what a high dose is?
Is it the RDA?
Because if you look at something like vitamin D, you know, but right now the RDA for vitamin D is like 600 IUs a day.
And 70% of the population doesn't have enough vitamin D. And taking 600 IUs a day, if you're deficient, isn't going to get you to an adequate level.
So in a couple of studies that I've read where people that were deficient in vitamin D took 4,000 IUs a day for a year, that was enough to get them up to 30 nanograms per milliliter.
So it's you know it's possible that it didn't didn't take a year, but the study was that they looked at it a year later after taking a year of 4,000 IUs a day.
But that was enough.
I think generally speaking, people that are supplementing between 2,000 and 4,000 IUs generally tend to have adequate levels if they're not severely, severely deficient to start with.
If you're severely, severely deficient, it can take longer to get up to an adequate status.
Yeah, so he also said that the data is clear and consistent that supplemental vitamins don't do anything.
There's no positive benefit from them.
That's what he said, no positive benefit.
And like I said, to his credit, I haven't read his book, so maybe he goes into some specifics that I'm not aware of.
However, to say that supplemental vitamins have no benefit is like, really?
You know, I mean, they've done, they've even done randomized controlled trials showing that omega-3 fatty acid supplementation, supplementation, lowers all-cause mortality.
So, you know, supplementing, and he actually refers to omega-3 fatty acids as an antioxidant, at least in that podcast he did.
So, you know, that's one thing.
Vitamin D supplements, people that have supplemented with vitamin D, 1,500 IUs a day.
I don't remember how long they did that for, but they had a 17, it was many years.
There was a 17% decrease in cancer, cancer risk, and there was a 30% decrease in cancer mortality, and like a 40% decrease in cancers of the digestive system, including colon cancer.
So that's one for vitamin D. Let's see what's another one.
There was another study where they looked at women that took multivitamin.
But this wasn't not a controlled trial.
This was, they did a questionnaire and found out like how many, how frequently women took multivitamins and how many times a day, or how many days a week they took them.
And what they found is that the ones that took vitamins on a daily basis had the longest telomeres.
They measured telomeral length.
So that's another one.
Magnesium.
So we're talking about, you know, taking supplemental vitamins helps you fill some of those nutritional gaps that you're not getting from your diet.
And the reality is, is that we're not getting a lot of those vitamins and minerals from our diet.
For vitamin D, you'd have to really be living in a place that was exposed to the UVB during winter and summer, and you'd have to be out in the sun for 15 minutes, you know, because getting it from fish, well, maybe fish has a good bit of it, but you'd have to eat fish every day.
And also to get the omega-3s, you'd have to eat fish like every day.
Like I personally, I agree with Offutt and that goofball dunning in some instances where, you know, you should try to get all your micronutrients as much as you can from your diet.
I agree.
You know, and, you know, case in point, I do my smoothie.
I, you know, I definitely try to eat my greens and healthy meats and fish.
I really like fish.
But I do supplement.
You know, I take omega-3 fatty acids.
I take vitamin D. I take a multivitamin, which has my, you know, selenium and some of my trace elements, my iodine.
And what else do I take?
I also take a B complex, even though most people aren't, they don't have low levels of the B vitamins due to like fortification and stuff now.
I actually take a B complex because it's really kind of interesting.
But our lab has shown that, well, it's partly shown this, that as we age, I talked about how your lipid membranes get more rigid.
And a lot of, so this includes your mitochondrial membranes.
They get more stiff.
And over time, what happens is metabolites and stuff can't get transported as easy.
And also what happens is these proteins, they bind cofactors.
Like B vitamins are really important for a lot of proteins in the mitochondria that are necessary for metabolism to generate ATP.
And these proteins require B vitamins.
And a lot of them are embedded in the membrane.
So when the membrane gets stiff, the protein binding constant changes to that B vitamin.
And it's been shown that you can overcome that, meaning you actually can overcome that, messing up that binding constant because it screws up the structure of the protein by increasing the level of B vitamins.
I've always found that interesting when you look at some vitamins, you look at multivitamins, and you know what the RDA is, and you see their percentages fucking off the charts.
In the case of the B vitamins, you know, like I said, most people aren't deficient in them, and they haven't really shown any toxicity of taking too much of these B vitamins.
And they are water-soluble, so you end up peeing them all out.
I personally am taking them just because I've seen some of this data where it shows that some of these proteins that are when your lipid bilayer is kind of more rigid and gets screwed up over time.
And also when your oxidation does that or eating rancid fat, things like that, changes some of the structure of those membrane proteins that require B vitamins.
And like I said, I don't know how much more you need.
So if you look at the, so omega-3, there's three, there's EPA, there's DHA, and ALA.
So the major plant form, like flax seed oil or flax seed, walnuts, for example, have ALA.
Okay, and that's, they don't have EPA or DHA.
Now you can convert a very small percentage of ALA into the EPA, but it's like 5% of it.
It's very inefficient conversion.
And women may be able to do a little bit better of a conversion.
I can't recall off the top of my head what their number was, but the point is, is that if your only source of omega-3 is flax or walnuts, you're not getting your DHA anymore.
Yeah, that's really, the vegans, if you're vegan, really, I just, microalgae oil, I mean, the phytoplankton, or essentially are what making these omega-3s.
The fish eat the phytoplankton, it gets concentrated in the fat.
Microalgae oil, I recommend for people that are vegetarian, vegan.
So if you're vegan based off of philosophy where you don't want to eat like any type of creature, phytoplankton is a creature.
It is.
It's kind of a creature.
So I guess that could be a problem.
But if you're doing, if you're a vegetarian or vegan for health purposes and there's not like a philosophical component where you have a problem with eating these phytoplankton, then well, I mean, vegans, shouldn't they avoid, I mean, there's certain probiotics that are, I mean, that's a creature too.
So, but the omega, the DHA and EPA are really important.
They're really, really important.
And so you asked, can you take too much?
I mean, for one, you know, EPA is a very, it's got a very potent anti-inflammatory effect, which is, you know, important for a variety of different mechanisms.
You know, inflammation, chronic inflammation over time can lead to a lot of age-related diseases.
And DHA, as we, I think, even discussed last time, it's a really important component of your cell membranes, particularly in the brain, like 40% of it.
So you can actually buy EPA, like just, you know, there's companies that'll sell it.
If you're really just looking at the anti-inflammatory part of the fish oil, you can buy EPA.
It's a little more expensive.
But what it does is it inhibits that whole arachnidonic acid pathway, which produces prostaglandins.
So it's like it's like upstream where it's inhibiting the production of arachnotic acid and then prostaglandins, which activate COCs and like all, you know, you've got this whole cascade of inflammation going on.
It plays a major role in that.
There's probably other mechanisms that I haven't even read about, you know, other things going on as well that I'm not even sure, you know, feedback mechanisms, stuff like that.
But that's the major way that EPA does.
And they've even shown that like taking two grams of EPA a day can lower, can like reduce your C-reactive protein levels.
Oh, gosh, I don't remember the exact amount by how much it was, but it was pretty significant where it's like it really, you can measure, it lowers inflammation, system, like systemic inflammation.
Yeah, there is something to be aware of with the omega-3 fatty acids, and that's because they're polyunsaturated fatty acids.
They're very prone to oxidation.
So keeping them at four-degree, well, keeping them in the fridge, sorry.
Yeah.
Lowers that oxidation process.
And also just smelling it, you know, take a sniff of it and make sure it's not rancid smelling when you're taking when you're taking it because that's the one thing with the omega-3 fatty acids.
I mean, like I said, I take a lot of omega-3 fatty acids, and I think they're really important.
But I think it's important to be aware that they can go rancid.
And if they go rancid, consuming them can be not as good.
It says here on this website, krill oil actually influences your metabolism and genes to improve.
The reference study found that although both fish oil and krill oil contain omega-3s, they differ greatly in how they affect the genes controlling your metabolism.
Krill oil enhances glucose metabolism in your liver, whereas fish oil does not.
Krill oil promotes lipid metabolism, whereas fish oil does not.
Krill oil helps regulate the mitochondrial respiratory chain, whereas fish oil does not.
So DHA and EPA, in addition to the anti-inflammatory effects of EPA, and in addition to the lipid membrane part of the DHA, these fatty acid molecules are signaling molecules that actually bind to different DNA regions in your gene and activate them, much like vitamin D does.
And DHA and EPA do this.
So DHA can activate genes.
So, you know, if they're talking about, and it's been shown to activate mitochondrial metabolism genes.
So when they say krill oil does and fish oil does not, they're just to me.
You have to be specific.
What is it you're talking about?
Are you talking about DHA?
Because they're in both, you know, what else is there?
If you're saying just krill oil, well, you're talking about other things in the krill oil because if we're talking about gene activation, DPA and DHA is doing that.
DHA is activating genes.
You know, that's what it's doing in addition to what it's doing for your lipid memory.
Yeah, this is so confusing after reading what you said because it's saying some studies have shown that krill oil may be 48 times more potent than fish oil.
It means you'll need far less of it than fish oil as confirmed by a 2011 study.
And the reality is understanding mechanism, like when I'm saying mechanism, I'm talking about DHA can activate, you know, promoters in certain genes to increase the expression of mitochondrial metabolism genes.
That's been shown.
And so when you say krill oil is better, can do that and fish oil can't, that makes no sense to me.
You need to tell me what specifically is in the krill oil that's not in fish oil because, you know, DHA and EPA are in fish oil.
A unique marine-sourced flavonoid that creates a special bond with the EPA and DHA, which allows direct metabolism of the antioxidants, making them more bioavailable.
It's, you know, with the DHA and EPA, the really important thing, in my opinion, is getting it, getting enough of it, like getting, you know, taking a good bit of DHA and EPA because most people aren't getting any of it.
And all this other stuff, I'm just not sure how significant it is.
Maybe it does increase bioavailability of a little bit.
So for the folks that are taking or they're getting their omega-3s just completely from a plant source, what can they do, if anything, to try to – I really think the microalgae oil is the best.
Well, I'm going to send you some of these studies on the krill oil to see if you, unless you get bored reading it, you can't do it.
It seems like it's just such a boy, it's such a mess.
There's so many different supplements.
And just going into all the contradictory arguments, the back and forth about all these different ones, it can be incredibly taxing.
I mean, your website is a great resource of this.
If people want to go to foundmyfitness.com and try to figure out what you've already sort of described and you've already explained, but how does a person start?
I think a really good resource that I like is the Linus Pauling Institute.
So if you go to the Linus Pauling Institute, they are pretty good about writing a very, it's a scientific research institute that's associated with Oregon Health University or Oregon State Health University, something like that.
But they do a very balanced review on a variety of different supplemental vitamins and vitamins and minerals and essential fatty acids.
And that they give you both sides.
And now if they go into the krill, sometimes they'll go into things like that.
But generally speaking, I really like the Linus Pauling Institute.
I think one of the companies that I am familiar with is Wellness FX.
And I have no association with them other than I did a couple of guest blog posts for them where I, for free, wrote about vitamin D and magnesium.
And they actually, I think they're pretty much in almost every state now where you can go onto their website and they have a variety of different assays they'll do where they'll measure different vitamins and minerals and omega-3 fatty acids.
They'll measure different things, superactive protein.
And you can go to any, enter your address and go to like a lab corp around nearest by or whatever and get your blood drawn.
And then they'll give you the data within a couple of days.
They'll help you interpret it.
They have a variety of different physicians and nutritional people that can help you interpret what your blood results mean.
So like I used it myself.
We also got a test for my mother-in-law to use and she lives in Mississippi.
So, you know, and it's, it's pretty much, I think it's pretty much everywhere now.
So I really like them.
And obviously you can go to your physician, your healthcare, your primary healthcare provider, but they might not measure everything that you want.
But the nutrition thing, I think it's making its way into medicine.
And that's part of the reason why people like Offit, who is an MD, you know, these people, they've been trained very differently.
They haven't been trained in understanding preventative medicine, understanding how these complex micronutrients are interacting with different proteins in our body and how that's important to prevent different diseases.
So they're not thinking about it from the same frame of mind as people like me that are PhD researchers or nutritionists and there's a variety of other, I guess, naturopathic doctors maybe have more.
Isn't homeopathic like that crazy thing where they like dilute things to like crazy amounts where you can't even there's like no active compound?
If you if you Google it or look at the Wikipedia of what is this hormonal sorry homeopathic if you they have their own measuring system too I think it's like they'll take a compound and they'll dilute it like a millionfold and it's like to the point where there's like no biological activity and they give it to people.
Homeopathy, this is on Wikipedia, lacks, this is all with references, lacks biological plausibility and the axioms of homeopathy have been refuted for some time.
The postulated mechanisms of action of homeopathic remedies are both scientifically implausible and not physically possible.
Although some clinical trials produce positive results, systematic reviews reveal that this is because of chance, flawed research methods, and reporting bias, which is pretty common.
So, no, getting back to my wisdom teeth, though, it's a kind of a cool topic.
I had to get them removed because they were like impacted and causing problems and pain and such.
So, I did some research.
I was like, God, if I have to get my teeth removed, there's got to be some kind of benefit from it.
And I found that our wisdom teeth have something called dental pulp stem cells in them.
And these dental pulp stem cells, so this stem cell research is like a whole, I'm really excited about the stem cell research field and where we're going with that.
But, anyways, our wisdom teeth have dental pulp stem cells in them that can actually form other tissues in our body, like bone, cartilage.
And they even showed recently they've taken dental pulp stem cells from people with impacted wisdom teeth, taken them out, and then transplanted them into mice that had damaged motor neurons.
And it was able to differentiate into damaged mode, like into neurons, neural type cells, and help replace that.
So I went and looked online to see if anyone was banking them because they do cord blood banking, where you can bank your cord blood.
And indeed, there was a company that's a couple of companies.
They're both associated with cord blood banks as well.
But they bank the dental pulp stem cells that you can, when you have your teeth removed, they send you a kit with like buffered saline solution.
Your oral surgeon will stick the teeth in them, and then they ship it off back to the company and they preserve it in liquid nitrogen.
They kind of do very minimal processing.
They don't actually remove the stem cells.
They keep it in the tissue, the dental pulp tissue, and they freeze it in liquid nitrogen so that you can later use it if you need it.
So it's actually really cool because you can use this if you have damaged cartilage, bone, possibly Parkinson's disease where you need to replace damaged motor neurons.
So I thought that was pretty cool.
It's like a benefit for because getting your wisdom teeth removed is not fun.
So you can, you know, your child is their tooth and you can bank it where you freeze it.
It's like $625 for the whole processing.
And then to store it, it's like $125 a year.
I personally think it's a great investment if you have kids and they are losing their teeth or also if you have your wisdom teeth and you have to get them removed.
The company that I went with, I can give it to you.
I actually talked to their cell biologist.
I was on the phone because I read through all the procedures in these scientific papers to see exactly how you process it in the optimal way and the best way to have the best viability after you thaw them.
And so I was like getting on the phone.
I'm like, okay, do you do this?
Do you do this?
And so I went with this company because I spoke with one of their cell biologists and they had done the things that I thought were the best.
So anyways, the whole stem cell field is cool.
Yeah, it's, you know, what's really cool is that they can take fibroblast cells from your skin, like skin cells that we slough off like every day, and they can add four different transcription factors, like four different genes that they can add by like a viral and add virus to them.
And they can reprogram them to become these pluripotent stem cells in your body, meaning they can form any type of cell in your body.
So you can take a skin cell and you can make it, you know, into a brain cell, a liver cell, a heart cell.
I mean, this has huge, huge implications for regenerative medicine, but I think also just for extending lifespan.
Because I've seen other studies that were not super recent, but what they did was they took like bone marrow cells, they did a bone marrow transplant and took, which obviously bone marrow forms are blood cells, from young mice and transplanted them to old mice, and the mice like lived longer.
So they took the blood of young mice, they injected it into old mice, and they had tremendous benefits, including regenerating different cells, brain cells, tissue cells.
I mean, this is stuff I'm really excited about now is this, you know, the stem cell research and reprogramming.
You know, the epigenetics is a really cool part where you can reprogram your cells to basically be younger.
You know, they're finding now that, so epigenetics, I think we talked about this a bit last time, refers to changes in gene expression.
And, you know, things like methyl groups and acetylation groups will sit on top of your DNA and turn genes on and off.
But now what they're finding is they're trying to look at patterns of methylation like in your DNA.
So they've already solved the Human Genome Project where they know genes.
And now they're trying to look at the methylome, the human methylome.
And they've been able to, over the past few years, they've been able to identify that there's patterns of methylation in your genes that happen with age.
And they've even been able to systematically identify, so they've taken blood from people various ages, like from 19 to 101, and they've been able to identify the age of the person, the chronological age of the person, based on their methylation patterns, like with 96% accuracy.
And they've been able to do this within four years.
I think they'll be four years off, you know, plus or minus four years.
So they can take someone's blood cells, look at their methylation pattern, and say, you're 50 years old.
And the person will be between 50 and 54 or 46 and 50.
So I think that's pretty freaking amazing.
And the thing that's really cool, I'm on this kick, this epigenetics kick, where they've been able to now also look at the cancer cells.
Like in a person, they'll take a tissue, a tumor sample, and then a tissue from the same person, another non-tumor tissue, and they'll look at the methylation pattern.
And they'll see that the cancer of the tumor tissue ages by like 40% based on the methylation pattern.
Wow.
And yeah, so it's like the cancer cells aging rapidly.
So what's really interesting is now they're looking at what genes these are, what genes these methylation patterns are happening around.
And they're finding it's like DNA repair, mitochondrial metabolism, antioxidant genes, like everything we've been talking about in this whole podcast, things that affect DNA damage and metabolism, all these things.
Methylation patterns are happening clustered around these genes.
And the cool thing about it to me is that if we're figuring this out, then we can figure out how to reprogram our cells to be young and extend lifespan.
And I really think that we're getting close to doing this.
So, I mean, if you think about, I'll give you an example, like stem cells.
Stem cells also have methylation patterns that are very distinct to stem cells.
And there's certain genes that are, when a gene is methylated, it's not being expressed.
There are certain genes that are not expressed in stem cells for a reason, because when they get expressed, they cause the cell to stop dividing.
And you don't want your stem cell to stop dividing because stem cells are what's repopulating the tissue.
And they found that like a certain gene is methylated in young people.
So when we're young, our stem cells have, you know, this gene's methylated.
But as we get older, the gene, the methylation goes away.
So there's enzymes that actually are called demethylases that take off the methyl groups.
And this gene becomes active.
And then the stem cell stops dividing.
It's like you lose.
You're basically losing your stem cell.
And then, you know, more stem cells you lose, the worse off you are.
You can't replenish your damaged tissue and all that.
But what they found was that the thing that activates that thing that takes off the methyl group is something called NF-kappa-B, which is an inflammatory.
That thing is activated by inflammation.
NF-kappa-B, inflammation activates NF-kappa-B, and then it activates this whole pathway of demethylases that take off methyl groups.
So what I'm thinking is that inflammation is a chronic signal.
It's a way that I've been able to link environment and the way, when I say environment, I just mean like damage, constant accumulation of tissue damage, the DNA damage I was talking about, environment to epigenetics.
So it's like you have a chronic signal of inflammation.
It's activating these demethylases.
They're taking methyl groups off of DNA.
And now you're expressing genes that are usually not expressed when we're young in stem cells that stops the stem cell from dividing.
So it's like a really cool link between environment and epigenetics as it relates to aging, which we know that environment regulates epigenetics.
So to me, it's kind of cool because as we're figuring out these programs, what that means is I think that we'll be able to reprogram our cells to become young.
I think that we're getting really close with that.
I mean, if you look at, like I said, with the stem cell research that we're doing now, where we can even take renal epithelial cells that we excrete in our urine and make it into a pluripotent stem cell.
We can make it become a cell in our liver.
So I think with the advances we're making with that, in combination with this learning, figuring out the human epigenome, where we're looking at methylation patterns and figuring out what's happening with age, I think we're going to make huge strides in the next decade.
I mean, hopefully if research, if funding doesn't go down, it's been going down the drain.
It would seem like, boy, if there's something to be made where there's money to be made, funding anti-aging research seems like, God, that's the way to go.
This mice thing is so fascinating because they show that after four weeks, stem cells in both the areas of the muscle and the brain got a boost of activity and were better able to produce neurons and muscle tissue.
And then they also discovered that injecting the old mice, or rather the young mice, with old blood was a huge setback.
It was a huge setback when conjoined to an older mouse, so the, you know, bringing the old blood into the new mouse, the creation of new cells in the young mouse slowed, and old blood seemed to cause premature aging.
I think a lot of it comes down to, you know, like I said, there's these, if you look at the epigenome, the methylation patterns in these stem cells, these young stem cells, even young cells in general, they're very different from old ones.
And that affects the way, I mean, if you're looking at epigenetics, you're talking about regulating a whole host of genes, like hundreds of different genes.
And so if these things are being differentially regulated when you're young versus old, then taking someone's young blood and transplanting into the old old transplantee would make sense because now you're basically taking all those patterns that we've been able to identify and gene expression things are now going back to young.
So it's like now you're not expressing genes that are causing your stem cells to senesce.
You're not expressing, you're expressing more things that are involved in DNA repair and things like that.
Well, although it is difficult to get funding, there are so many different, yeah, artificial blood.
Wow.
Patient ready.
This is from the-scientist.com.
And it's saying that, wow, this is incredible.
In the midst of news that engineered organs are being implanted into animals and people, researchers announced the creation of artificial blood for transplant.
This is very recent, too, April 16th.
It's nuts.
We live in strange times when it comes to these things.
Like every day or so, it seems like some new study from somewhere in the world is popping up that shows this incredible breakthrough.
The young mice study, this study, the artificial blood study.
If they can engineer some sort of a super potent blood and introduce it into your body, I mean, it's similar to like what the cyclists did when they were blood doping.
They would take their own blood, pull it out, inject it back into their body so they had more blood or EPO, which stimulated red blood cell production.
That kind of stuff is just, it's so trippy, the idea of sort of hacking and retweaking the components of the human body.
I mean, I know when I first, when I first got into the biological sciences, so I was a chemistry major in college.
I did research using these nematode worms, C. elegan worms, that have like a 14 or 15 day lifespan.
And they have a lot of the same genes that we have, but I could like inactivate one of their genes and literally double their lifespan.
So they went from living like 14 or 15 days to like 30 days.
And so this was, and actually it was, you inactivate insulin growth signaling, insulin growth factor.
And what happens is this growth factor then usually when it's active, it keeps this FOXO gene, which is a transcription factor, outside of the nucleus and doesn't allow it to perform all the functions it usually performs, which is involved in a bunch of stress resistance, like hundreds and hundreds of genes.
And so when you get rid of that IGF-1 signaling in the worms, FOXO gets activated and all those genes involved in stress resistance get activated and the worms live twice as long.
So it's like literally a genetic program in these worms that's controlling the way they age.
So when I first I remember that hit me, it was kind of like, holy crap, like that's pretty cool.
It's just such an amazing time with all this stuff because it seems like we're around at just the right time to catch this just incredible percolating of all these new studies and all these new things that are being developed.
It's just such a strange time to like try to pay attention to all of it and watch it all happen.
It's so exciting.
It must be really exciting for you because this is like your field of study.
Well, I feel like I'm happier now than I was when I was younger.
I'm smarter.
I understand stress better.
I understand all sorts of emotions.
I understand management, management of my body, of my hormones, management of my feelings, management of my energy levels, stress, relaxation techniques, stretching, yoga, all that different stuff.
I feel like I'm just way happier.
It's that old expression, youth is wasted on the young.
I understand life better.
I'm better at it now.
I'm better at being me.
It was like it was an awkward thing when I was younger.
And, you know, you might get to a point if you're 200 years old, you might abandon science totally and just fucking go down some totally different road.
My neighborhood came really close two times to giant fires.
I mean, we have fires that are so bad out here.
One time while we were doing it, and this was the time I got evacuated, I was filming Fear Factor and I drove from Los Angeles to Tojone Ranch.
To Hone Ranch is about an hour and a half outside of LA.
And as I was driving near Simi Valley, which is about 40 minutes from here, Simi Valley is where the fire kicked in.
And then from there, for the next 50 minutes of driving, there was no fire.
Well, when I got to work, we started filming.
We were doing the show.
And then when we were done and we left, the fire had reached us.
So the fire had reached, you know, an hour of driving.
So we were talking about, you know, somewhere around 60 plus miles.
And the entire right side of the road was like a Lord of the Rings movie.
It was like I was expecting a demon to ride a flaming horse.
It was insane.
For an hour, an hour of driving, all you saw to the right side of you was flames.
It was amazing.
The only thing that separated it was the highway.
And flames were jumping the highway.
And they had tried to keep the fire as far away from the roads and far away from structures, but it was so out of control that it traveled 50 miles plus in a few hours.
I mean, in a place like this, like LA or San Diego, where there's a lot of dry, you know, brush and like what kind of mechanisms do they have to, I mean, they obviously know this can be a serious problem.
Is there any sort of like there's not much they can do?
I mean, they try to stop it, they create fire breaks, they drop repellents on it, they drop this red stuff that's uh that that squashes the fire like in certain areas, but the this fire leaps.
The problem is these things cross highways, the embers fly through the air, they land on dry brush, and poof, they're off to the races.
Um, it's Found My Fitness, and it was just released like early this week.
And it's basically you can get my podcast where I talk about my information.
And also, I have a news section where I give news stories, and it's a community section.
If you ever used Reddit or Hacker News, it's based on that.
So, it's like that.
Yeah, it's trying to make an interactive community.
So, if you download my podcast, it would be really cool.
Right now, it's new, so it counts as twice the download.
Beautiful.
And also, foundmyfitness.com is where you can follow me.
I've got a bunch of gadgets on there you can click to download my newsletter, follow me on Twitter.
I also have a Patreon campaign where I'm trying to do these podcasts, and I have a couple of milestones where I'm trying to do one, you know, two, two podcasts a month or four.
So, I'm asking people to donate, or not, it's not really donate to pledge 25 cents a month to help me reach my milestone so that I can help give you the context that you need and the mechanisms for how science and health and nutrition and all these things are interacting.