Dr. Dean: Health & Steroids - Avoiding Death to Sleep to Hair Restoration

Dr.

Dean Saint-Mart, renowned for his knowledge of bodybuilding pharmacology, PhD in synthetic chemistry, and product formulator for supplement needs.

He is a renowned pharmacologist for his no-nonsense approach and open-ended transparency in regards to bodybuilding and the dangers associated.

Yeah, I only have actually like 1500 tabs up right now.

It's very typical for me though.

If I was to show you a picture of what my office looks like now, between

the last podcast I've done,

I ran into issues on podcasts after where my battery would die on the camera, so I had to invest in like a dummy battery.

So now I've got a cable running out of

camera into a power bank.

I've got a

fan on the camera.

You've got a nice new Shur mic because people are

complaining over the sound quality of what podcasts I'm doing.

So

I may as well pay back if people are going to watch, let them have some good audio quality.

This is a massive upgrade.

And we've got the hair, too.

Now, that's pretty cool.

You've got everything.

Yeah, the hair is back in full swing.

I think

I was in that.

I mean, I don't know what we're going to talk about today, but probably hair is going to be probably one of them considering my hair has sprouted out over the last four months.

I was in that ugly duckling stage post-transplant when we done the first podcast where you've got all this fluffy hair that's not even grown properly.

No, I get it.

Well, I mean, I don't get it yet, but I'm going to get it for sure.

I'm going to get it in December, actually.

Oh, wow.

Where are you going to go get it done?

Well, I'm hoping that you can sway my decision, but I am currently going to

now hair time.

Typical for a bodybuilder, right?

Following along, just following along, C-bums.

I'm glad to hear about the transplant going well.

I think it looks better than Ian's already.

Well, I mean, when you look at their

Chris's and Ian's,

I guess, when you look at what's available hair transplant-wise in

Turkey, you've got lots of clinics.

And to be honest, medical tourism is a big thing that's becoming very popular out there.

Like when you fly into Istanbul, whether it's the international airport, there's two airports.

The more like international based one is a little bit further out from, I think it's Sao.

Saw is the code.

I can never say the name of the other airport, but that is closer to their clinic.

When you go into the actual international airport, the amount of people walking around with bandages on their heads, bandages on their noses,

you know, swollen mouths from teeth procedures, it's huge.

Medical tourism out there is huge.

When you look at the clinics available, there's quite a lot of prestigious clinics available.

And now Hairtime obviously have been doing it a long time and they've got a lot of experienced doctors.

I guess what I was very impressed with like from my own personal experience is the time that they take to go through your consultation with you.

So when you go when you arrive at the clinic on the morning of your transplant

They basically ask you what's your expectations of the new hairline like what do you expect them to do surrounding

the shape of it, the alignment of it?

You can only have your hair transplanted to just above your forehead muscles.

So, they sort of check where they can go in terms of depth.

So, you're probably never able to go as low as it was when you were younger, but you can go pretty close to where it is now naturally and then develop the hairline from there.

Interesting.

And that's why I brought my wife with me because you get guys who will just allow them to create any hairline once the hair is put in their head.

But when it starts growing, you want it to grow in a natural pattern to your own hair hairline as it existed.

So

they spent about 20, 25 minutes making sure I was happy with the hairline.

They give you a rough outline: like, we're going to fill in here, we're going to fill in here.

We're going to do,

you've got two options: you've got FUE and DHI.

So FUE is the procedure that they do to implant the hair into a new hairline, to create a new hairline?

So they put the hair into an old follicle, and the hair then grows in that follicle.

And then they have DHI, which they use for density, where they basically just punch the hair into a follicle to create density on the top of your heads.

So they discussed with me, they said the hair on the crown area was thinning,

that they could do the crown area, but the failure rate is quite high.

And when you look at negative reviews of hair transplants, it's always generally surrounding the crown area.

The crown area.

And they make you aware of this because

the follicles within the crown region, if they do DHI to put a hair into that hair follicle to create density again,

there's a risk that you'll kill the follicle, you'll kill the hair that's already there or the thinning hair that's there, and the transplanted hair might die as well.

So now you've lost a donor hair and you've lost a hair in the crown region, and you've just sped up your balling process.

So, I mean, when you look at what causes hair loss or hair thinning, it's normally looking at oxidative stress, like what we covered in the first podcast, like enough antioxidants, enough blood flow going to the scalp, enough nutrients.

It'd be like anything.

If you didn't get enough nutrients to your muscle tissue, the muscle would shrink and eventually atrophy.

Your hair follicle is the exact same.

If it doesn't really receive enough nutrients, it's going to effectively shrink or minatrize.

And then you have all the other hormone things on top of it, like DHT, miniatrizing the follicle, causing local inflammation, an immune response.

Like when we're looking at hair loss, most guys jump and go, it's DHT, it's drugs, it's a high androgen level.

That's one part of the puzzle.

Like the bigger part is low estrogen.

So estrogen encourages blood flow to the scalp.

So you have to have a healthy estrogen metabolism for healthy hair.

And if you sort of look at a pre-contest setting, you're doing stuff that pulls your hair in reverse and lowers your estrogen.

And then you've got thyroid hormone imbalances.

So I think personally, looking back as my hair started to genetically recede in like my early 20s, when I got to my late 20s, when my celiac disease started to develop, or I think that's when it started to develop, you can sort of see in photos from when I got married into like my early mid-30s, where my hair was just slowly dying and moving back.

That

once the follicle is dead, to speak, you're not stimulating the hair to grow again.

So,

what I wish I knew, or I guess in hindsight, I wish I was a little more, less carefree with my hair that I paid attention to a little bit more because it was only when I see my hair, I think it was like 32 or 33, I seen a photo of myself.

And I was like, what's happened?

My hair used to be really thick and dense.

Started doing stuff like topicals for my hair growth.

Start paying attention to obviously how you nourish the hair follicle, derma rolling, microneedling, all these things that guys go down the rabbit hole of doing.

And I got really good density back, but the two receding spots on the side of my scalp were the damage was done basically through not getting that hair back.

And it was just weighing up: well, how long do I wait to see out that recession?

And so I gave it like four years until I was 37, well, 36 when I went for the transplant.

And at that point, like I said last year, with shaving my head before the shows,

you could see where the hair had receded back quite a bit.

When you start shaving your head and you look at actually where the hair follicles are dead, that bald spot in your head, you see how much you've actually lost.

Um,

so with like the transplant, they they create the hairline, they go through all these things, like they tell you about

whilst your crown area is thinning, it'll probably regrow with monoxidil and finastroid topically after the transplant.

So, they thought that did they have a really good um

i guess cosmetic doctor who looked at my hair even with the shaved head and said i can see that there's a thinning in the area but i don't think it needs a transplant that medication will fix that problem

and i i guess when you look at guys especially when i had a bald head you can see scalp thickening when guys have ridges in their scalp that's scalp thickening it's collagen deposition.

So that really like brainy looking shape to your scalp when you have all the ridges in in your hair with a shaved head,

that's impeding blood flow to your scalp, so it's creating,

I guess, laxity to the hair follicles.

So, one of the other suggested theories of hair loss is actually loss of scalp tension, and that's where you'll get people with like scalp massages,

even as far as there's some,

I guess, treatments that recommend Botox into your scalp as a method of helping with scalp tightening.

But

that was all argued back in like the 1950s, 1960s.

They argued backwards and forwards for about 40 years, they discredited that scalp tightening theory.

And it seems to be making the rounds again in terms of the research might not have been fully correct in dismissing it.

And that there might be something to look for there with supporting hair growth.

So when they do the hairline, they go through all the risks and everything else.

The hair extraction, you're lying face down.

The most painful part, I've spoken about this before, and other people asked,

it's not painful other than the local anesthetics.

So,

when you're getting the local anesthetic into the back of your head and into your forehead for the transplant procedure, they're about a seven or eight out of ten, but it's for about five minutes.

So if you can distract yourself, like have a good pain threshold, keep your mind occupied.

It's literally you feel the pain and then you don't feel the pain.

So it's a really sharp sting and then nothing, a really sharp sting and then nothing.

If you can sort of just put your mind, keep your eyes closed, keep your mind occupied before you know it, it's over with.

The hair extraction is fine because you're like on a massage bed sort of setup.

So you're lying face down.

You can potentially nap.

But then the transplant procedure is sitting in like an incline chair, and that's when you probably have to pay attention to staying very still because they're obviously transplanting hairs into that hair follicle with such accuracy that you're sort of afraid to even move.

But towards the end of it, my transplant procedure took, I think, just over three hours.

Towards the end of it, you're getting a bit like, I want to get out of here.

I've had enough of lying about because

they're working pretty much in silence.

The two

the surgeon has an assistant to him.

He's basically just working in silence, talking to his assistants throughout the procedure.

And you obviously have your eyes closed, and you've got a sheet over your face to protect you from the light that's shining on you.

You just sort of like you're just left with your own thoughts for about three hours.

That by the end of it, you're like, I just want to get out of here.

Like, people sort of, I've seen other people speak of other clinics that perhaps have you watch TV or other ones, but these guys pay so close attention to what they're doing

that they obviously can't afford to make any mistakes when they're dealing with something so delicate.

The recovery process, I mean, aside from the pain of the local anesthetic,

that's probably the

hardest part is the first three days or the first three nights because you have to sleep upright.

so you basically sit upright to go asleep you can't lie down you can't bend forward there's a lot of restrictions for the first couple of days and once you get past once you get past I think day seven you can lie on your back then but you still have to sleep with a neck pillow around your neck so the first 10 days are a bit

iffy that you can't touch your scalp, you can't bump your scalp, you can't rub your head.

And if anyone who's listening has had a hair transplant, it'll probably like a test to the itchiness that comes with your scalp, where you just literally want to rub your head, but you can't.

So the itch as the wounds are healing, obviously, you get all the scabbing on your head, and you wash the scabbing off.

That's probably the hardest part to navigate is

getting through that first 10 days.

And after that, then it's just patience.

And then eventually, hopefully, end up with a set of hair after about four or or five months.

And then you look as pretty as Dakie Dean.

You reverse time by about three or four years.

I'm excited.

I'm glad that you said that

they consult with you for a while on how you want your hairline because I'm going to be real, I have seen some hairlines that, and I think this is a shared opinion amongst most people that like view a lot of these like reels or clips of the hair happening, but that just don't look supernatural because sometimes they're just a straight line.

Yeah, that's it.

I think that was my biggest worry, to be honest.

And like, bring your partner with you to get her opinion.

Like, that's why I brought my wife.

I wanted to make sure that what they drew looked realistic to her.

That when it did start to grow out, it looked as I did when I met her in my 20s.

So she's very happy with the result, obviously.

She has

non-bond.

Yeah, and I'm very happy too.

It's like I said, it's very, very natural.

And

there's still actually,

you can't really see it when I even show on social media.

There's still little miniature hairs sprouting in this region that that's only going to get even more dense over the next four to five months.

I'm told.

So, we're really only at the halfway point of how you assess the results.

Wow, that's awesome for halfway point.

Um, obviously, the hardest thing then is navigating after the transplant in terms of keeping the hair that you've transplanted in.

So,

like, they will advise that you avoid any type of hormone replacement post-transplant for four weeks.

If you are prescribed under your doctor, consult with the doctor, obviously, around potential hormones that you might be using.

And then,

after the four-week healing periods, you're allowed to resume your normal medication if it's prescribed.

But they cover basically all the like what-if scenarios.

You have a translator who's available at all stages of the journey to speak.

So

the surgeons do speak Turkish, but you have a very good English interpreter who will tell you what they're saying to you, and you can explain back

what questions you may have or what concerns you have.

Even throughout the the surgery, you have the interpreter coming in out of the room asking you like, is everything okay?

Have you got any questions?

You know, is there anything you want to know about during the surgery?

Which is, which is always a positive thing that they're checking up on you.

And then the aftercare, I mean, every month they've checked in asking for, you know,

a WhatsApp.

Do you have an advisor on WhatsApp who follows up with you every month?

Like, you're now one month post-transplant.

Can you send photos for the consultants to review, please?

And they've done that pretty much now.

We're into this is month five.

So, for the last four months, basically, pretty much bang on Thursday when it falls to the new month.

I get a WhatsApp saying, please send the photos.

And the consultants will assess, you know, how your treatment or how your recovery is going.

But I think as the next sort of few months rolls on, it's probably just going to be more formality than anything really going wrong.

Right.

So, I guess regarding monoxidal and finasteride, is that something that they

like to implement afterwards?

Yes.

I know you were mentioning the crown area specifically, but.

Yeah, so they give you obviously a

post-operative care,

I guess, treatment plan, if you want to put it that way.

So they'll give you like a Medicaid shampoo that's to be used for four to five months.

They give you various different

probably the best way to describe it, like nourishing oils that would be like olive oil based with vitamin E and all these other nice extracts for to help nourish the hair.

But then they do obviously recommend that you either use oral finasteride or jutastero or topical, depending on your preference, and to use it in conjunction with monoxidil.

There's, I guess, in recent times, we've seen a lot of

content around like post-finasteroid syndrome or

potential issues that can arise with finasteroid use, which is completely warranted, like it is documented, that it's not something that is like

psychosomatic, that's in their head, that they think that there's these problems.

We can see in guys who develop these dysfunctions

issues in their blood work, or if they do a dry urine test for hormones, a Dutch test,

you see changes in their estrogen or their DHD metabolism.

So,

when we look at what potentially could happen with the use of these things,

it can fall down to a couple of different points.

When you inhibit the 5-alpha-reductase enzyme,

depending on what you do with that enzyme in terms of inhibiting it, the 5-alpha-reductase enzyme and the aromatase enzyme rely on NAD energetics.

So, everyone's heard about NAD.

So, in order for those enzymes to work properly, they require NAD to facilitate the enzyme doing its job.

So, when we see issues with post-fenastride syndrome, potentially the enzyme has been stopped from working functionally.

So, in theory, we have blocked that enzyme from working with a drug.

And then, when we start to reinitiate the drug or reinitiate the natural process of the enzyme working again,

there might not be enough energy substrates available for the enzyme to work properly again.

What you'll often see with guys who have potential issues with post-fenastoid syndrome, that there could be issues surrounding their mitochondria, with their NAD, with their overall cellular energy metabolism.

That

it's never

a case to say that it's in their head or that it's a neurotransmitter imbalance to speak.

I always go back to like step one: where do the neurotransmitters get created?

Where's the energy for cellular metabolism created?

You go straight back to the mitochondria.

So, for guys who are listening and they have potential PFS,

start from step one with the mitochondria: they're the guys that make your neurotransmitters, they're the guys that make your sex hormones, like testosterone that then leaves to convert with DHT and 5-alpha reductase or creates estrogen and aromatase.

So, in that instance, you then have to look at

where is your cellular energy potentially being diverted to in your body?

Is it to facilitate your body staying alive versus fueling this enzyme to do the hormone conversions?

I mean, you start thinking like that in terms of if there is an energy imbalance, what's your body going to preferentially use NAD for?

To fuel ATP, to make your energy, or to fuel an enzyme that makes DHT, that in theory, if you're making testosterone in your mitochondria,

your

body, to speak, is being fulfilled from a sex hormone perspective, although it doesn't have the same binding affinity as DHT.

it's not going to put as much importance over cellular energy production.

So guys then can pay attention to perhaps what is limiting NAD from being made in their body.

How is their overall carbohydrate or glucose oxidation operating?

How are the oxidizing fatty acids?

In theory, they might see some benefit from NAD supplementation.

But the problem is when you give the body NAD,

you're putting all this substrate in and then you're hoping that the body is able to recycle that substrate properly.

And when you look at, without getting into all the boring biochemistry, when you use NAD up,

you've got other things that have to feed in to get it to recycle back to NADH to fuel NAD plus again.

Things like vitamin B1, vitamin B2, vitamin B3.

Like looking at the bigger picture, that an IV drip of NAD might help you feel better for a few hours.

and that actually might make you feel worse if you don't have those underlying things supporting the energetics of what recycles the NAD.

So, right.

So, like a vitamin B complex in the morning or something, like say that you're injecting NAD plus with taking that supplement, would you find that beneficial?

With NAD plus, I mean, a little goes a long way, whether that is with NAD plus straight up as an injection form or an IV,

whether that's through

nictonamide riboside, Nor or nicotine

mononucleotide, NMN,

you're basically just giving the body

a convertive source of NAD.

So, when you're doing this, you have to think: if I put this in, what else needs support around it?

And with the mitochondria, you've got the complexes of the electron transport chain, and each complex uses a different substrate, basically.

So if you push a lot of NAD in for the first complex to work, the other guys have to pick up, and that's where feeding in obviously the B vitamins.

More so

riboflavin, which is B2,

which is what you use for FAD synthesis, which is another complemental type of donor-like NAD.

And obviously, vitamin B3, niacin, is what eventually converts to NAD in the body.

The vitamin B1 is more for helping with carbohydrate metabolism, so thiamine.

It's very important for our body to utilize sugars for energy.

So, an activated B complex would be a useful thing to consider.

But, bear in mind that if you're using an activated B complex and you're putting in a lot of folate, metal B12, peridoxin 5-phosphate, everything else that's in the methylated B vitamin or the activated B complex is feeding into other things as well.

So

this is where, like, taking supplements gets

can get complicated.

Where someone takes a supplement and expects it to work in a certain way and has a completely different effect.

Like,

if someone has issues with methylated B vitamins, and we see that carry over to methylation and potentially clearing out neurotransmitters too fast or slowing down their neurotransmitters being cleared, you're going to see symptoms like maybe overstimulation or the other side being very anxious and they're expecting this methylated B complex just to give them energy.

Someone told me B complex is great for energy.

I'm going to take it as a supplement.

That you have to really think about when I put this into my body, what effect is it going to have downstream?

Gotcha.

It's food for thought when you think about like taking different supplements, expecting one thing.

Like someone takes a B complex, expecting it, even general population, you know, people are led to think that B complexes are all about improving cellular metabolism, which they are, of course.

But then the other impacts, like what we discussed on the first podcast about vitamin B6 and dopamine conversion and serotonin conversion.

These are other things that are outside the energy metabolism that someone takes these products and then they experience these side effects without ever being told that these could be a side effect.

Yeah.

This is another reason that I think is just so valuable for a lot of people to, I think, dip into this space and listen to

figures like you because it just shows how much biology, neuroscience, just even steroid use and bodybuilding everything all of it is so into individualistic um but uh when you like zoom out and um look at the general population i think

there tends to be a very easy generalization of a lot of things you know yep such as all men are misogynistic

just a lot of different things just a lot of generalizations all the time

But

yeah,

I guess the good thing, though, about the finasteroid, post-fenasteroid syndrome, though, is that only maybe like 0.3% or so of the population that does end up actually having that

significant thing.

It's a very small percentage, but like anything, there's always going to be risks with any medication that's used.

And

that's where when someone chooses to take a medication on, obviously, the advice of their general practitioner, their conventional doctor, or whoever, healthcare practitioner,

that

they understand that whilst medicines can have positive effects, they can have most definitely negative effects.

And

it tends to be when the negative effect gets blown out of proportion at people and see a fear to a medication.

And then it's sort of maybe potentially sidelined when

if we then do like the sort of molecular biology approach, we can figure out why that dysfunction has happened.

But the problem then is most conventional doctors unfortunately don't have the time to delve into a complex issue like mitochondria energetics or enzyme dysfunctions.

When someone presents with these side effects, it can almost leave them thinking, well, maybe that person's just depressed, or maybe they're overly anxious, or maybe they're overly stressed.

That's why they have no libido or no drive.

That it's got nothing to do with a lack of

enzyme kinetics or the mitochondria or everything else, all the nitty-gritty stuff.

And that's where, unfortunately, in the past, guys were probably told it was in their head until enough guys start speaking out and people start to actually think about potential solutions on how we can address it.

And I mean,

five-alpha-reductase inhibitors are only one piece of them.

I mean, I see this with aromatase inhibitors, where the aromatase enzyme becomes dysfunctional from an energy perspective after using chronic dosages of AIs.

And again, that's not to say that every person is going to develop this, which would be incorrect.

But again, that is something in terms of the enzyme's machinery.

If there is a lack of energy being contributed to the enzyme, it's not going to work as efficiently as it should.

And I've seen it with roacutane, where roacutane has acted as an inhibitor of 5-alpha reductase, similar to finastroids, leading to symptoms of post-fenastroid syndrome.

And you see guys talk about post-roacutane syndrome.

But again, doing a level of groundwork, investigative work, looking at

organic acid testing, the Dutch test, looking at all these functional tests that might give us an insight into how the body's creating and using energy, you can potentially get an answer there to figure out how well, how can I fix the problem that has occurred from using this medicine.

I wouldn't say it's something that you take and you're doomed and gloomed forever.

It's just something that takes a bit of time to figure out where the actual root cause is lying.

And the other side of it, I guess, to be a bit fair on it is to not let it play into your psychology.

Because if it does start to play into your psychology, we know the power of the placebo that your mind is very powerful at what it can perceive and create in our environment that you don't want that to be compounded as a problem on top right right and then add on top of that that after your transplant you have to have four weeks off of all substances that's

and training put that in

put that in the grave i mean

it was one of the most epic rebounds and i started training again obviously muscle memory and going back to a more optimized hormone environment, still being physiological, but more optimized.

The rebound to speak of regaining your physique back from the dead and regaining your strength.

And I guess, I mean, during the four weeks off from training, I lined up a lot of different projects that I just buried myself into.

So

if you can't train, if you've got a surgery and you can't train or something has hindered it, find an outlet where you can invest the time that you would have spent training into something that maybe you've been putting off.

We wrote a scientific paper, me and two other guys,

Dr.

Guillermo and Dr.

Lucas, for the Strength and Conditioning Journal.

We wrote a paper together on that, and that took a good chunk of my time to write.

When you've got an anticipated downtime, I guess that's why I put off obviously getting the transplant done until I was very, very certain I was not going back to competitive bodybuilding.

That to me, that

ship had sailed and that sort of

draw to go back to doing anything like that ever again was completely finished.

Well, you know, someone else who told me that same thing about the rebound was Terrence Ruffin.

Because he just got his transplant this last winter, too.

And he had to take a good, I can't remember, I think it was at least four weeks off of training, maybe extended to six or so.

But

he had this really cool story where he actually finally exceeded.

There was like a weight cap that he couldn't get past, dropped back down to weight after he jumped off of everything, stopped training, obviously deflated right after.

He rebounded so well that he literally surpassed that weight that he couldn't pass by like almost 12 pounds or something like that.

So, I mean, and now he's got first place at the New York Pro and the Pittsburgh Pro.

So, yeah, that was an incredible package.

I've been a longtime fan of Terrence.

Very, very nice, just complete structure.

So, hopefully, he does very well this year at the Olympia.

Yeah, I'm really, I'm really happy for him and proud of him.

And maybe he'll listen to this podcast too because I know he's listened to you before, at least.

Yeah, I've spoken to Terrence a few times.

I mean, one of my first coaches years and years ago was Matt Porter.

So,

we shared that experience.

Obviously, he was Matt's client as well.

I guess with

that break from training,

it's very difficult to say exactly what happens, but we know from an epigenetic perspective that

with how androgens influence your genes, and we touched on this again in the last podcast,

your genes don't necessarily just revert back to how they were prior to using anything.

So the epigenetic control of the muscle in terms of the muscle memory is still there.

That when it's stimulated again, when the androgen receptor of the muscle is stimulated again, you have all these, I guess, favorable processes happening for the muscle protein to start growing again or growing back to the size that it occupied before.

So you don't lose the satellite cells to speak.

It's always like that argument with naturals that have used stuff, and then they put this sort of seven-year ban where you can't compete as a natural athlete, having used anything that you still have the potential for to grow that muscle mass.

It might not be as much as when you're on, but it's still going to be at a higher advantage of someone who's never exceeded their genetic limits of where their natural andium receptor expression was held as a natural athlete.

And

that is something that sent me down like a rabbit hole with the book I'm writing.

That

if we know these things work epigenetically,

what's to say then that you're not going to start breeding athletes down the line?

In that you're passing your genetics on to your kids.

And so that epigenetic control,

you're effectively, if your epigenetics have been more favorable towards

muscle protein accretion or changing the fiber type of your muscles in terms of like the actin gene expression, everything else.

When you have a child, you're passing your genes to that child, but you're also passing your epigenetic tags.

So, if your genes are expressed in a certain way, you're passing that genetic expression to your child.

That's probably one way of explaining why you often see elite athletes follow familial patterns, the genetic, the epigenetic expressions being passed on hereditary,

that

you might have

a very good amateur-level bodybuilder, but never really gets to the level of being a professional, might aspire to, but might never get to that point.

And then they pass that genetics to their child, and the child becomes interested in bodybuilding.

You're in theory potentially giving that child a head start with that epigenetic influence.

Yeah.

And at the best case scenario, if you don't become bodybuilders, you might have actually influenced their natural ability as maybe a track and field athlete or a strength athlete and a strength sport or combat sport.

That

secretly you've influenced your progeny with your choices of what you've chosen to do with your body.

Wow, that is interesting.

That is awesome.

Have you seen Chris Asito's son?

No, I haven't.

No.

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You should, I'm trying to remember what his username is, but you should check him out.

He's a, I believe he's natural.

He's 19 years old.

He's a natural bodybuilder.

And for natural, his physique looks phenomenal.

So much that there is, of course, a couple comments

that are not believing that he's natural and discrediting it and stuff.

But I mean, if you look at his physique and all, like,

it's got that natural look to it.

Does that say really anything?

No, but I mean, considering Chris Asito and his stance,

right?

And he's at his prime.

I feel like you would have to be really calling both of them liars when

you know, it's just, yeah, I mean, and then

there is potentially an example.

Um, but it's not uncommon.

You look at, again,

uh, sons of uh great historical bodybuilders like Lee LeBrad and Hunter,

Sergio, and Sergio Jr., that you have

this great example potentially of how the genetic line falls and then how that genetics

basically carries the next generation.

Because when you look at the physiques of the two children, it's surpassed what the parent has passed on.

Albeit, you know, we have advances in training, nutrition, supplements, whatever else.

It's a completely different physique, a much

more heavily muscled physique.

Which, obviously, there's other things to consider on top of, but it gives you food for thought that if you're just an amateur bodybuilder doing certain things with your genetics and then you have kids,

what advantage have you given your kids over other kids in the school whose parents might not have done certain things?

That

it would be interesting if you start having these ethical discussions on,

you know, your dad was a such and such a bodybuilder or whatever, strongman athlete, you're not allowed to compete because of your genes have been influenced.

Like, you start really questioning: well, what is natural?

You know, if you have a child of an enhanced person with potential genetic control,

is that child natural to speak because they've inherited your expressed genes?

And that just sent me down a rabbit hole when I was trying to figure out long-term what we're doing as a species, like as humans,

what we're doing in terms of expressing our genetics in certain ways and passing that down to our kids.

And then they're obviously passing those genes down to their kids.

Whilst we sort of look at like the £300 bodybuilder as being the like the pinnacle or the sort of cap of the human physique, like are we going to see someone on stage at £300 absolutely inside out shredded

as we continue going down in terms of that

progeny and you know, great-grandkids and everything else,

depending on what has been done with parents and the children, obviously, we could be heading towards like

superhumanism is a way of putting it.

And that

is obviously something that something like the enhanced games are very interested in is like creating a superior athlete with

all forms of enhancement.

Speaking of the enhanced games,

Chris Bell reached out to me in the DMs asking me, telling me that he thinks that I would have some valuable input for the enhanced games and would send them my way and referred to the doctors that I have on my show.

And I'm pretty sure that you're probably at the top of that list.

I was at the conference in December for the enhanced games where we

were very, very, very interesting discussion.

Um,

is it something that will go ahead?

I think so.

And obviously, there's an announcement tomorrow in Vegas surrounding the announcement of where the first games are going to be held.

Um,

whether it will go through to full fruition, I guess there's a few things that still need to be figured out.

Obviously, there's safety and health and ethics.

But one of the things that that really opened my mind during, it was basically a debate.

You got the 40 best doctors, scientists, pharmacologists, whatever into Oxford, Wit Aaron, and Dr.

Dan Turner.

That's where all you got all those super, super professional pictures.

Yeah.

And

basically got us into one room and debated all of our different backgrounds and what we considered, you know, appropriate, what we consider like things that should be cautioned or thought about.

And again, that was what I raised at one of the debates: was this whole thing about genetic influence?

Now, if you're a PD

using athlete

and you would then have a child and you've used these compounds, have you created

the next lineage of superior athletes from what you've used

without,

as crazy as it is, without the consent of that child coming into the world you've already enhanced their genetics

I mean stuff like

we were in a debate on internal versus external enhancements and

I remember going into it thinking

what what level of expertise can I add to this debate they had like four of us at the top of the room and then everyone else around the discussion table about external enhancements because I was trying to like think in my head what like what would I consider an external enhancement?

And all I could really think of was like,

as crazy as it sounds, stuff like AI technology, like

Neuralink or enhanced retina vision, you know, crazy things that seem far-fetched like science fiction, but will most likely become a reality.

That

other things like runners, we don't even think of runners as an enhancement, but you look at the top-level level

marathon runners, 100-meter sprinters, they all have specialized runners to like shave seconds after time, the clothes that they wear, wind sheets, whatever else.

That

when we're looking at like the future of enhancement,

it's not just compounds.

Like people think, oh, it's just take a load of steroids and throw a load of people onto a track and see who can throw the rock the furthest or whatever.

It's

like, how, how is we, how, as a species, how can we enhance the human life form to speak to have superior athleticism or superior dexterity?

Um,

you know,

you look at something like Olympic shooting, down the line once they say enhanced games don't have guys that have enhanced like optic nerves or contact lenses that basically tell you, you know, you're off aim by two degrees, readjust, and shoot.

So we think this is crazy, but

this is the sort of things that they want to see what we can do as a

human to surpass what was done in the past historically when there was like breaks put on athletic abilities.

So it's it's it's interesting.

It's not just see who can take the most trend and survive.

We already have that.

Yeah.

That,

I mean, when we went to myself, Vigorous Steve, Victoria Falkar, we were able to bring obviously a level of personal experience being within like the bodybuilding trenches and what practices go on.

And I mean, it's it's very interesting to see the other perspective because you had people from WADA, you had medical doctors, you had consultants, endocrinologists, that when we started getting into the discussion of things that are done just with bodybuilding, as an example,

it's so far removed from what they understand from research.

And I mean, one of my counter points during one of the debates was, how are you going to pick acceptable dosages?

I mean, one of the things that came up in the discussion was that

like, the athlete's decision is final.

Like, there's a whole chartered code of what we all agreed on, like the rules and ethics or conduct code.

That

I might not want to take 600 milligrams of TREN, but the guy beside me might not have any problem taking two grams.

Like, there,

but two grams could be an approved dose.

That

you, you have to figure out what is each person's accepted tolerance.

And for different people, I mean, if you want to win at all costs, then probably a lot of people say, give me as much as I can take.

Which is probably not the best way to approach it, but maximum tolerable dose.

Yeah, maximum tolerable dose.

But then you have to figure out, well,

your maximum tolerable dose from a psychological perspective or even physical perspective could be completely different to the guy beside you.

How do you standardize that?

How do you make it fair then?

Because you've removed one aspect of cheating,

but then it can become a free-for-all.

If it is standardized dosages,

where's the tolerance limit?

And then the other side to it was: well, we'll pick

studied dosages.

So, for example,

studied doses of testosterone have gone to like a thousand milligrams.

So, what we're going to approve a thousand milligrams is a safe dose for everyone, every male to use when

a thousand milligrams could have someone's total testosterone level from a UK measurement.

I'm not good with doing US off the top of my head, but it could be like 200 nanomole, which

probably to take a rough guess, maybe 4,500 nanogram.

You know, and you've got a guy who's

a genetically superior athlete that might have a total test level of a thousand, maybe.

You're allowing them to go up to 4,000, whatever,

without any second thought to what that's doing to our body

just because it's a studied dose.

You're right.

And

it's so difficult.

And

I can't

say how it's going to be done appropriately.

And I guess that's obviously why they've sought our expertise to try and guide the process.

It's very interesting though.

It's super interesting because I think I mean it just throws so many complexities because of course like you were saying the individualistic response per person but I think it also I mean I'm sure this is something you guys already discussed too but like tailoring tailoring the most optimal dose per athlete per sport, whatever they're competing in, like, you know, obviously going up to like a gram of testosterone is probably not going to be optimal anyways, for a majority of the type of sports that they're going to have at the Enhanced Games.

And,

you know, that's why we have like, I guess, bodybuilding and pro

and powerlifting, we already have a good many years of experience in separating out what types of gear and what types of doses that we're using per sport, you know.

But that's going to be a completely new field that's studied here for the enhanced games.

And I guess the difficulty there too is like

the long-term effects are the things that are going to be maybe a lot harder to dictate.

Yeah.

I mean, what I was fascinated by was the data collection that'll come from it.

You know, you have athletes who will

readily give their consent for everything to be tracked.

I mean, heart health, kidney health,

liver health, 3D diagnostics.

Basically,

when you view what it actually is, it's a giant human experiment to see how we can create

i guess protocols would be the best way to say it without calling like a like a pd stack or whatever a protocol a medical protocol that could optimize um general population health um

because when you look at the like

The core message I got from the conference, like if I was to take away from it personally,

to improve the human race as a whole, not just focusing on athletes.

The athletes are more so

the willing guinea pig to see what X, Y, and Z treatment does, what effect it has on,

again, motor control, neural health, strength, whatever, whatever we do in the sports.

And then, how can we make that research

accessible to the public to then

basically look at what effect it had in an athlete and then thinking, oh, I'd like to do that personally, or I can have that discussion with my medical doctor about a potential longevity treatment.

And that's pretty much the core message I got was: how can we start making people superhuman?

We're probably just at the tip of the iceberg as bodybuilders with creating muscle mass, and obviously, with strong men, uh,

I guess, weightlifting athletes,

we're really only touching the surface of then, what are the other things that can compound on top of it, um, as I guess, treatments, if you want to call them that.

Yeah,

it would be so interesting, too, to me, to, I mean, I guess this would help also expose just

a huge data pool of the genetic variants in responses to PDs.

You know, you'll be able to see people that really excel a lot at the use of PEDs and then people who probably don't really improve that much.

Yeah, I mean, whatever negative repercussions

you could look at, like you've seen in recent times, people go on about CAG repeats and the efficiency of the androgen

receptor binding to compounds.

We might end up seeing some level of data that they can delve a little bit further and see can they almost predict who the elite athletes are going to be when they're born,

if they have their genetic sequenced immediately.

And then

I guess long term to me,

when we touched on genetics the last podcast,

the thing about knowing your genetics is that it's not written in stone.

Like if you have genetics for heart disease, it doesn't necessarily mean that you're going to develop heart disease.

It means you are at risk.

But depending on how you live your life, your lifestyle, your nutrition, sure, if you have a genetic issue where you make more cholesterol naturally, yeah, it's probably not going to be something long-term that's going to benefit you of not having heart problems.

But it doesn't necessarily mean that you're doomed to have a heart problem.

And that's where I feel if we're able to sequence that elite athlete, not an elite athlete, elite athletes, that the bodybuilders that potentially might not have had amazing genetics, to speak, but then proved themselves with hard work, dedication, intelligent training, nutrition, some PD usage.

If it becomes that strict surrounding your genetics, dictate how you can become an athlete, it gets very, uh,

I guess, very

you're not being very inclusive, is probably the correct way of saying it.

You're pretty much writing someone off based on their genetics if they were screening everyone as an athlete.

So, I think you know, there's pros and cons, and quite often not knowing your genetics

can often be a good thing because it's a level of ignorance, it's bliss.

So, you're not worried about X, Y, and Z thing that's found in your genetic analysis.

I mean, right, right, from personal experience with my genetics, we touched on it again the last time.

My genetics show that I have Apo E2 and 4, which are basically Apo E is the lipoprotein that carries cholesterol into your brain.

So Apo E is associated with Alzheimer's disease and dementia and cognitive dysfunction.

And when you have two out of the four variants, you're at like 50 to 60% risk of developing Alzheimer's or neurodegeneration when you get older.

And this has occurred familiarly with grandparents.

But

when you look at what potentially can be done to offset neurodegeneration, what can offset that APOE carrying of cholesterol and fats into your brain and plaque formation,

just because you have that 50% risk, you don't go around living in your life worrying that, okay, when I'm 60, I'm going to have a a one in two chance of maybe having some form of neurodegeneration.

If you were to think that way all throughout your life,

you'd spend more time worrying than experiencing or enjoying life.

So, you're the genetics, when you do genetic testing,

they are right in saying that you have to have a level of emotional stability to

understand what's being said to you, but not sort of take it that it's written in stone.

Yeah.

Yeah.

I think that's always always super, super important.

But it can be hard in this field, especially when you're doing something risky like bodybuilding.

I mean, depending on who you are.

Absolutely.

Do you feel like

is there any like

do you know of any altering of uh epigenetics with neurology in the brain?

Um, say that someone jumped on PEDs

and then

you know, curious if that might ever, I guess,

control their offspring.

I guess in terms of genetics with neurodegeneration, neurodegeneration is a consequence of oxidative stress.

Again, we keep coming back to oxidative stress, but when we experience neurodegeneration, we've either

poisoned the nerve to speak with too much neurotransmitter, so you can have excitatoxicity, which is exciting the neuron too much, and the neuron just basically fizzles and doesn't know what to do.

And eventually you kill the nerve.

Can you say like living a lifestyle that's too dopaminergic over a long period of time be like one potential cause of that or is that something different?

I would say

more so probably from dopamine deficit symptoms, most definitely.

If we look at

I guess we'd have to split out what all the different neurotransmitters do in our brain.

So if we've got dopamine being the main like driven neurotransmitter, you've got acetylcholine as your main memory forming neurotransmitter.

And then you've got serotonin and norepinephrine.

Norepinephrine plays into your concentration.

So norepinephrine and acetylcholine sort of work hand in hand with one another.

Acetylcholine helps with

consolidating memories or helping with memory formation when we're trying to learn something.

And norepinephrine is what keeps you engaged to want to learn something.

And then one step back is dopamine, which is motivating you to want to learn something.

If we're looking at what potentially could happen with like PD usage with anabolic steroids,

in one instance, you could cause

an excessive amount of dopamine to be made in your brain.

You damage those dopamine neurons long term.

And that's where some of the rat studies show potentially that things things like 19 NORS are neuron toxic.

And that

although it's a case study or I guess a cohort analysis where they looked at,

as far as I remember, they were college level

PD users and looked at their memory,

I guess their subjective memory

prior to using PDs and after using PDs.

And the guys who used PDs and 90 NORs to speak showed deficits in their memory versus prior to using them.

That

would then tell us: well,

there has been some level of neuron loss or potential choline or acetylcholine deficiency forming where they're not able to form memories correctly or process or bring memories forward from their brain, which is obviously the neurons dying in regions of our brain where we store information.

That

I guess

would one PD of itself

or the group of them contribute to just one particular thing when it comes to neurodegeneration?

I don't think so.

I think it's sort of a global

insult to the brain, to speak, as opposed to just killing dopamine neurons, killing serotonin, killing acetylcholine.

You're basically just causing dysfunction in a group of neurons in a part of the brain, whether that nerve transmits dopamine or acetylcholine or serotonin, it's probably more so the area of the brain that's become damaged as opposed to the actual neurons and what information and neurons are transmitting.

You know, although certain parts of our brain obviously will influence different behaviors, you know, your amygdala controlling your emotions,

your hippocampal area with memories and where we're learning things, your prefrontal cortex for reasoning.

Depending on what part of the brain has experienced oxidative stress,

you're going to see potential deficits develop in that person's

intelligence or their personality.

But it's not

brain area specific to speak.

Like it's not saying

taking a lot of trend is going to destroy parts of your amygdala or destroy parts of your frontal cortex.

I think if oxidative stress is going to happen, it's going to happen globally within the brain, wherever there's not enough antioxidant, unfortunately, takes the brunt.

That

the long-term strategy to offset,

I guess, neurodegeneration

are taking things like antioxidants or looking at strengthening the connections between neurons with neuron plasticity.

but again, there's only so much that neuron plasticity can carry forward if you start actually damaging neurons, like what we've began this with.

No amount of like certain peptides like Adamax or Dihexa to speak is going to overcome you destroying parts of your brain.

Basically, you're going to improve the speed of transmission of the neuron, but it's such a scary risk when we look at PD usage,

cardiovascular disease risk, renal risk, liver disease, we can pretty much keep on top of with blood work and imaging and everything else.

You don't see someone go in and go, I'm going to get an MRI in my brain and I'm going to track my brain every two to three years.

When I'm competing with bodybuilding of what effect is

the exposure of these PDs causing to the neurons in my brain, like what parts of my brain are becoming dysfunctional?

Where am I potentially seeing small little lesions form in the brain from oxidative stress,

that

it's

scary when you think about that what you do in your 20s,

you might not necessarily feel that neuron deficit because of when we're young, we have billions of neurons in our brain.

It's only when things from a cellular perspective start to slow down as you age

that it could start off as simple as something as forgetting where you put your keys all the time, like your short-term memory, forgetting people's names or places,

you know, trivial things.

You know, guys are

really start getting a bit angsty here.

Oh, God, I'm forgetting all of us right now.

I was going to say myself included.

I'm horrible with remembering names.

But it could start as something as simple as that, where you don't think about it.

You just think, oh, that's just normal.

I forget where I put my keys.

But

in theory, that could be signs of slow onset neurodegeneration that you're not aware of.

And that's why, you know, it is very important that with this community, that we do have these conversations about mental health and neuron health as a...

A big thing to consider when we're all so focused on not dying of like more public things like heart attacks or kidney disease or a small extent, liver failure,

they get all the attention.

They're all like the, oh, what are you going to do about your heart health or kidney health or blood pressure when you're using PDs?

And the brain is sort of like a second afterthought that

I guess when you get into like your 50s and 60s or 70s,

you don't want to have these mental deficits where you can't remember things.

You can't remember good memories.

So, if you had a good bodybuilding career to speak, not being able to remember that, not being able to remember childhood memories or even your children's childhood memories.

It's a scary thing to consider that

you get to that point, and it's a consequence of not taking something like brain health or oxidative stress of the brain very seriously.

Yeah.

Um,

so we were

sorry, I went down at a little dark, dark rabbit hole.

You're like talking about like forgetting childhood memories.

And I'm like, I'm glad I forgot those already.

Anyways, but

not trying to get a little too dark.

We're discussing oxidative stress being probably one of the most important factors when it comes to all of these situations, right?

Cardiovascular health, renal health,

you know, your brain.

And I think

this is something that's like discussed a lot over at bodybuilding,

which I'm really appreciative of nowadays.

But

I feel like it's not pressed enough still.

so my audience does consist of a lot of bodybuilders, whether or not they're natural or not.

But I would just have to say, honestly, in general, Americans in general tend to,

through their lifestyle, induce a lot of oxidative distress on themselves.

And then you add bodybuilders on top of that, whether or not they're from America or not.

And it's just in the extremes.

So I guess this is something we discussed in the last podcast regarding supplementation.

What would you recommend for the top three supplements for oxidative distress?

And at the time, it was gluten, glutathione being first, vitamin E second, and then NAD and CoQU10 being third.

As you can tell, I've been trying to be on top of my supplementation and oxidative stress from my memory.

But

if we're looking at oxidative stress as a whole,

all the way to the foundation of the things that we should, you know, kind of check off in our lifestyle, I guess, what would you

What are all the things that we can say, just simplifying it down to like a list of all the things that someone should check check off in their lifestyle.

And then, all obviously, from lifestyle, supplementation,

and then obviously, finally, probably going to medication for us to reduce our oxidative stress as much as possible.

I guess the very top one,

sleep.

Sleep.

I mean, sleep is where,

as complex as it is, as

a routine to humans, it's a detoxification process where we're

basically our brain has its own immune system, it has its own microglial system

where you have it has its own lymph, it has its own white blood cells, as obviously a big blood barrier.

So, the blood-brain barrier, our brain is very selective at what it will allow into it to influence it.

And that's why some medicines fail to have certain efficacy in our body because it's not able to pass across this very selective barrier.

So, with sleep, you're allowing all of the junk to speak from throughout the day, like the lymph and everything, dead cells, everything to sort of drain out and be detoxified by the liver and kidneys.

We have obviously our actual sleep process of dreams, deep sleep, hormone secretion,

neurotrophic factors being made in our sleep to help strengthen our neurons.

So, sleep,

if there's one thing that most bodybuilders will neglect, thinking that you know there's some level of armor to hold with having less of it, it is sleep.

So,

really

looking and paying attention at a metric, perhaps, if you wear a fitness watch or a whoop or an aura or or whatever, your HRV

makes you not to wear your aura ring where your wife sleeps, yeah, yeah,

or fitness watch, but something like HRV won't be impacted by someone who's beside you.

So HRV is basically the

time it takes for a heartbeat to occur, the distance, the time between heartbeats, basically.

And what they suggest is a shorter HRV is a faster time.

So your heart is beating a lot faster.

And a longer HRV means there's a longer gap between heartbeats.

And we're talking milliseconds.

I can't even measure this.

So when someone's like, oh, well, my heart rate is 50 beats per minute.

We're looking at like milliseconds between those one second beats to say.

And so when you have a low HRV,

it could be genetic or it could be a sign that you are under sympathetic nervous system, stress, that you're not getting enough sleep.

That you might perceive that I operate fine on four or five hours of sleep, but really, underneath the surface, your body's telling you I actually need more to function better.

And

one of the things that

again, coming back to Android's influence on dopamine, trying to stay asleep when perhaps you have a heightened hormone environment, it can be difficult.

So, you often find, you know, if you're on prep,

very rarely, if your recovery is pretty good on prep,

you don't have an issue getting out of bed in the morning, or you don't have an issue of motivation to get out of bed in the morning.

You get out of bed and go and do fast at cardio or do whatever you need to do.

If you're a business owner, getting up early hours in the morning to do whatever needs to be done ahead of your day.

But

that

drive to have a lack of sleep, to speak, in terms of like five or six hours is enough for me.

And how I feel, your HRV could be telling you something different.

But the other side of the argument, and this is why I hate sleep trackers or things like that, as a ruler of your sleep, they could be completely wrong.

You know, if you wake up after five, five and a half hours of sleep and you feel amazing.

And you feel amazing all the time,

who's to argue how you feel versus what the research is saying on seven hours being more optimal?

And against just the generic variance of people's biology and their habits and rituals and everything else.

But there is some trade-off that if you are sleeping less in terms of like five, five and a half hours, and this is like sleep time

as opposed to time in bed.

Maybe see what effect trying to get six or six and a half hours of sleep time will

yield to your HRV or to your overall recovery?

Because in the long term, you're looking at this sort of future protection as opposed to like the short-term energy gain that you get from a five and a half hours sleep.

You don't know long term what that could be doing to your brain.

So, sleep,

it's a difficult one because

it's

rooted in what you do prior to going to sleep, like what we talked about, about, but also then how you stay asleep, your underlying biology and your neurotransmitters.

That

if you're not capable of staying asleep from that dopamine drive, where really you should be staying in bed,

let's say you wake up at 3 a.m.,

no problem, and you wake up at that time every single day.

But in reality, sleeping another sleep cycle to maybe 4:30 a.m.

or 5 a.m.

might serve you better long term.

In the short term, the 3 a.m.

awakening doesn't disturb you, doesn't create any problems to your natural day-to-day energy.

But long term, that extra sleep cycle, that extra 90 minutes of sleep, could have helped with brain detoxification further, helped with neuron development, like neurotrophic factor release, and everything else.

That

you, I hate saying you have to sleep for X amount of time because it's so variable, but pay attention to when the research is saying aim for like six to seven hours try and achieve that number

you will you will get away with four and five hour sleeps we've all done it and that sometimes is four and five hours in bed

because again with sleep trackers that's probably the beauty in that it can tell you when you potentially went to sleep and

Similarly, we've probably all experienced times where we've gone to sleep,

Your tracker is telling you you were asleep, but for the whole night, you sort of felt consciously awake.

You didn't feel like you ever went to sleep properly.

Yeah,

it can give you an insight into, okay, well, maybe I did sleep, but just mentally, I was so consciously aware of my environment that I personally don't feel like I've slept, but it's telling me I have.

those nights when you have that type of sleep, again, is that the most conducive to your immune system of your brain, to your memory formation, to the nourishment of your brain.

So, sleep, it's free aside from having a bed and a warm place to speak or a safe environment, is how I put it.

And the time, I think, is also what most people will discuss

is different for them.

That's it.

I mean,

playing to a chronotype similarly, like if you're, you know, an a late owl or an early bird,

there is no right or wrong, and depending on different stages of your life, you might be two different types.

You might be, you know, night owl at one stage of your life in your 20s, and you could turn into an early bird in your 30s and 40s.

That

just,

like anything, listen to your body, the same bodybuilding, you listen to what your body's telling you with recovery and everything else.

So, it's sleep sort of nailed, you're getting your deep sleep, you're sleeping in a warm bed or a cool environment is probably the better way of saying it, that it's not disturbing your sleep.

The next thing, probably, to step up in terms of offsetting the oxidative stress is probably nutrition, you know, making sure that we're covering the basics, which I don't really need to go into micronutrients and making sure we're fueling the brain adequately.

Like the brain uses quite a lot of glucose.

So

when we look at what energy sources it uses, it uses quite a lot of glucose, but also uses fatty acids.

Do you mind if I pause us for a second?

Yeah, yeah, go.

Yeah.

So before we move to nutrition regarding sleep, so I know we already discussed a lot about sleep in the last podcast, including some supplementations

and I guess

preventing catecholamines from raising too high whenever you are trying to go sleep.

I guess what would you feel?

Because you and I both already discussed like one of the issues with melatonin, how it varies

individually per person.

Some people don't really react so well.

Sometimes they'll wake up in the middle of the night if you're not using something like vitamin B,

B5 and B6,

particularly to

maintain that melatonin production naturally throughout your sleep cycles.

If one wanted to take advantage, though, of just how powerful melatonin is as an antioxidant, I know there are quite a few people out there that are proponents of high melatonin dosing.

And I know both Dave Lee and Martin Fitzwater are two people that do that currently.

I think, I don't know, Martin probably does somewhere around like 50 milligrams or something like that.

But

I guess

if someone was able to titrate themselves up to that dosage where they were able to take that much, how much would you recommend that?

So historically,

prior to all this, I worked as a shift chemical engineer.

So I flip-flopped between a month of day shifts and a month of night shifts.

And I personally, you know, when I started talking about things on social media during that sort of journey phase of my life,

I spoke about using melatonin as an antioxidant, which is a great thing to bring up because people don't ever look at melatonin as an antioxidant to speak.

They think it's this sleep hormone.

But if you do work night shifts and you do certain practices, like now I've got lights here in the office, it's what half nine, twenty to ten in the evening.

I've got a daylight lamp shining here to keep me awake.

That I know that's going to put some effect on my melatonin.

That

tonight before I go to sleep, I'll probably supplement with a small bit of melatonin to help with my circadian production or release of it.

That historically, I would have done 20, 30 milligrams of melatonin after night shift in the morning time prior to going to bed.

Knowing that, again, when I was on night shift, I'd do practices like this.

I'd sit in front of a daylight bulb all throughout night shift at my desk to basically tell my body artificially, actually, it's daytime, don't worry, stay awake.

That

if you're doing practices like that, where you're offsetting your own production or release of melatonin,

then supplementing with it as a strategy, again, as an antioxidant for brain health and everything else that carries over from that.

I've seen 50, 60 milligrams recommended.

Again,

there's no set

amount that is going to yield a specific response like what we talked about.

If you metabolize it very quickly,

that's not to say that it didn't work as an antioxidant in your body.

So

if you do go on the high side,

I know from speaking to Steve,

him personally, when he doses his melatonin quite high, it leaves him very, very groggy the next day.

I can't personally say it's ever done that for me.

But again, it shows the genetic tolerance or the interindividuality of what we're using that compound for in our body.

That

I I don't see there being too much of a contraindication to seeing what's a tolerable dose, other than potentially that grogginess the next day of you've interfered with your cortisol secretion the next morning to wake you up.

But I won't have any like secret recommendation to start at 30 or 50 or whatever.

20 could be enough.

I mean, even trying to track melatonin

is a difficult thing.

The only

tests that I'd encounter day to day would be the Dutch test would have your waking melatonin level.

And what you're trying to do there is correlate the waking melatonin level to your cortisol, but also to potentially your serotonin, knowing that that melatonin, that morning melatonin level has probably come from serotonin conversion.

So, I wouldn't have a strict recommendation, being fully honest on it.

Um, it's one of those ones that it's like a an experiment trial and see what

where you sort of sit.

But again, even with those large doses that I personally done,

I can't say that I felt any like

brain health benefit to speak, like short-term brain health benefit.

Most

probably definitely a long-term benefit where I've helped with my overall brain oxidative stress and keeping that under control with that exit and a supplementation.

But I can't say that taking 20 milligrams was better than taking one before bed.

That there was no appreciable difference between the two for me personally.

Gotcha.

I think my interest comes from just how I am right now, for example, which I think a a lot of people in my audience probably are.

Is I'm I feel like I'm about maximizing my doses on my NAC intake, my glutathione intake, and a bunch of various other, you know, anti-inflammatories and antioxidants.

And melatonin being one of the strongest ones, I've just always found like in

I just found it very intriguing that some people would just titrate up their doses to super physiological levels in order for just the long-term benefits of,

you know, it being an antioxidant so

i guess uh

if one were to experiment with this like we we we discussed how like melatonin supplementation uh at the beginning of the night can sometimes lead someone to still wake up in the middle of the night um

did you or would you ever recommend uh continuing also supplementing with something such as ltryptophan and vitamin b5 and six while you're using that melatonin just to prevent that from happening yeah i mean you're

when you take melatonin prior to sleep, you're

sending a signal to your brain in theory that it's nocturnal, that it's nighttime.

But, like what we spoke about, the actual thing that keeps you asleep is your brain's own melatonin, your own production of melatonin.

And that's not necessarily what you made during the day from sunlight exposure, it's what you're converting from serotonin in your sleep.

So, yeah, most definitely augmenting what the melatonin prior to sleep is doing to get you into a sleep pattern and then supplementing with B5, B6, tryptophan, 5-HDP, whatever way you want to get to serotonin,

is just ensuring that once you are asleep, your brain has enough cofactors to the building blocks of melatonin itself.

Bearing in mind that the gene that does that conversion of serotonin to melatonin

is what's considered a clock gene a gene that runs off a circadian pattern so that that it's called a anat

don't ask me what that stands for off the top of my head um but it's an amino acid transporter off the off from recollection um with a anat

you are basically converting serotonin to melatonin within a nighttime period, running off your circadian rhythm.

So, if someone is working a shift pattern, that gene isn't going to be as efficient at, or that enzyme, I should say, is not going to be as efficient at creating melatonin from serotonin when you're trying to sleep during the day of a night shift.

And that is where, again, you're coming in at the angle of taking such a high dose with night shift work potentially as that antioxidant and also as a way of trying to keep you asleep during the daytime and you should really be awake based on what your circadian rhythm would be telling you to do aside from that

nutritionally from a sleep perspective i guess

magnesium another big thing that we we covered the last time

such an easy thing to control and the impact it has over onto your

your neurotransmitter neurotransmitter clearance and then obviously a calmer brain is obviously potet well obviously obviously it's helping with the clearance of these neurotransmitters that could be stimulating your brain to wake up so you're staying asleep for longer the the impact that magnesium can have over onto

glucose regulation while you're sleeping like one of the things that has to be managed while you are sleeping is your pancreas managing your blood sugar.

And

when you think about it, when you go to sleep, it is one of the most vulnerable times,

you know, even historically, that your brain is perceiving that the environment is safe for you to basically switch off consciousness.

That it has to perceive that the

local environment is safe, but also has to

sense that the internal environment is safe also for you to go to sleep, that your blood sugar is not going to crash, that you're not going to have a hypoglycemic event and fall into a coma while you're sleeping, that

your body is still having control over regulation of your metabolism, your digestion, everything else.

Although it all slows down in your sleep, it's still running in the background.

That parasympathetic nervous system is still doing its job while you're resting.

Magnesium playing over into your glucose metabolism and energy turnover,

you know, mitochondria, everything else, they're still operating while we're sleeping.

So we want to make sure that you have enough nutrition to allow us to do that job whilst we're resting.

Okay.

Yeah.

I had a discussion with Austin Stout where he was saying, like, sometimes, I mean, you know, as you grow heavier and grow bigger, you know, and like, for example, a bodybuilding sense, oftentimes your magnesium needs increase as well.

But a lot of people don't really take that into account.

Yeah, I mean, like what we covered, the milligram per kilogram recommendation is normally 10 milligrams per kilogram body weight.

And so, you know, a kilogram, I think, is 2.2 pounds.

So if you sort of convert that, it's like 22 milligrams per 2.2 grams body weight, but pound body weight.

which as you get bigger, you've created more cells of your body and more cells of your body need more nutrition so it is one of the ones that as you get bigger and bigger and bigger you do potentially require more and more magnesium and

that 10 milligrams per kilogram from the research is just a starting point you've got guys then that could need more depending on their gut health their absorption their stress level

you know the more stressed you get the more cortisol you produce and the more cortisol you produce potentially the more magnesium you're using up to dampen that cortisol and adrenaline response.

So, that is a very good thing to consider that as you get bigger.

Again, coming back to sleep health, I mean, that's another

nice thing to sort of consider: that

is there the possibility of sleep apnea when you're sleeping and the impact that that's having to your neural health.

And if you're a bodybuilder with, or even someone who's just at the gym, that

unknowns to you, you could have developed a laxity in the jaw or in the tongue that is collapsing back onto your airway in your sleep, especially if you lie on your back.

You could be having these like micro apneas throughout the night that is effectively starving your brain of oxygen for a period of time and you start breathing again.

the impact that that has on your long-term neurochemistry as well or your neural health, aside from the lethargy, the increase in red blood cell counts to try and compensate for it.

If

you wake up in the morning time and your mouth is extremely dry

from mouth breathing or snoring,

you have excessive thirst in the morning time, you're waking up to urinate more than once per night,

you're in a position where potentially you are having some level of microapnea that might not be clinical, might not be enough to have a clinical prescription for a CPAP,

but you might see benefits to

things that help keep the jaw more aligned, whether it's mouthpieces, mouth taping, nasal strips, everything to sort of try and optimize that jaw structure so it doesn't collapse.

Or you seek a private prescription of a CPAP and see what benefit it brings.

And that's something that guys, again, just they could feel fatigued during the danger offseason and just think that it's a combination of training, food, PDs,

unmanaged recovery, if you wanted to put it politely.

But really, at night, they're snoring for two or three hours in their sleep, and they're not having the most restful sleep where

their brain again is,

I guess, subconsciously trying to keep you you alive, but then you're starving out of oxygen for a period of time.

It's waking you up, but you're not aware of that awakening for your breathing to begin again, and then you're back into another sleep cycle.

But there's still sleep disruptions that you might not consciously remember waking up these micro awakenings, but then the next day you're feeling them.

And then obviously, long term, your neural health will play into it.

That's another silent thing that known,

you know, there seems to be, I wouldn't say a taboo, but a lot of people don't really want to say, oh, I use a CPAP machine for to enhance my sleep quality as opposed to a strict medical need that you have full-blown sleep apnea.

If you have

high levels of snoring, you have issues surrounding,

like I said, the tongue relaxing in your sleep,

there's things that can be done to optimize your sleep that

what you've said to gain from correcting that is a lot better than

feeling that there's a stigma attached to having a CPAP.

And you see a lot of time, like guys, have a resistance to

going down the route of looking for a CPAP because they think that, oh, they're loud, they're noisy, they're uncomfortable, you have to wear a full mask.

There's, you know, at at this stage, we've got non-invasive like nasal pillows, we've got like CPAP poses that move in your sleep, that go on the top of your head.

That you might not look the most attractive to the person beside in the bed.

But

if you're gonna, if sleep's your priority, and you know, when all's said and done, the bedroom and you put on your CPAP, you know, who cares?

So

it's

again, it's a longevity strategy that guys thinking about this as a

way of protecting their brain health might be something to consider.

That it's not just looking at the

snoring and the disturbance that the snoring brings.

Yeah.

I guess the one thing that I would recommend, so I haven't even tried this yet myself,

but I guess the one thing that I feel like

I find interest in for the people that are like me that don't quite have sleep apnea or aren't fully qualified for sleep apnea and a CPAP, but are on the verge and do have snoring.

I know they recommend that mouthpiece that you were discussing.

That does help push the tongue out of the airway.

That's, I know the tongue is the main issue for me, at least I believe that causes me to snore and causes those issues.

So

I don't know.

I think I'm sure it'll vary perversion, but that's one of the things that I think I'm going to try to experiment with.

And then I'll probably have some results for people, you know, here soon.

And then the other two things that I know other people have

when they sleep, they have issues with is

peeing too frequently and then overheating in the middle of the night, even if you set the AC really low.

I guess, do you have any recommendations for those?

So, with the peeing multiple times during the night,

the first thing I always jump to is apneas.

So

when you have cumulative micro awakenings,

you're going to get to a point potentially where you have then a

your kidney filtration in terms of the fluids that's being managed by your body will shift.

And then you're subconscious, well, you're consciously aware now that you're awake and some of it can become habits.

So you then wake up and you're like, oh, I need to pee.

You just get get up and use the bathroom.

And then

the other side of it, if that isn't a psychological habit where you wake up and you just think, oh, I better pee just in case I pee in my sleep.

You know, you feel an urge, so you think I'll just get up and go to the toilet and get back into bed.

The other thing is low anti-diuretic hormone of your body.

So

really, what should happen as you head towards nighttime,

your body's production of antidiuretic hormone will increase.

It's called, well, here we call it antidiuretic hormone.

It also can be known as vasopressin.

So, you do have medications that will act as synthetic vasopressin or synthetic antidiuretic hormone.

And that's one of the

mechanisms of how

in the past people would have done like water loading prior to shows to

decrease their body's

ability for storing water, but also

to

suppress anti-diuretic hormone.

So now you are basically suppressing the thing that keeps water in your body, so now you're going to pee out the fluid.

When it comes to night time, you want to have a high amount of ADH or vasopressin so that you stay asleep.

There's certain things in the environment, there's certain toxins, there's,

I guess, stressors to our brain that can diminish ADH production.

Electrolyte balance is another thing that

guys tend to completely ignore with

what's called nocturia.

Nocturia is waking up to pee in the middle of the night medically.

If you have a very like high sodium diet and you don't have enough potassium, all all of your fluid and tears being moved into your vascular space, into your bloodstream.

And then, when you go to sleep at night, your kidneys are going to filter that excess of fluid and salt that's in your blood, and you pee it out.

You can have fluid pooling in the lower limbs, in your legs, whether that is venous insufficiency, like varicous veins, where you don't have veins operating properly to bring blood flow and lymph drainage back up your leg properly when you lie down you've pulled probably quite a significant amount of fluid in your lower limbs if you think about your bladder's capacity

most

likely in around your lower limbs on each leg you can probably hold around

500 milliliters of fluid relatively easy distribute across the whole leg that you're not going to necessarily feel but when you lie down at night you're down, your blood pressure relaxes

interior.

When you're in your sleep, your blood pressure is at its lowest point, and fluid can drain from your lower limbs back up the body to the kidneys, get processed, your bladder fills, and now you're excreting that fluid that collected in your legs during the day.

If that is a root cause, well, then you can correct your electrolyte balances potentially.

So, look at your potassium to sodium ratio, make sure that

really, the RDA for potassium is 4,700 milligrams.

So, if we say 4,500 potassium, 2,000 sodium, it's like a two is to one ratio almost.

That most bodybuilders are in the other direction where it's more sodium-laden and not enough potassium.

Or they're getting some level of potassium, but it's not in the correct ratio to sodium.

That's a way of potentially making sure that your cells are hydrated.

So, potassium pushes water into your cells, sodium pulls the fluid out of your cells into your bloodstream.

Alongside, obviously, making sure you've got adequate magnesium, calcium, and phosphate.

They're the other important guys that do fluid management as well.

Raising your legs, you see, guys do it backstage all the time.

Raising your legs prior to sleep, doing about an hour before you go to bed or two hours before you go to bed.

If you've had a busy day or something works on your feet, you don't have the most appropriate footwear, your arches aren't properly stabilized in your foot,

all the things that can sort of play into the fluid dynamics of pumping fluid back out of your leg,

raising your legs above heart level to allow gravity to let the fluid drain out

is a simple strategy if that is one of the contributors to your

nocturia.

and if that is the case, then if you do have something like venous insufficiency or varicus veins, there's not much you can really do other than surgery or take an appropriate rest when you're on your feet to try and alleviate that fluid building in your leg.

The electrolyte side of things, you can do it, diet manipulation,

environmental toxins.

I mean, people discount like mold toxins

can lower anti-diuretic hormone in your environment.

So, if a bodybuilder is waking up more than three times per night with a full bladder, you'd start to question what's going on in the environment as opposed to what's going on in their body.

You can probably correct if you're at

two awakenings to pee with a full bladder.

Probably the first one is that lymph drainage and fluid dynamics from during the day and the salt balance.

And then the second one might be psychological.

You wake up, you feel like you need to pee,

you feel that you're within two hours of having to get out of bed.

So you just feel, I'll get up, use the bathroom, and get back into bed.

That

if you ignored that psychological urge, unless it was really at you to go to the toilet, you'd probably go back into sleep again and your body would hold your bladder until you wake up again.

The psychological part is very inter-individual, but

nocturnal awakening is most definitely again something that will disturb your sleep and disturb then the quality of your sleep and the impact it has on your brain health.

So,

once per night, I think the rule generally is if you wake once in the middle of the night to have to use the bathroom, again, it comes back to fluid throughout the day, electrolyte balance.

That can be just put down to being quote-unquote normal.

But once you start going above that with multiple bathroom trips, if you think about it,

you're breaking your sleep up into

numerous shifts.

And

long-term, that can obviously then have a big impact on your recovery.

And I mean, that happened to me personally.

I got exposed to toxic mold years ago.

And that was one of the ways eventually that I was able to,

I guess, verify what I thought was the problem in terms of being exposed to molds and going and doing the like the urine test for mold toxins.

But I was waking up every two hours with a full bladder.

Like

full bladder, like could not like if you were like, oh, some of it's psychological or it's salt balance.

I've done absolutely everything to try and manage that.

And I was waking up with a full bladder every two hours that eventually I got to my wits end that you'd sleep for two hours, full bladder, go back to bed.

It literally was like a clockwork.

You go to bed, wake up at 12, wake up at two wake up at four and then you got up at six that

it it my sleep quality was just completely ruined

when you start addressing obviously the mold toxicity doing things to help with um

clearing it out of the body detoxing it that was like the biggest relief when you start to have like a full night sleep where you don't actually get up to go to the bathroom um I think from personal experience and maybe some of the listeners that if you have like a a night of sleep where you don't wake up to go to the bathroom, it's like success.

I've had a night where I've not had to get up to use the bathroom.

You've had like complete undisturbed sleep.

That

absolutely killed me.

And eventually it was one of the, alongside a few other things where I had my suspicions, it was like the

straw that broke the camel's back.

Where I said to my wife, there's something not right

in terms of what's going on.

And I verified my ulceratoxin level was sky high when I've done the urine test,

and that was about five or six years ago.

Yeah, well,

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Makes me feel a little bit better because I guess whenever I do go up to P, the bladder's not full.

So it's probably a little bit more of, yeah, the other, the, the, the other issues that you were talking about, such as just like if it's not psychological, then maybe

that's sort of apnea where I am kind of waking up anyways.

Yeah, I mean,

once I'm awake, that that's something to see what happens with the uh mouthpiece, see what, what change.

I mean, like I said, you hit, you hit the jackpot, you sleep all night and you wake up and go, woo, in a full night's sleep without waking up to use the bathroom.

Yeah, for real.

Cool.

So what about last thing regarding sleep?

Because I know we were talking about a lot.

We love sleep.

Overheating in the middle of the night.

So I know there's a lot of solutions these days.

There's a lot of new mattresses that are coming out about like, oh, we have cooling features and all these things.

You know, some people will just try to turn the AC down, even though.

There are those issues.

There are those couples where it's like one couple, once it hot, one couple, once it cold.

So then you got to figure out how to split that up.

Yeah.

But yeah, I guess, do you have in do you have any recommendations for that?

So

when we look at like thermoregulation,

how you sense the environment's temperature,

one of the things, and I mean, we're going to bring up everyone's favorite molecule, Trent.

When we look at like Trent sweats or when guys have thermoregulation problems from Trent,

on the surface of our skin

these thermal receptors on our skin are trying to tell us well is the body at risk of overheating does it need to perspire does it need to sweat to cool the body down is the internal core temperature gone too high

um

that

looking at what

estradiol and progesterone and progestins can have in enhancing the sensitivity of these receptors

you then start to see why women, even more so when they have estrogen problems, have it have sweating issues as well in their sleep.

When we look at like menopause, perimenopause.

Yeah, yeah.

Estrogen comes really low.

Like, if we look at

how to try and correct that, yeah, of course, you can try and regulate the temperature of your mattress.

Something as simple as the duvet tog, you know, are you using the appropriate, You know, do you have a winter time and a summertime TOG?

I'm not too sure on how things change in the US, but to put it in perspective, like at the moment in Ireland, we have like 22 degrees heat, which is extremely hot for us,

and then you've got winters where it's like minus four outside.

That

the house temperature, like I'm in my office now at the moment, and at what yeah, 10 o'clock at night, it's 24 degrees in my office with no temperature on, although there's no windows open.

If we're looking at the optimal temperature for sleep

being reported around like 17, 18 degrees Celsius, I'm not good with it, but US,

I'm pretty sure that's below 68 degrees Fahrenheit, right?

Well, I wouldn't know off the top of my head.

Again, I'm horrible with Celsius to Fahrenheit, but for us,

I guess, real quickly, let's see:

degrees.

68 is 20, 26 is 30, 105, 104 is 40.

So at the moment, 24 would be 75,

and then like minus 4 would be 24.

So like when you when you look at the overall,

I guess, overall

impact that environmental temperature is going to have and how your body's developed to those temperatures.

Normally, our house sits at maybe 17 to 18 ambiently, like between the thermostats and running the heating.

In the winter time, it's probably not uncommon for the house, if there's no heating on, to be 15, 16 degrees,

which again is quite low.

That

if we're trying to optimize the room's environment between AC, where one person runs hot, one person runs cold, I don't think you're going to win the argument of where the AC should sit,

and that might be down to then, well, what duvet cover is used in terms of like the thickness of the duvet.

So, here, again, with the UK, with such a variable temperature

and the Ireland, we'd swap between a winter duvet sheet and then a summer so a lighter togged bed sheet so that you're trying to offset some of the impact that the duvet is having on you when you're sleeping.

One of the simplest things I've often said with guys, if they have issues with sweating at night time, is to sleep naked, which people laugh at.

But if you sleep naked, your body has no inhindrance from bedclothes and also

maybe a bed sheet as opposed to a

duvet, depending on again the heaviness of the duvet.

A cold shower prior to sleep, about now, not immediately before sleep, otherwise you'd be too stimulated from a

nor epinephrine release perspective.

But if we can expose our body to cold with a cold shower, maybe two hours before bed,

might not be practical for someone.

But if they can expose their body to cold, you're going to lower your core temperature prior to sleep so that whilst you're sleeping, you've already set the pace for your body to adjust the temperature from a lower colder exposure rather than the actual ambient temperature.

So I've always heard,

you know, you do a hot shower to lower your core temperature since it, but is that are people trying to discuss like immediately before sleep?

Is that why they say hot?

Yeah, so if you're doing it immediately before sleep, you do hot.

Okay.

And then if you do cold, I mean, this, this is coming from someone who's excessively sweating.

If we're looking to optimize just normal sleep, then yeah, we do a hot shower, lower core temperature.

Doing the sort of reverse and the cold exposure, the norepinephrine release, the shaking, the termogenesis that comes from shaking,

you're trying to almost get ahead of your body having to adjust its temperature set point when you go to sleep.

So

it's one of those ones, like you said, where you sort of look at it and go, well, a warm shower looks more appropriate from a core perspective.

But if you're at risk of sweating and you can't correct your core temperature before getting into bed, where a hot shower actually has you feeling probably

more warm than normal, depending on the environment of the room,

your adjustment to that temperature is going to be offset.

So, the cold shower, sleeping naked, a bed sheet over a duvet,

there's not much else rather than looking at the hormone perspective, then, of what could be enhancing that thermal receptivity.

You know, most definitely looking at a cooler material for your mattress, making sure that your mattress can breathe to speak, so that there is air exchange from your bed.

If you have the budget and you have two people that are fighting over the temperature of the room, then

being able to climate control your mattress, although it's something I've never personally experienced,

I can say that when I was younger, colder pillows were much preferred by me than a warmer pillow.

There's something more comforting about a colder

pillow going to bed.

That I can only assume a colder mattress is probably similar.

That it's not freezing, but it's a little more inviting than a warmer one.

The other things on top of that, there's nothing really supplementally that I could offer

other than come to a compromise on your toggier bed sheet and look at potentially having that summertime versus wintertime bedsheet if your environment changes and you're not using AC.

I guess we're lucky here that we don't have the problem that when it's too hot like it is here now, it's a temporary thing.

So you just sort of deal with it.

It's not like it's a consistent problem where you have to run AC to control the room's temperature.

Quite often here, it's actually you need to run the heating to get the room to 18 or 19 degrees to be comfortable.

Yeah.

DNP.

Internal, yeah, internal.

Uh, just uncouple your body's energy dynamics and let it heat itself up.

You know, I mean, even like

excessive sweating in your sleep, um,

it can be a sleep disturbance.

So

we've, we've all been there, myself included, where you wake up and literally your bed is just soaking and you can't figure out how that happened.

Just

I've always been fascinated to like

if you had like a time-lapse video of what's happening in your sleep when something like that happens, like how

much sweat has been released from your body to leave your bed sheets, like you've basically done 45 or 50 minutes of cardio

just as a consequence of your body sensing that it's too hot so it needs to cool itself down with sweating.

That

there is nothing other than getting the habit of bedclothes might be appropriate, but they might not also be, depending on how you respond to the temperature of your room.

I'm glad we discussed this because

I think many of us too who are on gear and PEDs are just freaking on fire all the time.

So I think it's probably

a common thing a lot of us encounter, regardless of whether or not we're on trend or not.

No, and I mean, even like your bedtime nutrition and your metabolic rate while you're sleeping, what you've eaten prior to going to bed, what digestive processes are going on.

Like I touched on a very

broad level of

your skin's thermoreceptors and the environment.

If obviously food creates energy, it's thermogenic.

That heat is released from your body.

So again, if that heat builds up and you're underneath a heavy duvet, it's going to invariably create some level of like

sauna, to speak, under the duvet.

That's what happens to me, bro.

I love eating most of my calories towards the end of the day.

So I know that's my problem.

Well, we're not having problems.

And that can contribute then that heat generation from burning the food, to speak, is creating the problem.

So

you've got, well, to put it in another perspective, perspective, sweating is a detox pathway.

So you're just enhancing detox with sweat.

Let's go.

All right.

So I guess let's just wrap up the

oxidative stress portion so we can jump to the QA.

But we covered sleep and then nutrition.

Nutrition.

You know, I'm assuming just the nutrition that most people know, right?

Eat your fruits and vegetables, et cetera.

Supplements, then, or even like peptides.

I mean,

this is a rabbit hole of what you want to do with your brain.

Like I touched on,

once the unfortunate thing, and the reality is, once you kill a nerve or a neuron in your brain, that's it.

Game over, it's not coming back to life.

But what you can do is you can

make the other neurons compensate for that nerve dying.

So it's like

having a ton of telephone lines or telephone wires, and you cut one of them.

Now you've got less lines for transmission.

I think I explained this in the last podcast: that what you do then is you do neural branching where you're connecting all the phone lines together so that the speed of transmission is relatively the same as what it used to be with that neuron missing.

The only problem is, obviously,

neurons store neurotransmitters inside them.

That when you kill a neuron, you're reducing your neurotransmitter level potentially of your brain long term.

That

just because we create these neural branches to speed up the transmission of the signal, it doesn't mean that you have the same capacity to carry as much information as you could before.

So,

if, for example,

if we look at a nerve that carries acetylcholine, and acetylcholine is involved in your memory formation, in

I guess, accruing new information,

if you killed or

a neuron containing acetylcholine was to die,

but now we are improving the transmission of the other guys of communicating with one another, creating more branches, the speed of how we send that information or recall that information

is probably going to be improved.

But our ability long-term then to retain information from having a lower level of neurotransmitter is something that we wouldn't be able to correct.

We could have obviously optimized our neurotransmitter creation from nutrition and supplements, but you're not going to make up for the fact that you're now down one neuron that could have stored X amount of neurotransmitter.

So

the most prevalent strategy of improving like brain health and overcoming that is increasing brain derived neurotrophic factor, BDNF.

And people have probably all heard this acronym.

BDNF really again just stimulates nerves to branch with one another.

So if we can improve the amount of neurotrophic factors within our brain, we're going to encourage these new connections between neurons and improve the speed of transmission.

You've got various things like coming back to like nutritional supplements, lion's mane,

bacopa,

relatively a lot of the adaptogenic herbs act as adaptogens by lowering oxidative stress.

It doesn't necessarily mean that they improve neural branching or BDNF, but a lot of adaptogens will lower the impact that stress will have on our brain.

And that interior then will carry over to how the brain sends information as an overall.

So adaptogens can be a useful thing to consider, but they're not strictly going to improve that neural branching.

Stuff like lion's mane.

Probably at the very top, hardcore-wise, that was investigated clinically was dihexa as an angiotensin-4 derived peptide, which was shown to increase BDNF levels in animals anyway by seven times the control level from what I remember from the study, which is huge.

I think they but wasn't there like some discussion though of like the worry that it's so strong that it also increases it could increase brain tumor size?

Well, this is the thing when you look at any sort of thing where we're improving um

like BPC or TB500 we're improving andiogenesis.

If we're improving blood flow through the body, you could influence tumor size.

So there is most definitely a cancer risk with the andiotensin 4 aspect of dihexa.

Again, it's not been fully tested in humans to speak.

So if it's something that

you choose to experiment with, you have to be fully aware of these consequences.

And

that goes for something as serious as dihexa or something as benign, like we touched on with a complex, a B-complex.

So

we can use something like that in theory that is available

to perhaps influence BDNF in a very large manner.

You have other things like Adamax or Semax, which improve BDNF expression in the brain as well,

which

more so probably from

a nasal application perspective is more appropriate than an injectable due to that blood-brain barrier.

So when you use something intranasally, depending on the molecular size and the carrier, interior should be able to cross over the blood-brain barrier.

I'm actually currently micro-dosing that

several times per week, maybe like four or five times per week.

I mean, would you consider that reasonable and reasonably safe to just microdose for a significant increase in BDNF?

Again, coming back to

if we increase BDNF expression without any negativity,

what would be the worst case scenario to happen

to our brain?

And

looking at like the very top level, I couldn't see anything hugely negative that would result from improving neural connectivity

other than being able to recall information a lot more readily or carry an emotion.

Another thing, you know, carry neurotransmitters that influence our emotions a lot quicker as well.

When we look at improving cognitive health,

you have like two aspects.

You either want to look at improving like your memory or your information retention

or you want to improve like your speed of delivery or your speed of critical thinking to make decisions faster.

And both of them rely on that neural diversity of branching out to other neurons to either recall information really quickly or be able to deliver or recall and deliver that information as quick as possible.

So you'd have someone who

potentially could be thinking of something and then they're waiting for that, like information to come to the front of their brain, and then there's a delay in how they're able to communicate that out.

You'll find with improving BDNF and neural plasticity that your

verbal fluency, how you're able to get words out, is a lot better.

And you'll find that guys who do these sort of practices of influencing their brain chemistry

see this change in terms of how they communicate, how they're able to have quicker conversations, or they're able to

say what they mean in a more timely fashion to speak.

You know, and sometimes people

might go on, I'll go on big tangents, but you're trying to convey what is being thought about in your head a lot quicker.

So

using Dihexa,

Adamax, Semax,

again, there's nothing in my view that there's like this strict protocol because there really isn't.

We know what they do from a mechanistic perspective, but it's not until you actually start subjectively trialing things for yourself on what you feel from that experience or from that exposure to that chemical of your brain

that

someone might see a huge benefit from a microdose of Adamax or Semax, and your person might not see anything.

Does that mean that it didn't work?

Very hard to say.

I mean,

what's the expectation you're having on that

BDNF increase without

objectively measuring that BDNF number?

You might perceive that being able to remember something you've learned immediately as being valuable, the other person might not necessarily see that increase of a scale with the use of that peptide.

And so their perception of how it should be working on their brain is a little more grander to speak.

And so it comes back to what, again, what you subjectively feel when you do these increases.

Gotcha.

Okay.

Yeah, I feel like we can talk about oxidative stress for honestly an entire day.

I guess

if I were to wrap this up,

because

I want to be able to go to the Q ⁇ A because there's a lot of questions in there.

And I'm going to be real.

I actually was thinking before the podcast started, like, oh, it'd be great to go to the Q ⁇ A halfway through.

And

big tangent.

I always have so much to talk about whenever I talk with you, which I freaking love.

So, I mean, that's my favorite part about it.

But oxidative stress, I guess, um, if we want to wrap this up, like, I know there's a lot of other supplements and, uh, that we can go into,

I guess,

man.

It's a, it's a wormhole.

And I mean, that's where,

as someone who like formulates supplements, I am always going to be the first person that's very blunt in, well, what is the dietary need for using these supplements?

or what is the environmental need for using these supplements?

For example, like if someone is extremely stressed mentally,

that cortisol is going to have an impact on their sleep and it's going to obviously going all back to what we've conversed about there a moment ago.

If they were to take something like an adaptogen to lower the response to stress, they're going to see better sleep, they're going to see better mood, they're going to see better work performance, everything else snowballed.

does that mean everyone should take an adaptogen no no and then does that mean that you would recommend an adaptogen as the first thing for a stressed worker to take no

so it's

it's always really interesting when someone asks you know what's your top recommendations of these supplements and then when you turn around and say well i have no recommendations because X, Y, and Z context,

they're almost shocked because they're expecting you to have some sort of sales pitch on, well, if you take this, you're going to be so you know, super optimized in terms of like family, work, career, sports, whatever.

And it's just not the case.

And that was always

a vital part of like my integrity of the sort of supplement business that

you ask someone what they need to take, the answer back from me is, well, it depends.

And it's a long, long list of depends.

Gotcha.

Okay.

I say, if you're down for it again, if you're ever up for coming on again for a third time, then we can expand a little bit more on

ancillaries and reducing oxidative stress through supplements and even maybe medications if there are potential possibilities there.

But I know in the Q ⁇ A, some people actually asked some specific questions regarding things like medications and supplements.

So I think that would be a little bit more effective right now.

Yeah, so let's just move on to those.

There's one more thing that I was going to say before we move on, but I completely forgot because I brainfarted again.

Per usual.

Whatever.

Well,

if anyone else, though, in the audience is interested in delving a little bit deeper on, I guess, neuroprotective methods

and maybe peptides and stuff.

I had this podcast with Biohacking You, Brandon, who...

has done a lot of pretty extensive research on peptide use and neuroprotective methods.

So we also, we discuss things also just like calling up regulation for memory and some other various things that I think could be effective.

Um,

yeah, Brendan is a good guy.

I've spoken with him a few times, and he's well tuned in, so it's definitely something I'd recommend people to listen to.

I was actually listening to it earlier, so it's nice to

see you know

all this information going out there to the right audience that,

in my view, are in critical need of having easy accessibility to stuff that isn't talked about mainstream or won't be spoken with their healthcare practitioner, or just stimulates thoughts that they can bring these questions to their healthcare practitioner of concerns they might have.

And then they know, do you know, sort of

it's almost cheating because they know where they want the conversation to be guided if they are seeking medicative help because they're aware of what medications are available, how their mechanism of action works, what potentially they're doing with their nutrition, et cetera, that they might need this support from the healthcare practitioner.

Awesome.

Yeah, I really like what you said earlier, too, regarding, because it was literally the,

it aligned with the thoughts that I had as well about how just, you know, a lot of us, especially in the bodybuilding industry, for example, will focus so much on organ health, but then, you know, people aren't getting these regular scans of their brain every two years or so.

You know, most people kind of just disregard what happens to the brain.

So, um,

until like we're, you know, later on in life, where we're like realizing we're forgetting more things and etc., and then it's a little bit panic occurs.

So, I think it's really cool that there are a lot of people like you guys that are discussing this openly now.

I mean,

as much as we all fear

as bodybuilders, like having a sudden like cardiac event,

the other thing, you know, that makes you realize you're like the master of your own destinies.

You don't want to be in your

60s and 70s and being

not to be strict speaking, but

to be a burden on someone because of your mental health, of not being able to remember things.

And obviously, then your life experience is completely impacted because it's it's something that is very difficult to fix.

And a fix is putting it lightly because

like we covered once a neuron is dead it's it's done you're you're trying to optimize the brain's compensation of that that

dysfunction that

me personally

do genetics aside I'll do everything to try and ensure that brain health stays at the the forefront forgetting where I put my keys aside

are there any neuroprotective things or ways or supplements supplements that you recommend people do to, I guess, avoid their neurons from dying?

It's,

you know, when you look at

what triggers nerves to die aside from excessive

neurotransmitter, like excessive dopamine, we're all aware of like dopamine.

Glutamate transmission, when we have too much glutamate in our brain, glutamate is an excitatory neurotransmitter and it's a relative of GABA.

Glutamate

will

in theory poison our neurons.

Now, are there things that we can do to help with glutamate

metabolism?

Most definitely.

Can we look at the foods we eat and potentially what can be broken down into glutamate in our body as well from the food we ingest?

ingest absolutely but

it's

i would not say there's something that you take it and it's a an insurance policy that your brain health is going to be protected that you take this compound and nothing will ever happen to your brain that

again it comes back to like the the very basic things are the antioxidants if you've got good glutathione

good vitamin E slash vitamin C, CoQ10, you've got the building blocks of what are really going around your body doing a lot of the internal protection, controlling your iron, controlling your glucose,

controlling your exposure to electromagnetic radiation.

You know, we all discount that

because we can't feel it.

I always get scared because I always carry my phone right next to my balls.

But in that, you know,

I've spoken about, we went on honeymoon to New York and Times Square.

And I remember opening my phone, I was like, there must have been at least 300 Wi-Fi hotspots around me.

It was insane.

And you're in this

small enclosed area with tons of electromagnetic radiation around you that you can't feel.

but your cells most definitely are feeling it.

But you're using melatonin glutathione and all your antioxidant cascades to keep that damage that's trying to come into your body, that energy coming into your body at bay?

That

something as simple as that, you don't

think about, you don't think about where you travel to, you don't think about the impact that flying in a plane has to your oxidative stress.

You know, things that we take for granted, driving on a motorway with pollution, you know, if you're stuck on a motorway with

an accident,

one of the things that you could consider doing is having the air recirculate through your car so that you're not pulling all the exhausts of the cars that are stopped in front of you through your car, through your car's air itself.

So you're not exposing yourself to all the toxins in the air while you're stuck in a traffic jam.

You know, simple things surrounding that impact on your antioxidants and your oxidative stress without even thinking about what you're taking is doing to your body.

So

it definitely

makes you think of the broader thing that

there's no one singular supplement or food or strategy you can do to offset this effect on your brain.

It's like

what is readily available to you from a nutrition perspective?

What are these core basics?

We talked about antioxidants.

What can I maybe do with EMF?

Whether that is like EMF shields, as woo-woo as it can be, grounding, you know.

I'm glad you said that as woo-woo as it could be because I got a couple of those little black metals that you can put on a necklace that I used to buy my laptops and shit.

I have one here on my phone.

I've got, I forget the name of the company now, but yeah, it's sitting on my phone here on the desk.

So

I mean,

anything a little like that, I'm talking to you now.

And as much as I get comments about banging on my table and making noise,

my hand is on top of a grounding mat at my desk.

So, I've got a grounding mat where my keyboard's on top of the grounding mat.

Again, as crazy as it is, I'm just thinking consistently of what are little

things that I can do that maybe in the grand scheme of things

will offset a small amount of oxidative stress.

And in terms of like long-term health, it's like compound interest.

You're doing these small little things in hope of when you get to, like, I don't know,

let me throw a number,

say, 70 years of age.

And

from a cellular perspective, you've managed to maintain a lot of your youth, to speak.

And it's because you've managed to slow the rate of aging from keeping your cells functional from reducing oxidative stress.

That

these silly things that might seem benign have

played up into the bigger equation of things of keeping oxidative stress under control.

And

whilst it's all a rage, it's good to see that in the last two years, like research is bringing a lot of disease back to oxidative stress and mitochondrial dysfunction, where we're going into the nitty-gritty of

why did this problem happen?

And we're starting to really zone in on, well, the mitochondria became dysfunctional, and then everything played off that, whether it's cancer progression,

cellular dysfunction, glucose problems, iron dysfunction.

I'd say probably by the time I'm 60, so like another 22, 23 years,

that we'll look back like on the conversations we're having now about oxidative stress and mitochondria, and we'll be almost looking back at how we view early 1900 medicine.

Audi laughed at you know, the guy who proposed washing their hands prior to surgery because there's bacteria in their hands,

being sort of ridiculed by doctors going, you don't wash your hands, don't worry about that.

That we look back and say, you know,

when we viewed

problems occurring in the human body as compartmental problems, so diabetes being a problem of

glucose management, where it's the pancreas, where it's the liver, where it's the insulin receptors on your cells,

we'll start looking back potentially and saying, well, what happened in the beginning was the mitochondria just couldn't facilitate the glucose from being utilized correctly and it all fed upstream where the final thing that really took it was insulin sensitivity or lack of insulin production, et cetera.

That I think we're on an exciting time where people are starting to really shift their analysis into

where the key guys in our biology that are keeping us alive and driving a lot of the problems that we encounter day to day.

And,

you know, we look at how we appear visually in terms of age now.

You know, we've got 40-year-olds today who,

from better words of putting it, they look maybe in their 20s.

If you compare that 40-year-old of today back to a 40-year-old in the 90s and 40s or 50s, where, again, there wasn't much attention or lack of awareness to oxidative stress, there was a lot of mental stress from the environment and whatever else we want to consider back then, economy, everything else, lack of technology.

As we progress through time, again, with that whole like

human evolution,

we'll start to see: well, if we can intervene at a very young age on oxidative stress, and I guess this is an important thing to touch on before we go into QA, is

without going on a tangent,

oxidative stress is important to our body.

So, oxidative stress, when we look at like what induces hypertrophy, it is a stress to the body.

So, there is going to be reactive oxygen species made

to create a stressor on the body to overcome that stressor.

If we are chronically hammering our body with antioxidants and keeping oxidative stress like completely diminished,

then that's going to set problems because

we're going to interfere with our adaptation process of our body, where we have to create these reactive oxygen species to see a knock-on effect within the body.

So

that's the important thing that if we're constantly hammering, hammering, hammering at glutathione injections, IVs, it's important to sort of understand how is that glutathione

playing into the grander scheme of things?

Because we do want to have a small level of oxidative stress for how our body operates.

It's just not good for having

excessive oxidative stress where chronically chronically you have low antioxidants i guess that's why it's um

uh it's pretty smart to be aware of like um i guess timing when it comes to uh reducing oxidative stress though like uh i guess say doing like uh glutathione shots or ivus on like rest days particularly or um rested periods of time um I know one of the things that I also use as an example, like arachnidonic acid, only timing those, using those on specific days where I'm like, oh, this muscle group I feel like is the most important for me to grow, like leg days,

in order to increase the inflammation on those days.

Yeah.

I mean, even like cold exposure, where you should really avoid cold exposure within 48 hours of resistance training because you're interfering with the inflammatory process.

And I mean, creating oxidants in our body.

I guess saying having a level of oxidative stress is probably not the best way to describe it because oxidative stress would mean you don't have enough antioxidants.

Oxidation and oxidants is probably the best way of saying it.

We need a certain level of them in our body for these processes.

And if we're constantly mopping these oxidants up before they have an ock-on effect to create the change we're looking for,

that can be a problem rather than having a small amount of oxidative stress.

Okay, gotcha.

That makes sense.

So

any level of oxidative stress is probably a bad thing because it means that you've got a lack of antioxidants.

I should clarify that before anyone comments down below what I've said is incorrect.

We want a level of oxidants.

We most definitely want to keep oxidative stress under control.

So, yeah, think about that before you start piling all these antioxidants in again as supplements that I'm going to hook myself up to an IV of glutathione, NAD, vitamin C, just give me as much as I can take.

It's probably going to have negative consequences than positive benefits.

Awesome.

Cool.

Let's move to the QA.

Sorry about that.

It's probably my trend coming in.

Andrew,

if you have to answer the front door, go.

Oh, no.

I'm sure it's probably just like an Amazon package.

I was just joking around.

Cool.

All right.

So,

well, so many.

Everybody loves you, Dr.

Dean.

I greatly appreciate the love.

It makes doing these things worthwhile.

Elijah Sigur asks, is the rate of lean tissue gain the same on mastron as comparable compounds?

So

there is a

cellular paper.

There's a paper with Hirschberg assays, which are done on rats.

And you look at the rate rate of tissue growth in

basically the levator antimuscle versus the

seminal vesicles of the rat.

So you look at the androgenic to anabolic ratio of the drugs with Hirschbergers.

This paper basically

shows that all steroids roughly caused the same rate of development of tissue when you looked at the drugs that were used.

So to note, there was

anivar,

Winstrahl, Nandrolone.

Mastrone was not on it.

But the consensus from that paper was that all drugs built muscle at the same rate.

When you look at, in theory,

that may be true, but then you look at the broader picture.

And

to give credit, Dr.

Scott Stevenson has a brilliant presentation of this with Scott McNally about

this sort of question:

does mastron build the same amount of tissue as primobolin?

If you were to just take strictly mastron or strictly primabolin and compare them to one another,

again, looking at rates of genetic clearance, how everyone expresses the androgen receptor, the CAG repeats, everything else with that.

A broad assumption would be, in theory, possibly that they all build muscle at the same rate.

But in practicality, people are taking two or three different steroids at one time.

That

you can't say that if I swap mastron in, it's going to build the same amount of tissue as if I took primobolin because it's a very

broad assumption from a distinct assay in an animal.

Simplistically, in interior, you could say yes, but

in the grand scheme of things, probably not.

And this is again where this whole argument stems from Mastron not being an anabolic versus primabolin.

Mastron,

you know, people will argue can't build muscle tissue.

When we look at Mastron's molecular structure versus primabolin, it's it's very similar

aside from

a substitute that's been made on the A ring, and then the other one has a double bond.

Aside from that, they're relatively similar structure-wise, but then when you look at the molecular weight, the molecular weight of the compound is slightly different.

And this is what I try and get people to think about: that when you take a medicine or a drug or an anabolic, whatever way you want to phrase it, whatever whatever milligram you take of that compound,

you're not taking it for the milligram.

You're taking it for how many molecules of that drug are in that milligram dose.

And we're talking billions, quadrillions, trillions.

It's a huge number in that small dose.

That

when we compare different steroids and their molecular weights, they vary quite differently.

So

if you look at

nandrolone, you've removed that 19

metal group, the CH3.

That changes the molecular weight of the compound versus testosterone.

So now you have

a compound

that has,

in theory, a lower molecular weight than testosterone.

So if you have 100 milligrams of nandrolone and 100 milligrams of testosterone, there's a lot more molecules in 100 milligrams milligrams of nandrolone than there is in 100 milligrams of testosterone because of the molecular weight difference.

So

you couldn't ever say if I take 100 milligrams of nandrolone and I take 100 milligrams of testosterone,

that they're the same because the number of molecules is completely different between the two.

And that's where in theory you start to see nandrolone, trembolone being potentially stronger drugs because they have lower molecular weights, which means there's more molecules in that dose, and more molecules means more interactions with the receptors.

So

when we're looking at compounds and milligram dosages,

in reality, it should be well, how many molecules are in that set dose?

And this is something I spoke about years ago.

I know Steve has done a video on it before about like look at exactly how many molecules are in that compound based on your dosage, and then you can't really strictly compare

apples and oranges.

You can make a broad assumption that okay

on paper, it looks like most

steroids will

have nitrogen retention at the same rate as another one,

but then you have to consider

that is just in a

simple system, not in humans where you have,

I guess, liver metabolism, kidney excretion, other things that impact steroid hormones binding,

that it sounds great as a discussion point.

And sometimes it can be an easy way to try and explain to someone when they're like, what steroids do I choose?

And you're like, well, in theory, they all build muscle the same way.

Practically, when you start stacking steroids, and this was the whole beauty of Scott's talk,

is that this polypharmacy makes it so murky that you can't say that

because I added in this compound, it's building more muscle than primobolin, or it's building more muscle than nandrolone.

So it's very hard to give

a direct answer that Mastron is going to build the same amount of muscle as any other steroids, but it's always a great discussion point.

You don't happen to remember like

his comparison of the amount of molecules of TREN versus EQ versus Primo, for example.

So I have a post that I've done.

I can send it to you if, and if you want to overlay it here, which shows the number of molecules between

testosterone, nandrolone,

I think Tren, Mastron, and Primobolin,

and why

when we sort of look at Primobolin to make like a very abstract statement, where Primobolin is a relatively

harmless compound, where it's like

it's not as strong as the other guys to speak, if you want to put it that way, that like conversation terms,

100 milligrams of Primo versus 100 milligrams of testosterone,

there's millions upon millions less molecules in 100 milligrams of of primo versus 100 milligrams of testosterone.

So when you take 100 milligrams of primobolin, you're exposing your body to a lower amount of androgens versus 100 milligrams of testosterone.

It has different metabolic pathways to testosterone.

So it can be

the tree position of the steroid can be reduced.

So it has that tree keto position reduction that might not necessarily happen with testosterone.

And so when you look at primobolin being a quote-unquote safer compound,

on a milligram basis, it has a less number of molecules than testosterone, and it has a higher potential rate of metabolism within our muscle tissue before it even affects an androgen receptor.

So when we're looking at

when we're trying to assess

building a stack, you never really think that, well, 100 milligrams of Primo has less molecules than testosterone.

It's just like it's 100 milligrams versus 100 milligrams.

And really, the 100 milligrams of Primo is way lower molecular number than 100 milligrams of testosterone.

And conversely, you put 100 milligrams of nangelone in as more molecules than the other two.

So

you can see then you're not

if you're really like pedantic or you're really nerdy, you could probably work out like the molecular number on

you know the milligram level and how they're all balanced molecularly.

Then, from that perspective, if you put in, it could work out as abstract of

to make an example, like 134 milligrams of primobol into 96 milligrams of testosterone.

No one's going to do that.

It's going to be too difficult to measure it out, and it just creates too many layers of complexity that most people won't have the patience to work out.

You know, even myself included, I've never sat down and thought, I'm going to build a cycle based on the number of molecules.

But you have to think that way when you take these compounds, that's what you're exposing your body to: is chemical molecules that are going off to interact with receptors.

And inside that 100 milligrams, there's a defined number of molecules.

Gotcha.

Cool.

Sorry, it was perfect timing that just as you were saying that

the story expired.

Definitely intrigued to see that, and I feel like people should definitely watch Steve's video, whatever the video is titled.

I feel like that would be super neat.

I feel like I would expect Trend to just be in the billions.

It's great talk.

All right, found it.

Danny Brian07 asks ancillaries for HDL and LDL control if a Zetamibe isn't doing enough?

Great question.

I guess we're going to come back to our best friend again with oxidative stress.

When we're looking at cardiovascular disease protection or prevention,

ancillary-wise,

we have to view that when we take androgens, we're going to produce more hepatic lipase, which is the thing that breaks down HDL.

So

it is a losing battle to do anything to try and improve your HDL level if we're already suppressing its production or we're breaking it down very quickly.

What your strategy should rely on is improving the HDL's function or its receptor function to work better.

HDL,

really, the only thing thing that has shown good promise aside from like basics, like doing your cardiovascular activity to help raise HDL production.

To be honest, again, if you have high levels of testosterone or androgens, you're going to create hepatic lipase, which again is just destroying the HDL that your cardio is trying to create.

That your strategy really should be around how I can improve protecting my LDL from being oxidized

and what can I do to reduce the expression of apolipoprotein B which is the protein on your LDL that basically tells the LDL to dump its cholesterol into a cell.

So when you take something like a statin, a statin blocks cholesterol from being manufactured and as a consequence you block

Apo B from being created.

ApoB would be on your LDL particles.

So the statin is really trying to reduce your Apo B expression or your Apo B level than directly going to LDL as the

root cause.

But there's a particular reason why the stands are normally having a very low success rate, right?

Like you're basically just delaying.

And this is it.

And this is because when you

look at what drives arthrosclotic plaque production,

Apo B is one of the things.

The Apo B receptor, you bind the Apo B, and the LDL dumps its cholesterol off.

And if that happens to be an artery inside the arterial wall, and that interior then leads to a plaque accumulation alongside what we consider an immune dysfunction, in that when our LDL becomes oxidized, so if an oxidant like a free radical damages your LDL in your bloodstream and it's just doing its job of carrying fat.

It's just a bystander.

When your LDL gets oxidized, it's now unstable.

So free radicals basically steal an electron off a substance.

And now you've basically created a

best way to describe it, like a wibbly-wobbly LDL particle who's going to try and look to stabilize itself by taking an electron from someone else.

So it becomes like, who can I rob an electron from to stabilize me?

If that LDL can't stabilize itself by taking an electron from somewhere else, and this is where vitamin E comes in, vitamin E is the guy that comes along and offloads an electron to the oxidized LDL and goes, I've got you, here's your electron, you're now stable.

And vitamin E takes an electron from vitamin C.

That's how vitamin E is protecting your LDL from being oxidized.

But if the LDL gets oxidized and you don't have enough vitamin E to protect it,

your immune system, your macrophages, the little pac-men, come in and eat up that oxidized LDL because it realizes if that's in the bloodstream, it can damage the arterial wall.

It could take an electron off the arterial wall, take an electron off a nearby LDL particle and just set off a

guess a cascade of one to the next being oxidized.

What ends up happening is you create a foam cell whereby the macrophage, little Pac-Man, eats the cholesterol, and now it's sort of sacrificed itself where it itself has become very, very sticky.

But these foam cells know that if they stay in the bloodstream, they're going to cause their own level of dysfunction.

So they leave the bloodstream into the arterial wall space.

And slowly over time, these foam cells aggregate and stick together and clump together with bits of calcium to form arctosclerotic plaque.

And then that presses in on your artery, creating a bulge.

And then that bulge forms a huge amount of pressure.

So, if you imagine your arterial wall is getting smaller and smaller, these bulges are building in.

And then they rupture.

And then that big, massive mess of foam cells and calcium is in your bloodstream, your immune system, more so your platelets see this big, massive, massive dysfunction and they clot around it to try and protect the body.

And that's the clot that forms with

like a thrombotic clot that goes to your heart or goes to your brain for a heart attack or a stroke.

So, if we're looking at offsetting

arterial plaque formation and ancillaries for this,

azenamoib is more so working locally in the gut.

So, you have

to not get into all the boring science of it, you produce cholesterol in your liver, most of it goes to your gut, and then most of it from your gut is reabsorbed into systemic circulation to bring fats to your cells.

And then HDL brings the fats from your cells back to your liver for recycling outs, like excreting out in your colon.

When you take a zenamibe, you're trying to block some of that cholesterol reabsorption so that you basically poo out your cholesterol.

You have other types of medications that bind that cholesterol into your feces and you poo out the cholesterol, so you have bile acid sequestrants.

Very like old school medicines where they approached dietary cholesterol as being one of the root causes of heart disease.

And if we can pull cholesterol out of the gut, we're going to protect the body, which is useful,

but

zetamoib isn't going to come at the angle of if you're making Apo B protein on your LDL cholesterols, you're hoping that some of those guys are being pulled out from the gut with the azetamobe than going into circulation.

What

we should look at if you are at high risk of APOB expression

with high LDL is potentially looking at a statin.

And as crazy as it is, when people argue with statin use and

what risks come with them, there are most definitely risks with their usage.

But if we can selectively maybe utilize these statins

in an appropriate way to lower that cholesterol's production, so you're lowering the APOB

as a long-term strategy alongside managing oxidative stress, you're blocking the LDL and the APOB.

And how we tie this together with that sort of failure rate is most people who take a statin just take the statin and never focus on the oxidative stress and the damaging of the LDL.

So, to put it in perspective,

let's say you have a cholesterol level in US terms of 200 or 210, like a really high number.

And in theory, a statin lowers cholesterol production by about 50%.

That's what they roughly estimate it at, is about 50%.

Most statins have efficacy at blocking the key enzyme that creates cholesterol.

But let's say that 210 level of LEL cholesterol is being oxidized 100%.

And if that continues without a statin, your primary risk of having a heart attack, let's say it's two and a half years.

Taking that number from 210 down to 100, so let's just have or 105, whatever way you want to put it, but you're still oxidizing 100% of it.

You're still generating plaque from that oxidized cholesterol, but at half the rate, at slower the rate.

So, really, you've bought yourself maybe another two and a half years.

So, whilst you're heading for a heart attack in two and a half years, you probably have a heart attack in five.

And that's where you see a lot of statins still attribute themselves.

I mean, if the success rate of a statin

primary risk prevention, but stopping someone from having a heart attack,

absolute risk reduction is about 3%,

which then tells you the bigger picture is lowering the cholesterol number plays a part, most definitely.

But how that cholesterol is being managed in the bloodstream, whether that is oxidative stress or a lack of antioxidants, is probably more important to consider and the influence then that our antioxidant control has on our discriminatory formation.

You have other medications to consider with

heart disease risk that are becoming quite popular, although it is very specialized in how they can be prescribed and they are the PCSK9 inhibitors.

With blood work, again, most people look at LDL.

They can look at APOB and they can check their LDL.

They're the main things.

And what I love about the US is it's relatively easy to get an NMOR particle analysis to see whether you have large or small LDL particles, which is another context to take into consideration.

Because if we have very small, dense LDL particles

being the majority of the LDL fraction, they're relatively small enough to pass between the cells of the arterial wall to deposit themselves.

That

when we look at PCSK9 inhibitors, we're basically blocking one of the core receptors in the liver that tells cholesterol to be made, to put it in a very simple way.

And this is also a way of controlling lipoprotein A.

Most people

will probably have low genetic susceptibility to LPA, But those who have high LPA,

there's very little that can be done to address it.

And whilst there's a paradox that if you take a lot of steroids, your LPA level will fall,

that's a very poor assumption because in the paper that seeing this drop in LPA level from a high level of steroids, the LPA level was still very, very high.

So to say taking more steroids will lower your LPA

marginally, but it's still going to be out of range.

It's not a strategy to fall for.

That PCSK9 inhibitors alongside some form of statin or some way of controlling cholesterol production can lower LPA from being made.

So again, if guys are doing blood work, listening to this, check your LDL, check your HDL, check your APOA.

So, this is the protein on your HDL that helps it do its job.

And that's where we should target our support on HDL: is making what HDL we have functional.

So, again, protecting HDL from being oxidized.

And that's where strategies like citrus, bergamot, all these flavonoids and polyphenols play into it because they help protect dysfunction against your HDL.

They do have a benefit in a certain capacity to stimulate your HDL from being produced, but

it's madness to think that if you're on a superphysiological cycle and you're taking 2,000 milligrams of citrus bergamot, that your HDL is going to be above 40 or above 1 in UK measurements due to taking a supplement.

you're not going to circumvent the biology of what the androgen is doing by destroying your hdl and that that lowering of hdl is where the consequence falls where your liver tries to compensate by making more ldl so when you have a drop in hdl to try and maintain the the balance of the lipoproteins you'll often see hdl go down by 10 and ldl go up by 10

gotcha And that's sort of where your strategies rely on antioxidants to offset the oxidative stress.

You can do stuff like azetamibe or fiber, increase your fiber intake, like psyllium husk, apple fiber, stuff that will bind dietary cholesterol in your gut to try and excrete some of it out alongside what you make endogenously.

Um,

if there is a needs basis there for a statin with familial cholesterol risk or high APOB,

don't discount what that could do for your long-term cardiovascular disease risk prevention

but bear in mind that it's not

it's not going to have a successful or guaranteed outcome 100% of the time that you know if we look at that three percent

there's other things that have to be paid attention to that this is just something to

be in your arsenal that you're not afraid to consider because there can be again a bit of hesitancy when it comes to using medications like this, which is completely warranted because you see it affects to CoQ10, to the mitochondria, like statins can be mitochondrial toxic

that you could be creating a whole host of problems.

Again, you need LDL to transport fats through your body.

Your brain is no different.

You need LDL to transport fats to your brain.

That if your LDL value is extremely low, you're not able to facilitate fat transport to your brain.

So there's a healthy balance that if you do use them,

like an AI, you don't want to bury your cholesterol to basically nothing and champion it.

You need a small amount of it to help with your biology.

Gotcha.

Okay.

So I guess you just using me as an example, because I think

I feel like I land a little bit more with a higher percentage of the population, but someone like me who, when you're running something, when you're running gear, has a lower LP little A or a low LP little A, but then

has

obviously high LDL from the gear that you're running and then also a high APO B.

And in my units, in the blood work that I get from Lab Corp here in America,

they recommend lower than a level of 90.

However, I've had some personal conversations with Derek, more plays, more dates.

Obviously, he likes to err on the side of extreme caution.

So his ApoB levels recommended were really surprisingly low.

I can't remember what he said.

I think for bodybuilders, just something around like 40 or something he'd recommend or 50.

But and then he said, like, if you're, he had a conversation with Peter Attia, if you want to be super extreme and be like, oh, I want zero risk of cardiovascular disease or whatever in the future

to aim for like 25, which is,

I feel like, going to be like impossible for most bodybuilders, honestly.

In theory,

it

most probably would be, given that

if a statin intervention is giving you a 50% reduction,

at most maybe 60%

decrease in LEL production, as a standalone therapy, obviously at PCSK9 on top of it, that will lower a few more percent.

You add in azetamide from a gut perspective, another few percent.

It's not

impossible, but given that we're dealing generally with LDL values that are quite high, above 150 anyway, in US terms or above 3.3 in UK terms,

an APOB value of like 25

is going to take a lot of diligence to get down to that level.

But in saying that, you're looking at like zero mortality risk of APOB B contributing to your plaque formation

which

still allows a small amount of your LDL to be oxidized if you're not paying attention to the other thing of oxidative stress which I'm sure if you're going to all that trouble to completely diminish the risk from ApoB and LDL that you would be doing strategies to offset the oxidation of it.

It would be just a bit ironic to pay attention to all these strategies.

Put your APO B to 25, but the LEL is still, although it's a low number, is still being oxidized and then triggering foam cells to be produced that might take years upon years for plaque to form.

But the irony would be maybe if you went and then done an MRI and you found that there's soft plaque in your heart from doing all these strategies, and it was because you didn't pay attention to one of the pillars with it being the oxidative stress.

I guess

if someone is worried and they're approaching like their 30s, not to throw like age numbers, but they're approaching their 30s having done bodybuilding in their 20s.

When you sort of reach your 30s with bodybuilding, from my own personal experience with, like, I never had aspirations of being a pro, so I can't say when I got to 30, I was like, oh, it's now or never.

I've got 10 years to try and get into the pro league, and then I've got maybe another 10 years till I'm 50 50 to be a decent pro.

When you get to that age, bodybuilding is probably still an integral part of your life if it grew with you during your 20s.

But now you're starting to think about getting married and having kids and career, corporation life, or whatever, your own business,

that your focus on health shifts a little bit from your view in your 20s.

If I do these supplements, I live this lifestyle, there's very little that can happen to me.

Doing something like a

CT angiogram with contrast, so doing a CT scan of your heart with contrast will basically show up if there's any soft plaque, any calcification, or any, I guess, aggressive plaque that's formed in your heart.

When we look at calcium scores,

calcium scores look at

long-term plaque that has calcified and that tends to be plaque that has been in our body for at least five to ten years.

If you do a CT scan for a calcium score at like 30 and it comes back zero, that you've got no calcium, that you're you've got basically nothing's detectable,

that's looking for just calcium for long-term plaque.

Unless you've really done a lot of very like negligent things during your 20s, the instance of having calcified plaque heading into your 30s,

it's not uncommon, but if you are a very diligent bodybuilder with supplements and everything else, it's unlikely in my view.

The other side of it is if you do it with contrast,

you'll start to see small, soft plaque developments where you start to see some of this plaque form,

but not necessarily be an arteroma where there's an actual lesion with plaque forming inside it.

That

doing something like that then gives you like a 10-year risk analysis of if you do the CT scan with contrasts at age 30, it's saying roughly what you've done the last 10 years of bodybuilding has had minimal impact to your cardiovascular disease risk for the next 10 years, provided you continue doing what you're doing.

That

an echocardiogram, whilst everyone like champions this from a left ventricle hypertrophy perspective or septum thickness, it's very useful, it's not invasive, it's trackable, you can compare, you know, do an echocardiogram every two years, it's not a massive exposure to radiation.

A CT andiogram, with contrast, if someone is seriously thinking about going into their 30s on bodybuilding, haven't done it for a significant portion of their 20s on exposure to androgens and whatever else, doing that as like a sanity check of, okay, I'm going to really see what's going on in my heart based on my blood work.

And your blood work,

your blood work could have had skewed LDL

and relatively

lowered HDL for a number of years as a bodybuilder.

And you do the CT androgram,

and the contrast agent finds that there's nothing gone wrong with the heart.

There's no plaque formed.

Doesn't necessarily mean that that skewed blood work is healthy.

It just means that whatever you've done strategically in terms of the management of how that cholesterol is operating in your body has yielded a low risk.

But it still gives you an idea of

making a decision on whether or not I want to pursue bodybuilding for the next five years.

Because someone might have a risk tolerance that if a small amount of plaque is found with that CT androgram, even if it's soft plaque, that's the end of their career.

I'm done with bodybuilding, it's not worth having a heart attack if I keep doing what I'm doing.

It's a useful thing that guys should try and consider if they have access to or they have worries about their blood work.

Again, working with their primary care physician to maybe refer them for this sanity check.

But again, going back to the difference with an echocardiogram, a CT scan is basically a massive x-ray.

So there's consequences of being exposed to that radiation.

You know, everything comes with risk, so it's not like I'm going to do a CT scan every year to keep on top of my heart health because it would probably not be the most healthy thing unless there was a medical necessity for you to undertake that risk.

But supplements, ancillaries, we sort of covered like the medication side of things, nutrition, look at polyphenols, look at antioxidants, you know, simple things like turmeric, curcumin, CoQ10,

grapeseed extracts, Astoxantin.

I mean,

when I was looking at formulating our heart stack, I just basically looked at what were a lot of the key polyphenols and antioxidants that potentially could be useful to humans' nutrition, looked at potential dosages that could be considered, and basically put 15 ingredients into the one product to try and make sure that I was covering as many bases from a nutrition perspective that might be lacking.

But again, just to close it, that

when a supplement like HeartStack,

let's say your nutrition was

very devoid of overall nutrition and very ultra-processed and whatever else, thinking that taking a tub of heartstack per month and continuing to eat crap basically, that the stack is protecting you from what you're ingesting is a very bad way of thinking.

If we're looking at nutrition as being like the pillar of our health, that you're using the supplement to enhance your nutrition.

If you don't like having grapefruit or you don't like having certain vegetables or fruits, you're using this as a supplement to get them into the diet, not as like a

again, I'm going to take

ethanol, which is like all the forms of vitamin E as a supplement to offset me and burgers and pizzas all the time.

That it's it, the supplements have to come into the equation of supporting the pillar than being the insurance policy.

I guess what I'd hate to think that someone's buying supplements thinking that I have to take this product because it protects me from X, Y, and Z.

That can be a very slippery slope, both financially and psychologically.

Yeah.

And I think,

as I discussed with Austin, Austin Stout, like, if it's an issue to have a certain amount of vegetables or fruits or even specific vegetables that maybe even irritate your gut, at that point, if you're still looking for a supplement, I mean, it's even beneficial for you to at least supplement with some greens there.

Obviously, you should still try to make sure that you have

you're meeting your daily intake of fiber, but

you know, worst case scenario, and you need a supplement with something, like you still need a supplement with the fruits and the vegetables in some sort of sense.

Absolutely.

Cool.

Let's ask this one last one.

And then there are so many questions, but

I'll ask that afterwards, basically.

But Henry Pham asks, is the mitochondria stack of SLU, MOT C, and methylene blue beneficial under 30 years old?

Hey, that's a very good question.

I mean,

I have inadvertently brought this trifecta to the bodybuilding industry that

was a personal experiment.

That's the way I always explain it.

That

what I put out was what I've personally done.

And people, if they want to trial it on their own research, that's

their own discretion.

Under 30,

let's think about where we are in terms of our development.

And

let's say that this 30, well,

let's say they're 25.

Let's not even say they're near 30, where they're at that moment, let's say they're 25,

they have been following a healthy lifestyle, they've been following like some of the core basics that we all preach with steady nutrition, sleep, training, everything else.

Do I think that considering something like mitochondrial optimization should be at the top of their list?

Probably not.

Unless

they had some signs of mitochondrial dysfunction.

But

the argument to that would be fix what's causing your mitochondrial to be dysfunctional than looking to optimize how they work in the body.

And if we even keep this as a natural person,

if we look at how we began the conversation with mitochondria with hormone creation, neurotransmitter creation,

at 25,

would they have been exposed to so many things that would cause mass mitochondrial dysfunction?

Probably not.

Although, again, you have to look at the environment.

Have they been exposed to toxins, pesticides, all these things that we wouldn't even consider that could be causing issues with their mitochondria or their gut health.

In that instance, if we help support the creation of more mitochondria,

but there is dysfunction happening from the environment, you're creating them for them for them to be effectively poisoned or to be harmed.

And then they produce reactive oxygen species themselves, or their dysfunction knocks onto

DNA repair or the energy required to repair our cells and our DNA, that boosting the number of mitochondria again is probably chucking petrol onto a fire.

That

when we're doing this sort of mitochondrial optimization,

you have to think about, well, what is the end goal I want from this, like with the brain optimization?

If I increase the number of mitochondria

in biogenesis or I create more of them, I'm now creating more factories for energy production or neurotransmitters or hormones.

But I'm now also increasing the number of guys that make pollutants in my body.

So whilst I'm getting a massive benefit from having more factories to make all this material, they're creating a lot of waste that can I accommodate the waste that they're creating or do I have the practices to accommodate recycling the waste that they're creating.

And then you have the other side of it, which is improving the efficiency of the mitochondria, which is

how they're able to utilize glucose or fatty acids for glucose oxidation or fatty acid oxidation.

And that then comes back to what's called oxidative phosphorylation, where we're using oxygen to burn glucose or burn fatty acids and beta oxidation to feed into the electron transport chain.

That

if again, as the mitochondria efficiency to create more energy improves,

in theory, if we had a supported system of antioxidants to help keep the fires under control that are happening from the energy creation,

improving their efficiency is probably a no-brainer because you're improving how they're producing the energy in a more efficient manner.

But then that relies on

how your body is able to metabolize fats and glucose and bring them into the cells for the mitochondria to use, which then goes back to like insulin sensitivity and

how you digest and transport fats.

That it's not just straightforward that you get all these benefits, like you take SLU, you're stimulating more mitochondria to be made from the estrogen receptor-related

alpha stimulation, or you're improving how energetically efficient they are at making energy inside the mitochondria.

If

overall, the mitochondria being poisoned, to speak, are dysfunctional.

It just doesn't make sense to take something to basically, you're just keeping things in a level playing field.

You're putting something in that is getting you nowhere, really, overall, other than wasting money, in my view.

That you'd want to then try and remove the source of the pollution that's poisoning the mitochondria, if you want to put it that way, and then look at making them more efficient or giving you more energy out of it.

And that's, you know,

it's where we have to be very careful when we're talking about all these crazy things.

And people look at what I've done with this sort of trifecta and the amazing results that came from it.

It was

because I had to think about: do I have these underlying support pillars to allow me to push hard on these guys?

Most people will just look at the supplement and think I'm going to try that without taking a step back and thinking about the consequence of if I do this, what is going to happen at the end?

And again, it comes back to again the B complex.

You have to know what's going to go beautifully or what's going to go tragically when you do these things.

That

it's

again, we're talking about something that can dramatically change a bodybuilding prep.

And I proved that last year where you know you can prep on very little to speak.

You can get away with eating 3,400 calories on a training day, a body weight of like 202 pounds.

You can get away with 20 minutes of cardio and 10,000 steps.

That's on the surface of it, it looks like an amazing bodybuilding prep.

It's like that's some per person's off-season that you're eating the food for

because you've understood that I've built this pillar of support in these guys.

And once I turbocharge them to speak, they're going to give back positively provided I keep up with them, provided I keep feeding them.

So, again,

this is where when we're looking at how we burn body fat and fatty acid oxidation, one of the primary things that helps fuel fatty acid oxidation is glucose metabolism.

So

this is where for like in a prep and this is why it never made sense to me if your bodybuilder is consistently restricting calories

expecting well from carbohydrates expecting your mitochondria to burn fatty acids more efficiently because you've created this energy deficit from carbohydrates that are fueling the mitochondria in a certain aspect to produce energy that feeds into fatty acid oxidation.

You're basically blunting your ability to burn body fat.

So

you now have to view: am I fueling these guys adequately?

Am I eating a high carbohydrate diet?

Am I doing everything from a NAD, like the vitamin B1, B2, B3 perspective, magnesium?

All of these basics that I've never really spoken about.

That you have to understand this bigger picture before you start putting all these guys in.

But once you do have those guys in place, in theory, these things on paper

work

like magic.

It's not magic, it's playing off biology.

But a guy under 30,

I'd be saying

to me,

if we were very curious, I'm not going to stop someone's curiosity

for a what if, but it's really unlikely that they're, they're going to require it.

If they're looking to,

I'm going to use the word like cheat.

If they want to look at like cheating a prep, if they have everything in place, like what we talked about, well, then you've got.

nothing to lose other than your own personal risk and your own financial risk of getting the products and spending money on it.

That

I just, if someone came to me and like, I want to try this stack, again, it comes back to the basic questions of like, what's all the foundations underneath?

It looks great.

You know, it's this new fad to speak,

but it doesn't necessarily mean that

they require it on the surface level.

So it's just, I'm always just very cautious.

Okay, cool.

I guess that would be another cool argument, too, for, for,

I guess, advocating having a little bit more of a balanced diet when you're prepping, when you're cutting, rather than

there is a lot of people that will crash their carbohydrates really low and keep their fats fairly high.

I know originally it's

a better method for a hormonal perspective, especially if someone's not supplementing hormones.

But I guess if you're a bodybuilder,

it's not always a terrible decision to go the old classic bodybuilder route and have some fairly low fats and a more carbohydrate intake.

I mean, when we're enhanced bodybuilders, the whole fat intake, yes, you need a level of fat intake for cell membrane repair.

So your cell membranes are made of fats.

You need a certain level of fats for brain health and for

brain energy on top of carbohydrates.

Which I think some people can definitely tell whenever they're crashing their fats a little bit too low.

They can feel that when they're fat.

I mean, the way I set up my prep last year was

I

on average on a training day, I had 390 grams of carbs.

My fat intake, I think, was 45 grams, and my protein was about 280, 290.

And I was at a body weight of

the stage pictures in the end, I was 87 kilograms at weigh-in, which is like 196.

But all my fat came from fish oils or supplemental sort of sources of fat like macadamia nut oil.

Um, I kept all my protein like lean sources

with lactose intolerance.

I use we have a vegan isolate product.

I use that as my sort of protein shake.

But I've always lean into like fat intake strictly from polyunsaturated omega-3.

So

I'd have at one meal, I'd have six to eight capsules of our omega-3 fish oil products, and that's giving you three to four grams of EPA and DHA, which is what we sort of look at as a clinical requirement for EPA intake.

We have another like chewable fish oil product.

I'd do another serving of that at the next meal as a fat source with maybe five mils of macadamia nut oil.

And then the next meal, again, some omega-3

fatty acids with the macadamia nut oil.

And that was pretty much it.

That yeah, that was my fat intake.

And the omega-3s were playing into brain health and to membrane health, but

like that, that works for me personally.

Some people who take in a massive amount of fish oils can run into blood clotting risks.

The cell membranes can become very, um,

what would be the best way, very flexible.

So, they lose their rigidity.

So, there are risks to using a lot of omega-3

fatty acids as a supplement.

Yeah, that's what I was about to ask: is there like a

number that you would put a cap at?

To be honest,

really

a very good friend,

he's not as active on social media anymore, but Ben Kant is a very well-known Australian nutritionist.

And his perspective was

it's like one capsule of omega-3 omega-3 fish oil for every sort of missed serving of oily fish per week.

Don't quote me exactly, he has some good content if people go to his page.

He's very interested in omega-3 fatty acid intake and its effects on health.

He's a big proponent on like eating mackerels, sardines, you know, fish that are going to provide you with your omega-3s as opposed to supplementing.

That

the other side of it, then to pay attention to is

not all fish oils are created equally.

That the total oxidation, the actual amount of the oil that has been damaged by oxidation is important because you're buying cheap supermarket fish oil to pick on somewhere.

It might look like a bargain.

It might fill some nutritional voids,

but the oxidation of of that product could be quite high.

That

there's been research papers done on commercially available Omega-3 products.

They analyze the total oxidation of these things that are on just regular retail shelves.

And the oxidation values of some of them are like 40 and 50.

That above 26 is the acceptable limit.

The one I really recommend is the one I'm taking currently is Carlson's, the finest fish oil.

And they also have the options that you can just get it from a bottle so it doesn't have to be in pills where it's a little bit more easily oxidized sometimes.

And that we've won Omega Pro, the chewable version.

The totox of that is two, two to three.

It's basically to like, as soon as it's as soon as the fish is caught, it's manufactured, put it that way.

As soon as it's caught in the sea, they manufacture the oil and distill it.

So it hasn't got a chance to encounter transport issues, oxidation, and it's stored obviously in,

I guess, sunlight-protected containers and everything else.

That

paying attention and looking at that,

I guess, transparency when you're buying fish oils, that pay attention,

ask companies for Totox values.

Like, I got questions all the time of ours.

Have you got a Tote Tox value?

And I'll send the two values of our two products and the yard below the conformed 26.

Whereas other companies might be a bit hesitant to tell you that.

Just bear in mind that this then is a source of oxidative stress, that you think you're taking something that is a healthy supplement, but the consequence on your health long term is

something that you've not even thought about.

Awesome.

Well, I think, um,

I think that's a good place to wrap up this podcast for the day.

Yeah.

We had a record-breaking time.

it's uh quarter to 12 and

at night here approaching midnight so uh

i'm sorry about that

i'm uh i'm like we talked about tonight is most definitely going to be a melatona night with the the lights on here and wind down for an hour oh shit

oh man um well i really appreciate you for coming on man and i'm sure the the audience does too um and if you're up for it i have a fly ton of questions here in the q ⁇ A.

Plus, I also have my own curiosities, things such as like discussing peaking for a show with you and also GH.

And some of these people would love to hear about more things regarding fertility,

insulin, just a bunch of other topics that I think are all super interesting.

It'll be a pleasure.

Pleasure as always to come on and chat.

Awesome.

Awesome, man.

Well,

is there anything else that you would like to say or promote or whatever before we leave?

No, just thank you very much for the second opportunity to come on.

And if people want to, I'm sure they know where to follow me on Instagram at DNSTM and our supplement company supplementneeds.co.uk.

So

awesome.

Well, thanks for coming on, man.

Thank you.

Thanks a million.

I hope you get some rest tonight.

You too for this evening, anyway.

Later, man.

See ya.