Barbell Shrugged - [Cholesterol] How to Read Bloodwork for Lipids, Triglycerides, and Fatty Acids w/ Anders Varner, Doug Larson, and Dan Garner Barbell Shrugged #670
Episode Date: November 23, 2022In today’s episode of Barbell Shrugged you will learn: What are lipids What is cholesterol The difference between HDL and LDL cholesterol Why there is no such thing as “good” or “bad” chole...sterol What are the bloodwork numbers for optimal cholesterol What is the perfect ratio of HDL and LDL Ratios for Triglycerides to HDL for optimal health Mechanisms for regulating cholesterol in the liver Why saturated fats are not bad and how your body uses them Cholesterols role in testosterone production To learn more, please go to https://rapidhealthreport.com Connect with our guests: Anders Varner on Instagram Doug Larson on Instagram Coach Travis Mash on Instagram Dan Garner on Instagram
Transcript
Discussion (0)
Shrugged Family, this week on Barbell Shrugged, we are talking about lipids.
If you have ever been to the doctor and they go,
oh, your lipid panel is off, and you're like, what the hell is that?
And they go, well, it's like cholesterol and like fatty acids and triglycerides,
and you go, you just nod your head, because you go, okay, well, that sounds good.
And then they don't really provide all of the information on what you need to do
to help lipid profiles,
especially understanding cholesterol because it's an insanely lengthy conversation
that we're going to have right here for you today.
I also want to say, friends, happy Thanksgiving.
I appreciate you all.
It's super cool.
I'd get into this at the beginning of the show,
but I've met so many of you guys over the last couple of months, uh, talking about rapid health, all the, all the
pieces of health and performance that you're trying to improve. And, uh, just really grateful
for all of the shrugged family out there. And it's super cool meeting all of you. So, um,
I appreciate it. And as always make sure you get over to rapidealthreport.com. If any of the information inspires you, tweaks your interest, and you have a desire to come and understand what optimal health looks and feels like,
head over to rapidealthreport.com and schedule a call with me, and we will get you hooked up.
Friends, let's get into the show.
Welcome to Barbell Shrugged.
I'm Anders Varner, Doug Larson, Dan Garner.
Today on Barbell Shrugged, we're talking about lipids
and what you can see in your blood work
when you get your standard yearly blood work
and what does it actually all mean.
Bros, before we get into all of this,
I gotta go talk to the people real quick.
Everybody that has come from this show mean, gross. Before we get into all of this, I got to go talk to the people real quick.
Everybody that has come from this show and has scheduled a call to talk to me about everything that they have going on in their health and performance, I just want to say thank you to
all of you guys. It has been like a whole year since we launched Rapid. And the fact that every
week we get to see like numbers of downloads and people that
listen to the show, but they're just a number to actually put a face to all the names and
hear everything that we're actually able to help you guys with through the show and the content
that we put out. Many times, this is just like four dudes hanging out on Zoom talking about
things that we love. And the fact that you guys actually digest this stuff and it makes a big impact on your life uh i'm beyond grateful for for all of you that have
have come and talked to me and scheduled a call and uh all these conversations go so well and i
appreciate everybody that uh one just tunes in two if you've scheduled a call and been interested
in our programs over the years uh specifically this past year, since we brought Dan on full time as a co host, just very grateful. I keep going, I'll get
emotional. I don't want to I want to I want to add to that, though. Let me get emotional for one
second. Yeah, I didn't know we were gonna do this, man. I know. I've been thinking about it now that
we're coming up on our one year anniversary. And it's been it's been since I do all the talking
with these people. It's very, very cool.
Yeah.
Yeah.
Yeah.
Like when I kind of came on, I think my first episode on Shrugged, my first one was like in November, but then I became an actual co-host in February.
You guys found me in a cave somewhere in a basement in Canada.
And there's a lot of people that did not know me, what I did, what my philosophy was, what I like to do, all that kind of stuff.
I have met so many amazing people through this podcast.
The people that DM me, the people that message me, the people that email me, the people say that tag me when they're listening to a show in their car or something.
This is something that, you know, like I didn't really have any exposure to before.
So, yeah, you guys are all a bunch of freaking rock stars and you make me happy all the time. Let's talk about some lipids. Cool. Dude,
what is a lipid of all the things that we talk about, especially we've been on this like
testosterone kick. I totally understand all the testosterone. Um, but when people hear, uh, about,
uh, or, or see lipids in their blood work and their doctor starts to talk to them,
not everybody really understands like cholesterol and fatty acids and,
and how,
what,
what that actually means and how it applies to their health.
If we were to provide like the bird's eye view,
the 10,000 foot understanding of like,
what are lipids?
Where do we start this conversation where,
where people just aren't going to be able to get it at their doctor's office
when they get their blood work. Yeah, well, I don't think you get much of anything when you
get your blood work done. You get seven minutes of their attention. Yeah. So if I offer a 30
second explanation here, but in all seriousness, yeah, the lipids, the conversation surrounding
lipids is it's very deep, it's very complex.
And it's so much more than just, hey, this is your good cholesterol.
And hey, this is your bad cholesterol.
And nothing kind of annoys me more than imprecise language.
Like when someone could kind of just create an absolutist statement regarding something
as complicated as cholesterol that in many ways, we're still learning much more about.
There are new theories coming out on cholesterol involved in energy formation, even the the
explanation of like what a lipoprotein is like lipoprotein, lipo fat, protein, protein, when
something is say an LDL, a low density lipoprotein. The reason why that's even formed to begin with, is because that
lipoprotein acts as a transporter. So when someone says, lipoprotein, or what's what's your LDL,
that's kind of, again, a form of imprecise language, it's really LDL C, your LDL cholesterol,
because the lipoprotein is actually acting as a transporter. And the reason why it's acting as a transporter
is because lipids aren't water-soluble.
You kind of, that's what just where I went and said,
hey, glucose lactate.
These things transport very little.
Water-soluble things transport like absolutely nothing.
Fats are, they are not water soluble. That's why you see if you put oil and water, for example, it's a lot different than the blood. But for ease of
communication, oil and water, they separate because fats not water soluble. What basically
is happening in the world of lipoproteins is your lipo is your fat. And that is on the inside. So that is
hydrophobic, because it is it's going to stay away from water, something that's hydrophilic is
water soluble, which is protein on the outside. So when you have a lipoprotein, that is an
intelligent way that the body has structured something to transport things around the body.
And from a super bird's eye
view, and this is something that I want to actually do courses about in the future,
coming down, we eat food. Food has fat. Fat is going to be converted into something known as a
chylomicron. We're going to convert that chylomicron into a VLDL in the liver. That VDL,
you could just think about the V like vehicle,
it's going to drive and drop things around the body until eventually we lose the V and it becomes
LDL. Then we've got lots of LDL and circulation. And this cholesterol, whether you are looking at
it from a pure cholesterol perspective, or from an HDL or an LDL, it is the, the, um, the, like the,
a form of life without cholesterol, there is no life. Every single cell in the body,
every single cell in the body can synthesize its own cholesterol. So that alone tells you how
important this thing is. Every single cell synthesizes it. So when somebody says things, and this kind of kind of goes back to my original point in this, in this kind of opening rant here, when someone says anything is bad, I just kind of always go back to evolution. So why would we have evolved for a million years for the body to be so stupid, that it would make something only for the purpose of being bad for
us. It's like none of that ever makes any sense. I almost swore. Don't get too frustrated.
None of that ever makes sense. But someone says insulin's bad when someone says cortisol is bad,
when somebody says cholesterol is bad, all of it's absolute nonsense. They all have irrelevant
functions. It's like, this is the absolute nonsense. They all have irrelevant functions.
It's like, this is the good cholesterol. This is the bad cholesterol. But no one ever talks
about the balance of them or ratios or how they play together. Yeah. Or like, or why they're there.
Like cortisol does very important things. Insulin does very important things. Cholesterol does very
important things. And then it's just as important to look at the entire physiology in
front of you and ask why that current balance and ratio system is in place and what potential
impacts or benefits that may have on the current context of their goals and situation. And that's
really what what lab work offers. But it's really something you can do just as a coach, even in the
absence of lab work is really just assess somebody as a whole, look at it from every single angle, and really just take the vocabulary
of bad out of your vocabulary, but also good out of your vocabulary, things are just things,
and they have functions. So we know, we know, in the case of lipids, or cholesterol, that it's not
technically bad, you just pointed that out.
But why are people saying that it's bad?
Like, what's the what's the narrative there?
Why do people think that?
Why is that common?
Yeah, well, it's pretty common because where there's common things, there's correlations.
And where there's correlations, you're going to find a lot of absolutist statements being
born where there is elevated LDL that is
associated with things such as cardiovascular disease risk. But if you look at a very, very
popular study, and I would encourage people to check it out, the Framingham study, the Framingham
study was an excellent study. And if you only look at the LDL metrics, it's basically showing you,
hey, you know, mortality risk ratio goes up with more LDL.
However, when you correct that with a healthy HDL, mortality risk tends to go way down.
The statistical significance is absolutely not near what it was in LDL alone.
So this is where the idea of ratios come into play and why I always look at things in terms of ratios like LDL
being typically, and you know, depending on what data you look at, but there's plenty out there
that would suggest LDL to HDL being at a two to one ratio is very ideal for healthy longevity and
healthy physiology because LDL can get high. But so long as you have enough HDL around
to balance out, we'll use that term, the LDL, then you have a physiology that's functioning optimally.
You just run through like all the basic numbers for like normal healthy cholesterol and what those
ranges look like. Because people probably know, know their basic numbers, like at least like for total cholesterol, people might have an idea if
they're, you know, above or below 200 or whatever. Yeah, so this is this is a good. So basically,
what we're looking at here, when you have LDL, what's what's super important to just kind of
quantify here is really just HDL and LDL, because those are the ones we really want to look at. HDL, you'll look,
see it on a typical lab that if you have less than 39, they consider that unhealthy.
But there is no thing on the lab that suggests too high of an amount, which I think is that's also so imprecise and crazy to me when I see that on the lab. It's like, so I could have an HDL of
2000. And that'd be fine. Like, it's absolutely
absurd that it would just be considered less than 39 is HDL. Yet, when you look at the literature,
greater than 70 HDL in a greater than 70 HDL in your labs using American ranges increases mortality
risk, and greater than 75 has been associated with cancer risk.
So how come the lab reference is really just saying less than 39, when you can have a really
skyrocketed HDL, and it increased certain risk ratios, like I just, that's why I've always kind
of leaned towards, hey, this doesn't make sense, I need to start formulating my own optimal ranges
here, because people aren't even talking about this stuff. But, you know, conversely, I'd also imagine it's 100 times more common to have too low
HDL than way too high in most cases, right?
Yeah.
And that's why LDL is seen as the bad guy, simply because there's no HDL around to help
clean up the mess.
That's like one of the biggest things.
LDL being elevated is usually a representation of
an underlying pathology, such as hypothyroidism can create a very high LDL insulin resistance,
type two diabetes, these things can create a very high LDL. So it's not necessarily the LDL that is the creator of the mortality risk, but rather a product contributing
a contributing factor of what was the original mortality risk. So like, for example, when you
look at insulin, we'll use insulin because that's super common. Insulin resistance takes place when
you cannot get rid of the glucose out of your blood and deposit it into your muscle
cells using a healthy amount of insulin. So then your pancreas has to work overtime and create a
ton of insulin. And that ton of insulin is being used basically as a force method to get glucose
down and deposited somewhere. The problem with that is there's an enzyme known as HMG-CoA.
HMG-CoA forms cholesterol, and that's excited by insulin. So insulin will activate HMG-CoA.
HMG-CoA forms cholesterol. So did you have high cholesterol or did you have insulin resistance,
which resulted in super physiologic levels of insulin being created, which over activated HMG-CoA and
therefore led to higher cholesterol, right?
Do you need a statin drug or do you need to stop eating like an idiot?
That's like a, there's a very real conversation to be had there.
And this also goes like, for example, in the, in the world of bodybuilding, because well,
bodybuilders will just take insulin directly and then that can elevate cholesterol and create complications there.
But if somebody is on growth hormone, growth hormone is very popular these days,
even in the non-bodybuilding population. If you take too much growth hormone,
growth hormone actually induces insulin resistance. If you induce insulin resistance, you make your own
endogenous insulin more. Therefore, you make HMG-CoA activated and you make more cholesterol.
So things that people don't even would never consider, like my growth hormone, but what
happened in my cholesterol, they're going to be looking at all kinds of different things,
but they don't have that underlying knowledge of the enzyme activation that's taking place that contributed to that cholesterol.
Shrug family, I want to take a quick break.
If you are enjoying today's conversation, I want to invite you to come over to
rapidhealthreport.com.
When you get to rapidhealthreport.com, you will see an area for you to opt in, in which
you can see Dan Garner read through my lab work. Now,
you know that we've been working at Rapid Health Optimization on programs for optimizing health.
Now, what does that actually mean? It means in three parts, we're going to be doing a ton of
deep dive into your labs. That means the inside out approach. So we're not going to be guessing
your macros. We're not going to be guessing the total calories that you need. We're actually going to be doing all the work to uncover
everything that you have going on inside you. Nutrition, supplementation, sleep. And then we're
going to go through and analyze your lifestyle. Dr. Andy Galpin is going to build out a lifestyle
protocol based on the severity of your concerns. And then we're going to also build out all the
programs that go into that based on the most severe things first.
This truly is a world-class program.
And we invite you to see step one of this process by going over to rapidhealthreport.com.
You can see Dan reading my labs, the nutrition and supplementation that he has recommended that has radically shifted the way that I sleep, the energy that I have during the day, my total testosterone level,
and just my ability to trust and have confidence in my health going forward.
I really, really hope that you're able to go over to rapidhealthreport.com,
watch the video of my labs, and see what is possible. And if it is something that you are
interested in, please schedule a call with me on that page. Once again, it's rapidealthreport.com. And let's get back to the show.
Hypothyroidism is another one like just I just want to kind of cover blanket audience,
blanket audiences here, because we actually got a lot of feedback on that thyroid episode a while
back, and we could do a million more in the thyroid. It's a fascinating topic. But what
people don't know, before we move on to thyroid like along with
that like if they're they're producing way too much cholesterol by by taking insulin and whatever
else then simultaneously if they're taking a lot of anabolics don't your hdls oftentimes like take
a take a huge hit and go way way way low at times that'll that'll happen with anti-estrogens yeah
so like if you're taking anti-estrogen compounds which a lot of guys have to, a lot of guys
actually take anti-estrogens even if they're just on TRT.
So they're doing TRT basically improperly, which is resulting in estrogen dominance,
which is resulting in a need for anti-estrogens and anti-estrogens lower HDL.
So then it's not necessarily that your ldl
will go really high in these scenarios it's that your ratio will go off because you're suppressing
hdl in that yeah for people's hdl is getting down to like five like like super low in some cases
extreme you're saying below 39 is is really low and like getting down to single digits is
bananas and get and below 39 like uh i actually call them catch potato reference ranges it's not
very nice but it's just something that's just stuck in my head is that um yeah you know something
i say to my athletes is if you want to be as healthy as the average person use their reference
ranges so the reason i'm saying that is, is that is,
if you are less than 39, that's the couch potato reference. So you're you are at there,
if you're getting to five, then you're 35, you know, 34 points below the couch potato,
bottom end, let alone what would be considered optimal, which is really 55 to 70 in most populations for
the greatest protective effect with minimal risk. Yeah. So if you're a person that has,
quote unquote, high cholesterol, but then your HDL and LDL ratios are fine, even though you're,
quote unquote, high, you're still healthy. What are those ratios again? Is it 2 to 1, LDL to HDL?
Yeah, typically you want to see 2 to 1, LDL to HDL
for the proper partnership to be taking place.
Another good ratio is actually just total cholesterol to HDL,
and that's a 3 to 1.
So if you add a 3 to 1 and a 2 to 1
with respect to total versus HDL and LDL versus HDL,
then you're in a really good spot. You really want to know both those. Like if you're just
going to LDL and HDL and you're, if you're, I just had the example of having high cholesterol,
which is LDL, HDL, and triglycerides. And so there's one additional metric there that's not
being factored into the HDL LDL ratio. So so if you you really want to be looking at both of those
ratios not just not just one or the other right um total cholesterol to hdl and ldl to hdl yeah
right yeah absolutely and then even in the world of triglycerides like that's i think this is i
feel like i say this every freaking episode but i feel like this could also be in multiple episodes
is that try is this like like physiology like it's complex yeah yeah yeah you can't write it
on a napkin or do it in one podcast but we can say good or bad that's the truth here um no so
i'm glad actually doug brought that up so when you look at the literature and you elucidate mortality
risks uh with ratios triglyceride to hdl should be less than 3.8 to one. So you can actually incorporate
triglycerides right into the equation as well. And not everything is going to be perfect,
but it's good to be close to these things and at least use them as a proxy to know where you're at
for certain risk ratios, just like you would want to with any other biomarker for for health in any context. So how does diet influence these numbers,
like eating straight up eating things with cholesterol? I know people like used to not
want to eat egg yolks and whatnot, because it has a lot of cholesterol in it or shrimp or whatever
it is, because they were worried that's going to raise their cholesterol and give them a heart
attack or whatever. So there's directly eating cholesterol or just eating too much saturated fat
too much sugar, like how does how does intake affect your blood chemistry here?
Intake, it's like a, it's a bit of a mixed bag because your liver, so every single cell
in the body synthesizes cholesterol, right?
But certain times, certain cells have a higher cholesterol need. Like for example, cholesterol is a precursor
for testosterone, DHEA, the estrogens, cortisol, that that's coming from a precursor cholesterol
molecule. So at times in need, certain cells need more cholesterol. So therefore, the body's put in
a protective mechanism in place known as the liver, which makes more cholesterol
than any other cell in the body. So it's formulating its own cholesterol. Again,
you know, after a million years of biology, why would our livers formulate a bunch of this stuff
each and every single day? Because it's in every single cell membrane. It's what allows cells to
be permeable. It's also a precursor to a million things. But you know, I digress. When the cholesterol, sorry, when the liver makes a
bunch of cholesterol, it is transported around the body on an as needed basis. What's pretty
cool about that, though, is the liver will either increase or decrease cholesterol production based
upon dietary intake. So if you're having eggs every
single day, the liver is not stupid. It's not going to go, well, I'm just going to keep making
a bunch of cholesterol every day, no matter what. Everything in the body, there's a type of
adaptation mechanism taking place to where dietary intake of cholesterol does not have a very big
effect on cholesterol levels in the body,
unless you have certain predispositions to it. But those predispositions are typically
elucidated very early in life. If you have a cholesterol problem, it's not something you don't
know about. I mean, from a genetic predisposition perspective, that will be picked up quite early.
Like for example, there's something known as a, I believe it's Smith-Lemley-Opitz syndrome, Smith-Lemley-Opitz syndrome. And that is an
inability to produce your own cholesterol. And you can absolutely die as an infant. If that's
not picked up early, cholesterol is life. Every single cell needs it. That condition is associated
with basically, you know know any kind of problem that
you can think of and how is it remedied dietary cholesterol eat a ton of eggs yeah eat a ton of
eggs so it kind of depends you have genetic predispositions or you have an actual condition
or your liver is going to adapt to the current situation like any other smart organ would
um if we were to take i was gonna say uh if we were to take if we were to play to the current situation like any other smart organ would. If we were to take...
I was going to say,
if we were to play the egg game
all the way to the extreme
and the guy that's going to be editing
this video and audio for us,
he's a bachelor out in SoCal
that used to eat 28
eggs a day and went into the doctor's
office and they were like, your cholesterol is just through the roof.
Did he go too far?
Or is it something that can be regulated by the body if there is a system in there
that kind of balances that out?
Should he stop eating eggs?
Yeah.
Also keep in mind, he's totally shredded.
He's absolutely jacked.
Well, maybe not jacked, but he's shredded.
I heard you say that.
I just killed him.
Way to be skinny and jacked, buddy.
Yeah.
Matt, I want to help.
Colton doesn't need any more help.
He's better looking than all of us.
He's lean as heck.
He's eating all kinds of eggs.
This is, yeah.
I don't want to answer this one.
When he came to the suburbs
in North Carolina,
every husband in my neighborhood
had a good night that night
because their wives saw Colton
and they were like,
does he just wear no clothes
in your house like that?
Why doesn't he have a shirt on?
You know what?
Actually, in the theme of the episode,
when they looked at Colton,
no one worried about his cholesterol.
He must have high cholesterol.
He must be on a statin.
Back to his egg addiction. Yeah. So in a real way, you know, there's more context involved there because yes, your body will adapt even to extremes.
And that's why people can do the keto diet.
That's why people can do the carnivore diet.
That's why people have tons of eggs per day.
That's why there's been a lot of tribes and cultures that ancestrally speaking, have consumed
tons of cholesterol throughout, throughout many, many, many generations.
So there's absolutely an
adaptation discussion to be had there. But there's also the discussion of, you know, that's kind of
what his doc told him. Because, you know, one thing we didn't really get to is, on most reference
ranges, you're considered high LDL when you're above 99. There is so much, so much, so much literature out there that would
suggest that problems are really only going to start to occur after 170. That is a far cry away
from 99. So you know, if Colton comes back to you and says, man, my doc said my cholesterol was
crazy. And it was like 120. I would look at his HDL and say, Oh, it's 60. Who cares? Like, like,
I'm serious like that there is absolutely convincing
evidence uh so there is uh there are a lot of context would need to be had there even outside
of the conversation that he should active get sunlight and is a happy person yeah um you know
very similar to our our episodes on testosterone it's like if you have low testosterone someone
comes along and says well you have low testosterone let's just pump people on more testosterone testosterone without really
addressing why you had low testosterone in the first place finding the root cause things we've
mentioned many many times like you brought up hmg coa reductase and and statins so statins are hmg
coa reductase inhibitors and they basically make where you just can't produce your own
cholesterol and so your numbers go down but that doesn't really address why you had high cholesterol in
the first place. Um, what are the downsides to just going to your doctor and, and just, um,
getting, getting drugs to reduce that number without really addressing the entire system?
I mean, the, the downsides of, you know, know, the stressor that that would create in the entire
system, like the reason of your elevated cholesterol, unless it's a genetic predisposition,
is due to some sort of lifestyle issue that's currently happening, that's simply not being
addressed. Just like in the, you know, just like you said, in the testosterone conversation,
if it's low, there's many pathological reasons, and certainly non optimal health reasons why that testosterone will be low.
And the same thing can be said for cholesterol being high or low, as well. You there is going
to be reasons whether it be insulin resistance, whether it be mean, even just the statins,
statins are going to deplete certain minerals are also going to deplete CoQ10.
CoQ10 availability is its own heart protector.
So like you're doing something, but the back end, if you're not familiar with DINDs, which
is a drug induced nutrient depletions, and you don't know you need to replete your CoQ10
from the statin use.
There's a lot of, you know, downstream things that happen there.
Statins are also associated to lower testosterone,
which is unsurprising, since that person is unhealthy, and probably who's going to have
low testosterone anyways. And that's why they have higher cholesterol, because they have a
crappy lifestyle. But now also, they're taking a statin, which is reducing the amount of precursor
availability to create whatever testosterone they could have had. So then that person is going to
take TRT, and is going to take
a statin and is really going to change nothing about their healthy habits. And that's why you
see things like statins have the like, look at the research, the research on statins preventing
cardiovascular disease or preventing the amount of heart attacks taking place. It's terrible.
The research is not impressive at all on statins effects to protect people or increase
longevity. Why? Because that person never changed anything that led to the reason as to why that
statin was even prescribed. So it's just it's so unsurprising to me that these things take place.
And even simple things like three vegetables per day, I get That's not even that hard to do.
That's been demonstrated alone.
So not including any other factors,
three vegetables per day lowers LDL.
But most people just simply don't want to do that.
Just it's a lot easier to work with a statin.
It's a lot easier to take a pill.
Those vegetables contain the fiber,
which grabs onto the bile,
which gets the bile out of the body, which forces your body to make more bile.
How is it formed?
Through cholesterol, glycine, and taurine.
How is that bile secreted into the small intestine?
Thyroid hormone.
That's actually how hypothyroidism leads to higher cholesterol as well.
Because even if you form new bile from taurine, glycine and
cholesterol, yes, you've got all this bile ready to go, but it needs active T3 to be stimulated to
get released into the small intestine. So again, this will act, this will elevate cholesterol
over time, and it'll begin to rise. Do you have high cholesterol? Or you have a malfunctioning thyroid?
And then even in that conversation, what else is somebody with a malfunctioning thyroid is
probably going to be a little bit overweight. So then that cholesterol will be blamed on the
overweight situation. But then imagine, imagine that just kind of create that context in your
mind. Imagine hypothyroidism inducing high cholesterol. That high cholesterol
now is being blamed on that person being overweight. Now that person wants to try a diet,
but they have hypothyroidism. So they are more fatigued. They had legitimately have a lower
metabolism, they are going to have a hard time. And then people are gonna make a that person's
lazy, and that person's not disciplined, and that person it's like man this is a really tough situation and then that person's
probably gonna end up on a statin because they said i tried the diet i tried it it just i think
i'm just genetically programmed to be fat it's like no you're not people just aren't doing a
deep enough diagnostic on you yeah i feel for those people in a big way because like that sucks. Yeah. Um, digging into, uh, saturated first, uh, unsaturated fats. Um, it's kind of like another,
another area where like good and bad show up a lot. Um, if we were to dig into like the bad one,
uh, the saturated fats just immediately, cause people are going to be more afraid of those
things and have like more of a negative opinion of those. What is what is saturated fats
role? And why is it probably not considered just like the bad one, as we've laid out many times in
this in this show? I mean, again, even even evolutionarily speaking, we've eaten much more
saturated fats across human lifespan than we have unsaturated
fats. There's many, many animal consuming societies. And even when you're having monounsaturated
fats, it's usually almost always a 50 50 split or some sort of combination that contains
several fats rather than just one fat. The thing when you have unsaturated and when you
look at biochemistry in a in a a carbon layout, and Doug really knows
his biochemistry, so he might be able to help me here. But where there is unsaturates in a carbon
molecule for fat, that is where lipid peroxidation takes place. So yet, peroxidation, you can think
about inflammatory lipid response, that's just a super easy way. Lipids, fats, peroxidation,
oxidative damage. Lipid peroxidation occurs on unsaturated points in the carbon molecule.
Lipid peroxides can be picked up in a urine analysis. And it's already been demonstrated
in humans, by the way, that elevated lipid peroxides makes your lipid profile more damaging than it actually appears, if that makes sense,
because there is oxidative damage taking place due to the carbon situation in unsaturated fats.
And that's why things like seed oils have a really bad rap, because they have this carbon layout,
which allows for more oxidation to take place, which allows for more general inflammation and
unhealthy physiology to take place, which is for more general inflammation and unhealthy physiology
to take place, which is associated with a lot of general mortality risk, which is kind of what you
see in the world of cardiovascular disease is like a lot of epidemiological research, a lot of
observation, a lot of correlations, a lot of country samples, big things like that. And then
they kind of boil it down to certain fats. But yeah, seed oils have a really bad representation.
And saturated fats have a really undeserved bad reputation.
If they're not bad, why do they show up on my food intolerance list as like,
those things are really your bad thing?
Like, how do I develop as a relatively healthy
human being, like, such an intolerance to seed oils? I would honestly just assume that, like,
it says canola oil, it's all of the seeds mixed into one big bottle. And if I eat out,
next thing you know, it's going to be a disaster 10 minutes later. So like, how does somebody
kind of like develop an intolerance to seed oils if they're
not that bad? Did you have, oh, seed oils are bad. I'm actually, they're the ones that are
associated. Yeah. So that's already. I thought you were saying that they weren't as bad as the,
as people say them. Sorry. No, sorry. Maybe I misspoke. I meant CETO ales are quite, you know, demonstrated to be poor for physiology across a lot of
data.
And it was saturated fats that are not as bad.
They have the undeserved bad reputation.
Gotcha.
My bad.
Sorry about that.
So all good.
Like everybody or many people are going to have the same kind of intolerance to that.
Kind of like what showed up in my labs was basically
like don't eat at Chipotle, or at any other restaurant, because that's what they cook
everything. It's also like most things in life, like moderation is fine. Balance is fine. Not
eating like so long as you know, you're doing the right thing 80 to 90% of the time. I've always
I've been a big believer that there's
no such thing as a bad food. There's only such things as bad diets. Biology adapts to averages
over time. So if you're making more good decisions than you're making bad, especially if your goal
is just a good lipid profile, and not to be a UFC world champion, then you're gonna be doing a lot
of the right things. Yeah.
Yeah, like even just a second ago, you're talking about acetyl as being bad like most people consider like linoleic omega-6 fatty acids to be
pro-inflammatory and if they're it's way easy to get too many of them but at the same time like
they are an essential fatty acid like you do need some amount of them if you don't get them you're
gonna have all kinds of problems like those fatty acids convert into arachidonic acid a bunch of
other fatty acids that like are a big component of your brain and nervous system.
So, you know, those are the bad, the bad fats and, and they can be bad, just like sugar is bad if you get way too much of it.
But like a little bit of sugar is just fine.
It's going to give you energy and help you, help you train and work out and whatnot.
It's the same with, with industrial seed oils and whatever else, how they're processed and how they're heated and whatnot.
And they can go rancid and what, you know, what have you, like you're talking about,
there's, there's better, there's better and worse sources of them, but they're an essential fatty
acid. You definitely need some of them. You don't want to have nothing, but you don't want to have
too much. And so it's always a balance as you've, as you've continued to say on this show, there's,
there's a healthy range for pretty much anything. Yeah, 100%. And sometimes like I've seen,
I'm seen as like a radical with different ideas,
but like, I'm always saying balance.
It's like this guy, this guy's crazy.
There's people out there, you know,
on a carnivore only diet or like, you know,
like very extremes, like no carbs or no fat
or only animals or only plants.
And I'm like a guy like,
how I have a little bit of all of it.
You're an idiot. What are you talking about? Balance. And I'm also I'm a fan of the history
of science as much as I am science. Like, when you look at the history of science, you do identify
that people have been wrong more times than they've been right and what better example than cholesterol that all that all started with Ancel Keys in the 50s and it was like
cholesterol is bad for you oh wait never mind it's not you know why no actually
was fat it was fats bad for you never mind it's not a fact it's right I I just keep picking a new enemy constantly.
And I always just try to look at,
understand when you look at scientific history,
you have to remain humble.
That's like how you remain
on the right side of history with things.
Whenever you take such an absolutist stance, I've just been in the industry long enough. And you guys have talked to
way more people than I've talked to in this industry by being on shrugs. How many people
have you guys seen come and go that had very strong beliefs over the past 10 years?
I can answer that question very real. And it's typically like a stage of their career
yeah yeah like if you stay in it long enough you uh you go through many stages in which you then go
oh all of these things are right as long as you ask the right questions and meet people where
they're at you can use all of these tools to go but uh you have to do it for like 20 something
years before it makes sense
i'd say the biggest one there is like the entire paleo crowd came in very strong was huge like
when crossfit was huge and then the like paleo is still around and there's you know there's pros
and cons to having that kind of mindset around eating it's a it's a simple rubric for figuring
out what's you know what's generally healthy and whatnot but at the same time like that that there
was a big paleo wave and then all the paleo people kind of fell off. And I don't see
very many paleo people in the same way that I used to five or 10 years ago. No, no, there's
always those waves. There's the Atkins wave, there's the Mediterranean wave, there's a paleo
wave, there's the fasting wave, there's a keto wave, there's a carnivore wave, there's the vegan
wave. I mean, that's, again, why I kind of always lean on labs is don't follow a philosophy.
Follow your own physiology.
I'm going to need help with the name because I'm drawing a blank.
But he, Dan John.
Bam.
We interviewed Dan John like two years ago.
He's the man.
He's the man, right?
Why is he the man?
One, he's super smart. He's super man right why is he the man one he's super smart he's super
good at communicating just very basic concepts to people so they just get it in like three sentences
and he's a savage right he still competes in olympic weightlifting um when we interviewed him
he i want to say it was like five times he said he had seen basically the keto
diet show up in his career and like have a wave.
And like,
it's not that paleo is the keto diet,
but it's definitely like meat and vegetables,
which is a very low carb diet.
And then it was like,
then Atkins and then keto.
Like it was like basically those same principles show up over and over and
over and over again.
If you stay in the game and this is part of your career for 40, 50 years, you just see the waves and you go, oh, this one's going to die out.
And the next one shows up and then the next one shows up.
That was one of the moments where I was like, oh, this is why Dan John is Dan John, because he's done it for so long that he can tell you what the macro flow of the industry looks like.
The life cycle of the industry and how it's just reborn in the same way every 10 years or so.
And you got to be careful for the people who are even science-based sometimes,
because you can use the science to formulate a philosophy.
You can actually do that.
And it's a way in which you're appearing unbiased,
but you have the largest bias of anybody
else because your bias is so strong that you're actively seeking the literature that only supports
your idea. But then you start to see so many conflicting things like coconut oil was an
enormous craze, and to some extent still is. That's already been demonstrated to increase LDL
quite substantially. IL-6 is an inflammatory marker. It's been demonstrated to lower LDL.
So like you just, you start to see so many things that you have to actually do the Dan John and
take a step back and start looking at everything instead of these isolated things.
Yeah. Yo, real quick. Wait, wait, wait. Two minutes before we wrap.
Yo, real quick, dive one more time into how cholesterol produces all the sex hormones
and whatnot.
Just gives like a big overview of that, because I don't think people truly associate or often
associate cholesterol, which is quote unquote bad with producing testosterone, which is
quote unquote good.
And then all the other hormones, of course.
Sure.
So if you want to go to we'll go the testosterone pathway, you got cholesterol, and you're going to form it with some vitamin B5. You're going to combine these two. It's going to
go off to a cool area in the cell known as the mitochondria. The mitochondria are going to do
some gymnastics with it to spit out something known as acetyl-CoA. Acetyl-CoA is then going
to be formed into something known as pregnenolone. Pregnenolone is the mother of all sex hormones because you need it to make anything. If you want to make any of the estrogens,
cortisol, aldosterone, progesterone, DHEA, all of them come from pregnenolone. So following this
pathway, cholesterol, vitamin B5, mitochondria, and up acetyl-CoA. Acetyl-CoA gets formulated
into pregnenolone. Pregnenolone is
going to get converted to androstenedione before it becomes testosterone. If that testosterone
wants to become some estrogens, it can follow the aromatase pathway from there to become estrone,
estradiol, or estriol, or E2, E4, E16. If it wanted to go the other way, pregnenolone will first become
progesterone. Going back up the scale, pregnenolone can go over to become progesterone.
Progesterone can actually a lot of people don't know it can take a secret backdoor enzyme
to become testosterone. So if somebody is has quite a bit of progesterone, there is certain
enzyme pathways that you can you can promote, we'll say
in order for that backdoor to take place and you have more testosterone. But in a typical situation,
that progesterone would become cortisol, that cortisol can become cortisone. All of that
begins with cholesterol. So first thing I said for a reason, reason why it's in every single cell,
as well as mitochondria being in every single cell. It's the essence of life.
Dan Garner, tell the people where to find you.
I am at Dan Garner Nutrition.
I am also at CoachGarner.com.
I've got some courses there and you can hang out with us at Rapid.
There it is.
Make sure you go take those courses if you're a coach out there and you want to learn about all this stuff,
it's kind of like the backbone of all the training that we do with our
coaches as they go through all those things as well.
Also ask Doug,
Doug's just this sneaky guy who asks questions,
but also knows everything because I just said HMG CoA and he goes HMG CoA
reductase.
He,
he already knows the enzyme.
He thinks I'm not picking up on that.
He already knows all.
So if you got questions, you can also go to Doug.
He's the biochemistry whiz.
Doug loves hanging out in the DMs.
So send him all your chemistry questions.
And he logs on Instagram once every three months.
I've really been trying not to be hanging on Instagram all day.
Yes, it definitely helps to know things to softball questions your way.
You say that extra word, though, and I'm like,
this dude knows the answer to what he's asking me right now.
Sneaky.
Sneaky over there.
Doug Larson, tell the people.
You bet.
I'm on Instagram every once in a while at Douglas E. Larson.
I'm Anders Varner at Anders Varner.
We are Barbell Shrugged at Barbell underscore Shrugged.
Make sure you get over to RapidHealthReport.com.
That's where you can see Dan Garner actually talk specifically about my triglycerides,
HDL, LDL, and the ratios and how that lines up with all my labs.
And where it led to my low testosterone.
So get after that, too.
That's always fun, putting your low testosterone scores out to the world
so anybody can go look at them.
Real manly over here.
Real manly over here.
RapidHealthReport.com.
Friends, thank you for everything over the last year.
I really mean everything from the beginning of the show.
It's super cool that I get to meet all of you guys
that are scheduling calls
and talk about how we can help you.
Friends, we'll see you guys next week.