A Cardiologist's Guide to Hormones, Peptides, and Labs for Lifters Over 40 (Dr. Abid Husain) | Ep 406 - Wits & Weights | Fat Loss, Nutrition, & Strength Training for Lifters

Episode Transcript
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Philip Pape (00:01):
If you're over 40 and wondering about blood work
for cardiovascular health, theeffect of hormone therapy on
your heart, or which peptidesactually work for recovery and
heart health, this episode isfor you.
My guest today is a functionalcardiologist who works with
lifters and athletes.
He's going to reveal exactlywhich labs and biomarkers you

(00:22):
should be tracking beyond thingslike cholesterol, the real
cardiovascular risks andbenefits of HRT, and which
peptides have actual evidencebehind them for recovery and
heart health.
You'll also learn whethercalcium scoring is worth it, how
much lifestyle changes move theneedle, and the latest
misconceptions about lifting andheart health so you can focus

(00:43):
on what matters.
Welcome to Wits and Weights,the show that helps you build a
strong, healthy physique usingevidence, engineering, and
efficiency.
I'm your host, Philip Pape, andtoday we're going to get
specific about what you need totrack and monitor for
cardiovascular health.

(01:04):
What is cardiovascular health,especially if you're over 40?
My guest is Dr.
Abid Hussein, a triple boardcertified cardiologist
specializing in functional andintegrative medicine at Boulder
Longevity Institute.
Unlike, I'll say, conventionalcardiology that only looks at
very specific measures likecholesterol panels, I believe
Dr.
Hussein is a bigger thinker.

(01:25):
He's a systems thinker.
He uses advanced diagnostics.
He works specifically withathletes and lifters like us to
optimize performance andlongevity.
He's also an athlete himself.
So in this conversation, you'regoing to learn which specific
biomarkers, labs, things likethat matter beyond the basics.
You're going to learn the risksand benefits in terms of heart

(01:45):
health for things like hormonereplacement therapy from someone
who prescribes it.
We're going to learn whichpeptides have legitimate
evidence because there's so manyout there.
And things like calciumscoring, is that worth it?
How to think about the balancebetween lifestyle and
therapeutic options.
So you're going to come awaywith a practical roadmap to
monitor and protect your heartwhile still pursuing the things

(02:06):
we love when it comes tofitness.
Dr.
Hussein, welcome to the show.

Dr. Abid Husain (02:11):
Thank you for having me, Phil.
It's great to be here and uhhappy Halloween.

Happy Halloween, yes.
Yeah.
It's uh it's a supernaturalkind of day.
And we're gonna hope hopefullyground it in things that are
super and natural today.
That's right.
And I want to start, I alwayslike defining terms, right?
So we use engineering thinkinghere.
We want to be very objectiveand data driven.
And when we talk about ahealthy cardiovascular system, I

(02:35):
was grossing out my daughtersthe other day.
We saw a video of the heartlike unraveled.
And I understand it has kind ofthis spiral shape when you
unravel the entire muscle andthey were kind of grossed out.
I find that so fascinating.
Of course, I even talk aboutwhere our food comes from and
they get grossed up.
But uh, what do we meanphysically and mechanically?
What does a healthy heart andcardiovascular system look like?

(02:59):
And then I guess at the systemlevel, what does it mean to have
a healthy heart in a way thatcan be measured or observed, if
that makes sense?

Yeah.
Well, I love that you startedwith that analogy of the heart
uh unraveling and uh having aspiral sort of uh topography or
morphology to it.
Uh that's not something that'sreally well talked about or well
known.
You know, the the heart, it'scertainly a pump, but it is an
incredibly efficient,chemodynamic and mechanical

(03:29):
system.
And the way it's put together,that it's got cross fibers of
muscle.
And in the placement of thosecross fibers, the torsion
optimizes the ability of theheart to get the most amount of
squeeze per amount of movement.
It's incredibly fascinating.
Uh so it's not just amechanical pump like uh a piston

(03:50):
sort of a thing that we mightimagine from a car.
It is a really dynamictorsion-based system that
spirals the blood out.
So if you start thinking abouthow just the hemodynamics of the
heart, the way the heart is puttogether with the rest of the
system is like that.
It's not just a binary sort ofyou know serial addition of

(04:13):
components.
There are additive componentsthat amplify or reduce risk, and
this is what combines with oursystemic, you know, circulation
and inflammation, uh,metabolism, all of these things.
They're not just additive,they're they either amplify in a
logarithmic fashion or not.
So it's a it's a reallyincredible organ.

(04:35):
And uh, you know, there arewhen we think about it that way,
it's really naive to think thatwe can assess heart health
based on one marker, which ischolesterol.
You know, that's what the theuh the traditional viewpoint is.
Go to your doc, cholesterol ishigh.
Okay, you're screwed, put youon a statin.
You know, that's not the waythe heart works.

(04:57):
You know, we've got to look atit potentially mechanically, but
biochemically with riskamplifiers or risk reducers.

Okay, I love that you took it there.
And yeah, I agree.
Having talked to a few otherheart experts and seeing the
state of the healthcare industryand people who have issues with
their heart and being in thelife, the world of lifestyle
where I understand the benefitsof things like strength training
for all this, yeah, I knowthere's a more complex
interconnected web of systems.
And you mentioned uh bio, Ithink you said biochemical,

(05:26):
right?
You said not just mechanical,but biochemical.
So kind of tie that together tothe term health when we say
heart health, because people getconfused between cardio health,
like with running and movementtype of health, VO2 Max and
resting heart rate versus heartattacks and plaque and arterial
blockages and statins.
And like how does it all cometogether when we think

(05:48):
cardiovascular health withoutgetting too complicated and
overwhelming?

Yeah.
Well, you know, when we look atVO2 Max and we're looking at
performance, those areindicators of heart health, but
they don't necessarily give usan indication of what's going on
at baseline.
You know, those are peakperformance indicators, and they
have specific roles in helpingus understand what capacity a
person has, you know, what wecan push them to.

(06:13):
It doesn't necessarily give usa, and it is associated with
all-cause mortality, uh,cardiovascular events, but
that's at a certain level, andthen it can start to be a uh a
J-shaped curve where if we gotoo high or if we push ourselves
too far, they we can start toget uh degradation.

(06:33):
Now, how do we measure that?
How do we look at that in amore day-to-day baseline status?
That's when we take a look atthings like more of the
biochemical markers, things likeC reactor protein, uh,
myeloproxidase.
Uh, there are, you know, thereare we can look at the
cholesterol profile actually andsee the morphology of the LDLs

(06:54):
and see if they are going to amore pro-inflammatory state or a
less inflammatory state.
And that's simple, some simplecalculations looking at LDL and
APOB.
You know, when you look atreally extreme athletes that
push themselves really hard andtoo far to the point of extreme

(07:14):
fitness, they actually have thesame biochemical makeup as
people on the other end of thespectrum who don't do anything.
So we see similarities in theirblood panels, you know, on
either end of the spectrum.
So that's why, you know, thosemarkers like a VO2 max or
performance markers are great tounderstand how we can push them
and develop their performance.
But when we look at vascularhealth, cardiovascular health,

(07:38):
it's important to tie in thosebiochemical markers to see how
far we're pushing them.

Okay, I love that.
And I think I heard a podcastby Brad Kearns recently talking
about elite marathon runners andhow they have like symptoms,
measurable biomarkers of heartof a heart attack after they're
done with their race, and it,you know, and the body adapts
back and recovers and likeeverything's usually okay.
But we know it's a highly,highly stressful thing.
We're gonna assume that thelistener is maybe not in the

(08:03):
elite regime right now andthey're just concerned about
day-to-day heart health.
So there's a couple of topics Iwant to unravel.
One will be more about thebiochemical markers.
But before we do that, is ittrue to say that heart disease,
which again, we can define whatthat means because I understand
there's different elements,yeah, is a disease of obesity
primarily, or because I get intothese debates with some people,

(08:24):
is there a subset of thepopulation where it's genetic,
where it has nothing to do withobesity?
Like help us understand that.

Yeah.
I think that uh, so when wetalk about heart disease, what
we're really talking about isatherosclerosis.
That's the number one killer,the development of plaque in our
coronary arteries or in ourbrain, anywhere in our body,
really.
That's the number one killerglobally.
That's what causes heartattacks.
So let's that's what we'retalking about primarily in this
sort of in this part of theconversation.

(08:52):
Other cardiovascular issueslike hypertension, arrhythmias,
they do have some crossover withthese same systems, with these
same pathophysiologies, but thisis about uh mostly about
atherosclerosis, because that'swhat kills us.
When we talk about obesity,it's not necessarily a it's
about caloric excess.
It's about energy excess.

(09:13):
You know, obesity is that'swhat we're talking about when
we're looking at obesity.
And when our system is floodedwith excess amounts of calories,
energy, we're gonna store itand we're gonna store it in fat,
but it also that trickles downto oxidative stress that happens
on a molecular level.
Our body has an ability tomanage energy very well when

(09:34):
it's done in balance.
If we have excess, that excessenergy starts to leak into areas
that it shouldn't, and then ourbody has to figure out how to
manage it.
Is that part of obesity?
Definitely.
Uh, and it's part of what we'reeating too.
It's part of the macros.
If our energy is coming fromsources that are highly refined

(09:55):
and glucose rich, carbohydraterich, that's gonna challenge our
ability to uh to metabolizethose.
And we metabolize those with ahigher toxin load.
And that leads to the obesitypart of it is not only about the
higher energy component, butit's about uh managing, it's
about the uh the toxin that thatbuilds up.

(10:16):
We end up putting on fat to tryand manage that.
So that is the majority of whatwe see because we live in an
overly nourished society.
There is a genetic component toit.
There are people that do have apredisposition, and if they
know about that, then it's evenmore vital for them to take care

(10:36):
of what they're putting in tomanage at least these energy
management systems.
So is it a problem exclusivelyobesity?
I mean, when you talk aboutobesity, then you gotta talk
about type 2 diabetes, type 1diabetes, you know, the genetic
component, type 1 diabetes, iswhat we see predominantly when
we're looking at uh the geneticpart of uh glucose intolerance.

(10:58):
Some people do develop type 1diabetes in adulthood, and
that's uh an emerging conditionalso.
But the majority of what we seeis type 2, and that is
associated with obesity, but itdoesn't have to be.
You know, those are people thatbecause of inflammation, maybe
it's inflammation specific tothe liver, they may have uh
liver and pancreas, then theymay have uh development of uh of

(11:22):
glucose intolerance and sort ofthis type 2 pattern.
So we do see thin people withdiabetes.
So it's it's there is anoverlap.
It's not primarily a disease ofobesity, but obesity is part of
the characteristics of what wesee show up.

Yeah, no, I always like to ask that because I care
about the autonomy and theself-efficacy of the listener in
terms of what they can do,right?
And obviously, we can't controlour genetics.
And if there was a narrativethat heart disease is this
random thing that can be highlyinfluenced by genetics, that
would be kind of a scary thing.
Whereas I think in reality, ifyou went back a hundred years

(11:59):
pre, you know, massive obesity,you would see far less heart
disease.
So, you know, not to say thatyou don't see any at all, which
means means that's powerfulbecause we can do do something
about it with our lifestyle,which is what we're gonna get to
eventually here.
Okay.
So plaque and arteries, that'sheart disease, but we also have
markers along the way we want tolook at.
Now, you mentioned some of theinflammatory markers.

(12:20):
So C reactive protein, you alsomentioned APOB.
You did say cholesterol panelsare still helpful in context.
So help break that down.
If we want to track thesethings, the listener's like, I
want to get labs tomorrow andstart measuring before and
after.
What would they be looking at?

The panels that we look at look at high
sensitivity C reactive protein.
We look at APOB, APOA, andalong with that goes the uh the
LDLs and the HDLs,triglycerides.
And then when we when we goback to the inflammatory
markers, there are a fewadditional ones that can give us
some insight into what's goingon into the vascular system.

(13:00):
That's uh there's one calledLPPLA2, sometimes also known as
PLAC plaque, and then there'soxidized LDL, myeloperoxidase.
These are like a list ofinflammatory markers that can
give me an idea of what'shappening in the vascular lining
as well as what type ofmetabolic situation is going on

(13:21):
uh systemically to create thecholesterol.
Uh because cholesterol is isreally in it's an energy
delivery tool.
It's got it's used for so manydifferent things, and it when we
try and look at how it's beingmade, like the body makes it for
a reason and it's gonna make itat a higher a higher amount for
a reason.

(13:41):
Usually it's delivering fuel tosomething, like the immune
system, like cells that need itfor their membranes.
So it's doing it and it'sdelivering it at a higher amount
because maybe there'sinflammation, or the the uh
liver is cranking it out in acapacity or in a way that it
can't do it efficiently and it'sgot to just pump out smaller,

(14:02):
more dense particles.
So that's what we're that'swhat I'm looking for.
When I look for what kind of uhwhat kind of metabolic profile
a person has, I take a look atLDL and APOB, and there's a
ratio.
The LDL to APOB ratio, thecutoff is 1.2.
If it's below 1.2, this is thismeans that you have a

(14:24):
predominance of small denseLDLs.
If it's greater than 1.2, youhave a predominance of large
buoyant LDLs.
Why is that important?
They're at two ends of thespectrum.
Small, dense LDLs are likecannonballs.
So you've got little densebullets, cannonballs bouncing
around inside the arteries,causing damage, digging into the

(14:46):
lining, and creating what isthe beginning of plaque.
Large buoyant LDLs are beachballs, they bounce around,
deliver cholesterol energy whereit needs to go to, and then
don't penetrate and oftentimesget back to the liver and get
recycled.
So that's part of the problem.
When we have a lot of thesesmall, dense ones, there's a lot

(15:09):
of problem problems with it.
It's not just that they'reprone to getting under the
lining, they get inflamedfaster, they get clear, it's
more difficult to get themcleared, they stay in our system
longer.
And then these become, youknow, these are the
characteristics of inflammatorymetabolism.
And then when we add somethinglike a C reactive protein to

(15:30):
that, ideally a pie sensitivityC reactor protein, I want less
than one.
And uh that is going to give mean idea of how much
inflammation is associated withthese LDL particles.
Um, now this is now C reactiveprotein is a global inflammatory
marker, so it doesn't give mean idea of specifically what's
going on in the lining of theartery, and that's where things

(15:52):
like uh MP uh myeloperoxidase,plaque, and oxidized LDL come in
handy.
You know, oxidized LDL is theinflamed LDL, and and it will
oftentimes be uh elevated in thewall if there's inflammation,
but maybe not in the serum.
But if I do see elevations ofoxidized LDL, I'm guaranteed

(16:14):
that it's in the wall as well asin the serum.
So when you look at ifC-reactive protein is elevated,
if oxidized LDL is elevated,these are risk amplifiers.
I know this person has highdegrees of inflammation.
So we got to track these, bringthem down.
The other what creates oxidizedLDL is that plaque, LPPLA2.

(16:35):
It's an enzyme that convertsthe LDLs into something more
inflamed and atherogenic.
Uh and and then it in theplaque, it can also create
what's what are called the foamcells, which expand the uh the
inflammation and the size of theplaque.
So if we see that, that'sactually a really good lifestyle
indicator.
Sometimes if patients have thatelevated, it means it can be

(16:58):
elevated with smoking, highcarbohydrate diets, inactivity.
So, you know, this is andsometimes LDLs themselves can
elevate it.
So, you know, there aremultiple things that we can look
at to kind of tease apart whata person needs to do more of or
less of.
Uh, and then lastly, themyeloperoxidase also looks at

(17:18):
the lining of the artery, alittle bit more of a vascular
inflammatory marker.
It's sort of the first uh thefirst responder of the immune
system because it's it's anenzyme that's associated with
the neutrophils.
And if there is acuteinflammation or inflammation
that's just beginning in thosein the lining, sometimes we see
myeloperoxidase elevated.
So I can, you know, by lookingat those and tracking those, I

(17:43):
can see where uh it things areeither improving, reducing,
maybe dial in, what else needsto be done?
The you know, when we look atuh, as I said, with the LPPLA2,
there are medications that willreduce that and then activity,
exercise.
Well, that's a lot of lifestylechanges can impact that, C

(18:04):
reactive protein, basically allof these markers.

Yeah, okay.
A lot going through my headbecause one question I had as
you were saying that is which ofthese are leading versus
lagging indicators?
Like obviously the cholesterol,once it shows up, that's kind
of a lagging indicator.
But you meant, I think you saidthe myeloperoxidase maybe is a
leading because it tells youyour lifestyle.
So I like that you know,there's a pattern to these
things, and as each of them getprogressively worse, as you get

(18:28):
toward that end state of likebefore it becomes too late,
let's say, I imagine you see thepattern shifting toward that,
and then you can shift it backwith your lifestyle and maybe
medications we'll get into.
You mentioned neutrophils, youmentioned CRP.
A lot of people have autoimmuneconditions, which I know uh
present themselves through a lotof these markers.
It sounds like, and this couldbe a simple yes or no question

(18:49):
or may require explanation.
Sounds like when you take allof these markers together,
that's how you're playingdetective to piece apart that
the CR, the global CRP isrelated to this and not that.
Is that a fair way to put it?

It is, exactly.
Yeah, because if I will if Ihave patients that have
autoimmune conditions, andcertainly patients will show up
with elevated CRPs because of atemporary illness, you know, and
so that's when they got theirlabs done.
So it can be something chronic,it can be something acute, but
there is a global uhinflammatory burden, but it

(19:23):
doesn't affect their vascularsystem as much.
So their plaque and MPO may notbe elevated, oxidized LDL may
not be elevated.
So these are really good uhtools to tease that apart.
Uh and and it and they changein a day-to-day, sometimes
hour-to-hour fashion.
Like C-reactive protein willchange within a few days.

(19:44):
And uh, but something like uhwell, something like plaque,
maybe a little longer, oxidizedLDL, a few days longer.
So, you know, these do have atime frame to them, also, which
helps.

All right.
I do want to ask one more thingabout cholesterol.
Well, maybe a couple.
One is I know there's a biggenetic component to
cholesterol.
There are just people that havehigher baseline LDL, let's say.
And I I definitely have seendebates on this, even among
medical doctors, of whether ahigh LDL, if it's your normal
baseline, is as much a concernas someone whose LDL got to that

(20:18):
point over time.
So I guess let's give you athought experiment.
If you had a 15-year-old comein who one, let's say two
15-year-olds, because I want toI want to start young here.
One is got excess body fat,right?
And one seems healthy in termsof body fat, and they both have
elevated cholesterol.
And that could be elevatedtotal, elevated LDL, even even

(20:40):
HDL, even though we call it thegood, you know, could be high,
uh, say 220, 250.
I don't know what the numberwould be where you'd be get
concerned.
How would you what's kind ofyour first thoughts about those
two different patients?

I go back to those markers.
I see what the breakdown is,what the APO B numbers are, and
I look at the uh Apo B to A1ratio, because that helps me
determine how well the system iscalibrated to remove the
cholesterol that might begetting deposited.
Uh so if there's large fluffyLDLs, not too much to worry

(21:12):
about.
If there's dense LDLs, then Ithen something to be addressing.
Um if they have borderlineinflammatory markers, someone
that age should not have anyreal inflammation.
So there are definite ways totease apart who is at risk and
who isn't.
And if the finances areavailable, do genetic testing on

(21:33):
them to see if there's any anyuh uh issues with protection of
the lining of the artery.
Uh, because there are specificgene SNPs that show deficiencies
in compounds like nitric oxide,which are vital for the the
anti-inflammatory effect andrelaxation effect of the
endothelium, the lining of theartery.

(21:53):
So if they have deficiencies inthat, that's important.
I'm gonna look at their diet,I'm gonna look at their activity
level, all that stuff.
Yeah.
Um, you know, I think a bigpart of the debate uh right now
is there's an interestingsubtype of people that are
called lean mass hyperresponders.
And these are athletic, leanindividuals that have extremely

(22:14):
high elevated LDLs.
You know, and we're talkingabout in the 200s or more, not
total cholesterol.
I'm talking about LDLs.
Uh and then their but theirHDLs are equally elevated.
The the curious thing is whenthey go into a keto diet, they
sh their their LDLs go evenhigher, and their but their HDLs
uh tend to stay flat.

(22:36):
So they don't do real well witha uh with a keto diet.
But the question is, do we needto treat them with statins or
lower that cholesterol?
And you know, the the studiesshow that even these people with
that super high LDL, they mayshow an accelerated amount of
plaque in a small period oftime.

(22:56):
So there is something to besaid about just being cognizant
of higher amounts of LDL.
And this goes back to thatstatement I was making about
energy.
You know, if LDL andcholesterol is an energy
delivering tool, delivering toomuch energy on its own can still
be a problem.
You know, we need to our systemworks best in a window in

(23:19):
homeostasis.
So when we go outside thatwindow and each individual has a
different window, then we cancreate a problem that's maybe
you know a more hyper energytype of problem that creates
inflammation.

Yeah, yeah, it makes total sense.
I mean, there are lots and lotsof issues when we have a hyper
caloric.
I always get them wrong.
Too many calories and uh storebody fat, and then there's the
visceral fat concern as we getolder.
And if you're sedentary, notusing those calories, it gets
even worse.
So actually, let's hit on thatreal quick because you mentioned
keto, you know, I know youlistened to a little bit of this

(23:56):
podcast, and we're you we'rewe're diet agnostic.
We're we're, you know,obviously diet is highly
personalized, it's got to beflexible and depending on your
goals too.
So when we're talking withathletes or people who lift
weights, you know, they seem torespond really well to moderate
to high carbs versus somebodywho's not using those carbs,
right?
Uh and conversely, I'm prettysure high saturated fats is

(24:16):
definitively now linked withhigh LDL.
But just reiterate that for usor tell me that I'm wrong.

You know, the the debate about saturated fat
is uh, you know, it started wayback in the 50s with the seven
country study, you know, andthat's been difficult to
reproduce.
So, you know, the questionabout Ansel Keys?

Yeah.

Yeah, that's right.

Yeah, yeah, yeah, yeah.
Right.
With all the selective cherrypicking of data, yeah, I
understand.

Yeah, and so and even the follow-up data that
tried to reproduce it actuallyshowed that it was not the
issue.
And you know, saturated fat isnot necessarily the demon that
they thought it would be, and uhsugar is the problem.
So, you know, if we look now atwhat is saturated fat really
associated with atherosclerosis,I think it really depends on

(25:02):
the individual.
You know, there's certainthere's certain genotypes that
do don't do well with uh highamounts of saturated fat.
And these are Apo E4 genotypes.
Okay.
Um, and that's a pretty easytest to get.
They also have a higher risk ofof Alzheimer's because what
happens is they don't manage,they don't have the cholesterol

(25:22):
transport mechanisms as well uhas robust as the rest of the
population.
And so the cholesterol tends toget a little more inflamed.
The reservoir with the mostcholesterol is our brain.
So that's how the associationwith Alzheimer's occurs.
But these patients, thesepeople don't do well with a
saturated fat diet.
You will see their cholesteroljump up and then their

(25:45):
inflammant inflammatory markerswill start to change also.
So it's very individualized.
So I'm very cautious to makelike a an overarching uh uh
blanket statement about diet.
And but I don't, as long as thefats are wild caught and not uh
and farm-raised, organic, thenI'm okay with saturated fat.

(26:06):
And I'm gonna follow thosemarkers because I don't have a
full genome uh assessment on allmy patients.
I don't necessarily need to,and I can let them adjust their
diet and we can do that togetherand follow some of these
markers uh and then track what'sgoing on and make sure that
it's working for them.

Yeah, the genetic component's interesting.
I've talked to a few folks onthe show from different
companies because I know it'sit's a little bit of Wild West
still, but there's someinteresting work happening.
And uh I have had some of thosetests done myself and uh the
APOE four, you said, right?
I believe I have isn't theretwo SNPs, and you can have one
or you can have two, and havingtwo is like the highest risk,

(26:45):
and I think I have one orsomething.
Um, so I think I'm I'msusceptible to that.
But I also have foundpersonally when I measure blood
work, dropping body fat tends tomove everything in the right
direction, and then you know,and building muscle moves
everything in the rightdirection.
And I've seen that with clientsas well.
And so I I do like the idea ofit is personalized, you should
experiment.
I would say if anything is likeway out there, let's say it's

(27:06):
saturated fat and 50% of yourfat is saturated fat, that could
be a concern and you want totry, but same goes for too much
sugar or too much anything else.
Um, not too much protein,though, guys.
I think you're good there.
That's right for the most part.

We gotta hit our protein goals.

So, okay, all right.
I want to move into a coupleother topics and then kind of
tie them together a little bitmore deeply because we we also
wanted to mention um hormonereplacement therapy.
This is not a very good segue,but maybe it is.
A lot of folks listening areolder and we talk a lot about
bioidentical uh HRT, uh,especially a lot for women in
peri postmenopause and for menwith testosterone.

(27:42):
And people are concerned aboutalways concerned about risks.
A lot of it probably comes frommisinformation, like the
women's health initiative.
Exactly.
You know, and and uhconflating, you say, synthetic
with biodential and animalsversus humans and stuff.
So, what are the actual risksfrom a cardiovascular
perspective of any of these, ifthere are any?

Yeah.
The risks are actually when wehave deficiency of the hormones.
So when we look at individualswith, you know, testosterone,
specifically, these were studieswe're done in men with uh
testosterone below, I think, oraround 250 total, they have a
significant increase inall-cause mortality and
cardiovascular death.

(28:23):
Not only that, but they alsohave an increase in risk of
prostate cancer, particularlyaggressive prostate cancers.
So, and then when we when wekind of uh take that one step
further and look at deficienciesin estradiol, progesterone,
again, associated with adverseoutcomes.
So when we're replacingtestosterone, estradiol,

(28:48):
progesterone, doing it tophysiologic ranges is perfectly
safe.
And in fact, in in my mind,it's therapeutic.
You know, we are we arereplacing deficiencies that the
body has lost, but the the bodyis incurring over the years.
You know, the hormones are ouroriginal regenerative tools.

(29:10):
This is why we can bounce backwhen we're young.
This is why we can developmuscle very quickly, because we
have the hormones to stimulatemuscle protein synthesis.
We have the hormones to protectour vascular lining.
As we get older, because of youknow, mitochondrial
deficiencies, because of juststress uh oxidative stress, wear
and tear, whatever you want tocall it, these systems start to

(29:33):
become less efficient.
And the most sensitive systemsare our hormone systems.
We lose those first.
So as we get older, the firstthing you're gonna lose as a
male is testosterone, testicularfunction.
That's why your libido dropswhen you're stressed because you
don't have the reserve and it'sgonna take away that accessory
function.
So um replacing testosterone tophysiologic and even maybe

(29:58):
super mildly superficial.
Physiologic levels is safe.
The caveat here is we want tolook at dihydrotestosterone
levels.
Those, you know, that has somemixed data, whether elevated
levels are beneficial, benign,or if, you know, there is it
associated with othercardiovascular issues.
We know dihydrotestosterone isan anabolic hormone.

(30:23):
It's gonna, it's involved withprotein deposition, with muscle
development.
And that way we want it there.
But when it's in excess, it maycontribute to LVH, left
ventricular hypertrophy, maybearrhythmias.
There's a few studies thatallude to that, but don't
necessarily say it.
And it doesn't give us aspecific cutoff.

(30:43):
You know, we also know thatelevated dihydrotestosterone is
associated with male patternbaldness.
So, you know, multiple reasonswhy we want to just kind of keep
that in check and maintain itwithin a physiologic or mildly
superphysiologic level.
But wholeheartedly, I supportthe use of bioidentical
hormones.
I don't see a risk from acardiovascular standpoint.

(31:04):
If we take a step back and lookat what it's doing to the
vascular system, not onlytestosterone, but estradiol
improve nitric oxide and enosnitric oxide recruiting systems.
They improve the endothelialhealth and the ability to
stimulate endothelial progenitorcells, which are those

(31:26):
endothelial stem cells.
So if you get damage done toyour vascular system, you can
repair better when you're onthese hormones.
And they also help uh regulateyour, you know, your that
cholesterol metabolism, youknow, like the the that that
cholesterol that goes to smalland dense, part of that is
hormones being deficient.

Yeah, it's all interconnected.
So I'm glad you brought it tothat.
Well, you mentioned physiologicranges that therapy is
perfectly safe once we're inthere.
I guess there's confusion aboutwhat those ranges are because
we've seen the quote unquotenormal ranges on like your GPs
labs uh change over the decades.
You know, I I know there's somemisinformation about oh, men
produ are just way lower intestosterone than they used to

(32:08):
be.
I know there's some, there'ssome half-truths there.
Maybe we can get into that, butI know the population range
seems to have either broadenedand dropped or whatever.
You can help us clarify that.
And then there's likeperformance ranges, and then
there's like guys who want toget jacked and hope it's really
up here.
So I have to get TRT ranges.
That's a difference.
Yeah.
Well, what do we make of that?
And for women as well.

(32:29):
Like for all the hormones, whatrange can we trust?
And what does that mean?
Physiological, you know,because a doctor might say, Oh,
you're 300 testosterone.
Well, that's right in range.
That's fine.

Yeah.
You know?
It goes, it comes back to whatyour goals are.

Yeah.

Yeah.
Like you said, it's if you'rewanting to get big, then we've
got to push those not only yourtotal testosterone up into
1500s.
You know, I I will say thatwhat we look at less, we don't
look at total, we look at freetestosterone levels.
So that's uh, you know, the thetotal is what everybody kind of
keeps in mind in that ranges,in those ranges, but it's the

(33:05):
free that we really want tofocus on because that's what's
available for your muscleprotein synthesis and
development.
And the same thing for womentoo.
Uh, and it's it's highlysubjective, and it depends on
your goals.
Uh, you know, women are aperfect example of this.
I have women that can toleratea total testosterone in the 500s

(33:25):
and don't have any problemswith hair growth, hair loss, you
know, acne, and they feelfantastic, and they will kill me
if I reduce that dose.
And then I have women that thatare, you know, I'll put them on
a minimal dose and they willstart to get acne, and it will
be in and their test totaltestosterone might be touching

(33:45):
100, and their free is touchingfive, you know, and it's it's
highly subjective.
So it's hard to give a ageneralized sort of range, but I
will say that for the mostpart, I like to shoot for a free
of about 30 to 35 in men, maybe25 to 35 if picograms per

(34:07):
milliliters, yeah.

Okay, 20.
You said 20 to what?
About 20 to 35, depending ontheir goals.
I have personal interest inthis, that's why I'm asking.
Yeah, because I think mine'saround 20, so you know, which is
not bad, but it's no, it's not.

And so, you know, you can if you're looking
to put on masks, then it's gonnabe in a higher range.
If you want to just stay fitand uh and all this is is is a
healthy range.
It's okay for yourcardiovascular system.
If you want to uh justmaintain, maybe stay a little
lean and muscular, then stay on,you know, you can hover in that
mid-range.

(34:39):
Uh, women, I tend to go up toabout a free of 10, maybe a
little higher.
Uh, and when I go higher thanthat, then you know, that's more
often than not, there might besome symptoms, but it's around
that range.
But uh again, highly subjectiveand depends on your goals.

Okay, cool.
All right.
So, some other things that thecommunity is really interested
in is peptides, uh, and alsorife with information,
misinformation out there.
Um, even I'm trying to sort itall out, and I see requests from
supplement companies all thetime, and just everybody's
pushing their peptides.
I I want to I want to get thestory from you about the

(35:16):
evidence and how we can kind offocus this and think what are
these?
What's the benefit?
Yeah, why would we usepeptides?

Well, I mean, I guess just to give you a little
bit of background, I mean, I'vebeen working in the peptide
industry for probably seven toten years, you know, and so very
steeped in it and use it on adaily basis on most of my
patients.
So it comes with a lot ofexperience.
I love working with peptideseven more so than supplements.

(35:42):
Uh, I feel like peptides arevery they're incredibly
bioactive compounds.
You know, the the promise ofwhat we think is going to happen
with supplements doesn't oftenhappen, but it happens with
peptides.
So because they are compoundsthat our body knows how to use
and it gets into the cellularspace where it's supposed to,

(36:05):
where where the action happens.
That's why I think they're sofantastic.
You can imagine them, you canconceptualize them as like mini
hormones.
Hormones large molecules thatneed middlemen, you know,
receptors to do to send theirmessage and do the action that
they do.
Usually it's something on thecell surface, binds a hormone,

(36:26):
transmits it downwards.
Peptides don't need amiddleman, they can go into the
cell and talk directly to eitheruh DNA or pathways that are in
the cell, which is why they'reso powerful.
You know, the in thiscommunity, I would say the
peptides that uh should probablyget the most attention are the

(36:48):
basic ones.
It's BPC157, thymus and beta-4,and then the secretagogs, GHRHs
and GHRPs, growth hormonereleasing hormones, growth
hormone releasing peptides.
The most common combinationthat you guys see in the in that
category is CJC and ipamerelinor tesimerolin, ipamerelin.

(37:10):
So let's unpack all three ofthose.
BPC is derived from gastricjuice, but it stimulates so many
different gene pathways.
It stimulates a nitric oxidepathway, so it preserves
vascular function.
It can actually improve bloodcell formation.
It works on the cellularcytoskeleton.
So it helps the immune systemuh deliver compounds to where it

(37:34):
needs to go, deliver immunecells to where it needs to go,
and it strengthens thecytoskeleton.
And it does it, so this is whyit's so good when you're
healing.
It lays down parallel collagenas opposed to disorganized
collagen that might happen toform scar tissue.
So it's a magical compound thatworks in so many different

(37:55):
places, everything from brainhealth down to uh you know
ligamental health.
Thymus and beta 4 is a greataddition to that because it also
works on the cytoskeleton in adifferent compound, but together
they are really potent inhelping heal from any types of
injury.
And uh and it is also so thymusand beta 4 focuses more on

(38:18):
immune cells, platelets, uh, andactually BPC does on platelets
too, but uh more on immunecells, but also but definitely
plays a part in thatcytoskeleton.
Uh and then when you're lookingat the secretagogs, those so
CJC and ipermoralin, theyinfluence growth hormone.
And you can think of those likeone of them is filling the

(38:40):
tank, filling the amount ofgrowth hormone you have to be
able to release, and the otherone increases, optimizes how
much you release.
And so by improving growthhormone, you improve IgF1, which
is our major healing hormone.
So many like trickle-downeffects of growth hormone
benefits.

Yeah, no, that was that was a good summary.
I was definitely familiar witha couple of those, like BPC 157,
which I briefly took from myshoulder.
I don't know personally that itwas overly beneficial, but I
had other mechanical stuff goingon that I'm still dealing with.
But are these still um becausesome of the logistical issues
were like, well, they'reinjectable and and it's hard to
like find practitioners you canwork with and to get it legally

(39:21):
because there's this wholeunderground of buying the powder
and getting it mixed and allthat.
What's the state of that today,both with access and also form,
you know, form?
Because I'm hearing aboutliquids and and and oral and all
this stuff now.

Yeah, yeah.
This is this is a hot newmarket right now.
Um, there's a lot of companiesthat are trying to bridge this
gap so so that we don't have touse injectables.
And you know, the problem withthis industry of injectables is
that there's all these internetcompanies that are research
only, you know, and when you geta research-only peptide, you

(39:55):
are getting no guarantee thatthis is a safe compound.
In fact, it will say on thelabel, not for human use.
For human use.
And not for veterinary use, noteven for use on your pets.
Okay, so be careful if you'regetting that.
I mean, they're they claim thatthe sources are reliable and
they will have third-partytesting, but ultimately they're
not being held accountable forany adverse events.

(40:16):
So, and that's dangerous whenyou're injecting something.
When you're doing somethingorally, you could probably get
away with a little bit more,there's a little more
flexibility there because it'sonly getting into your
gastrointestinal tract andyou'll be able to get it out.
It's not a sterile situation.
There are a host of companiesthat are now creating oral
forms.
Some are liposomal, some are uhbuckle-derived oral strips, and

(40:41):
some are just you know uhcapsules.
Most peptides, unless they havespecific binders to them, and
we don't know actually, mostpeptides do not survive the
gastric environment.
There are a few that do.
BPC is one of them, and westill don't have a definitive
way to make most of thosesurvive the gut.

(41:01):
There are some technologiesthat are trying to keep them
preserved and deliver themthrough the gut lining better.
And then there are some claimsthat liposomal technologies
preserve it so that it can getthrough into this into the
circulation better.
Problem is we don't have anyreal data to support if that's
actually happening.
We don't have uh pharmacologicdata or biochemical data to see

(41:24):
if it, you know, what the levelsare, you know, after it's
absorbed.
And part of the problem is thenature of peptides.
Peptides are such short-livedcompounds, most of the time
their peak action occurs withinless than an hour, 20 minutes.
So it's really hard to measurelevels in the system.
Uh, you know, there the wadascreens for peptides in all

(41:46):
their athletes.
The reality is that I don'teven know if wada has a
definitive way to measurepeptides.

So the short half-life.
Yeah.

Yeah, because it's such a short half-life.
So making uh, you know, arandomized control study to
actually verify that is verydifficult.
There are some companies thatare looking at that right now.
My advice would be if you'regonna get it, try and get it
through a practitioner that uhknows what they're doing.
It uses a compounded pharmacythat has a tracking method as

(42:17):
well as guarantees sterility.
And if you're gonna try orals,you know, you could give it a
shot, but know that unless it'sBPC right now, the data is is
not out there, and you'll haveto decide on your own by trial
and error if it's working.
You know, there are manydifferent uh delivery mechanisms
that are being tested rightnow.

(42:37):
And I'm I'm curious to seewhich one kind of pans out.
And I'm excited too, becausethis actually makes access for
all of these much easier.

So, related to the ones you mentioned, you said it
would be relevant to thisaudience and you gave a little
bit of an overview.

Yeah.

What's the context for these?
Because, you know, one onemessage that I always have is
8020, right?
Like, like fix the foundations,work on the big things.
Don't try to just get 10different solutions to a problem
in parallel, right?
Like build your lifestyle, liftweights, move.
Like there's some big hittersthat will move the needle a lot
for individuals.

(43:12):
Yes.
Uh, before necessarily going toeven supplementation, but at
the same time, there's certainsupplements that I would say,
hey, from day one, this could behelpful, whether that's
creatine or fish oil ormagnesium if you're deficient.
And I imagine peptides have asimilar story where, you know, I
know there's a recovery andrehab piece of it, an injury

(43:32):
rehab, and then there's aperformance.
Like, when should someone say,This is the decision point when
I should consider peptides?

Anytime you got an injury, consider a peptide.
Okay.
All right, because it willimprove your recovery time.
That combination, BPC, TV4, andthen some sort of secretagog,
that will do a lot.
Uh if you're cycling up toprepare for an event, that's a
time to consider using peptidesas long as you know that they're

(44:02):
not testing.
Or if it's a substance positiveevent, so to speak.
You know, if you're arecreational athlete, they're
not going to test you, and youcan use peptides to increase
your performance, increase yourincrease your personal times.
And then if you may want to useit periodically, uh just to
within your down trainingcycles, because it will they

(44:24):
help recovery.
I mean, when do you want tostart?
It really depends.
So I'll say this start usingpeptides when you start feeling
like your system is notrecovering the way it used to or
the way you want it to, to meetyour goals.
If your goals are you have arace or a competition coming up,
then that's a great time tostart using it as you're

(44:44):
training up because then you canallow yourself to be more
resilient.
If you have an injury, thendefinitely a time to use those
as options because they'rereadily available now.
So I, you know, it's really itdepends on where you are in your
trajectory.
Yeah.
I can tell you for myself,about five years ago, six years

(45:05):
ago, I mean, I've I've been anathlete my whole life, and I
just started noticing uh adownward trajectory in a lot of
my performance, or it kind ofplateaued, and um I started
saying, okay, I've never reallyused supplements and these
tools.
It's probably longer than thatago, about 10 years ago.
Yeah.
So uh once I started feelingthat, I said, okay, I've got to

(45:30):
support my system.
How am I gonna do this?
I started with the basics, Istarted with the right
supplementation, tried that,that didn't work, or if that
held for a little while, then Iwent to hormone replacement
therapy and then added onpeptides.
So go in stages, start with thetools that have the widest
benefit.
And that would be firststarting with testosterone,

(45:54):
basic hormones, and then add onto those afterwards.

Okay, so that's interesting because that it
sounds a little ambiguous to me,no offense, right?
Like there's not like bloodmark blood tests that would be
like you should take B2PCbecause of this blood test.
Yeah, maybe we'll get to that.
But you that's an interestingcomment about the testosterone.
So, what about a guy like me?
Because this is what I loveabout podcast interviews, is I
get some free coaching.
Um no, seriously, where I thinkmy total testosterone is 600,

(46:21):
my free is 20, decent.
You know, I'm 45.
Um, it's actually gone up alittle bit over the years
naturally, which is cool.
But you say use testosterone oruse consider TRT.
Am I a candidate where I'd belike, hey, there's a performance
element here that I care aboutand it's still safe to have TRT,
or is it like, look, I don'thave symptoms, libido is good,
all that.

(46:41):
Like, jump to peptides, ormaybe I don't need either
because recovery is fine.
Like, where would a 45 or 50year old like that is fairly
healthy fall on that spectrum?

What's your goal?
That's I guess that's thequestion.

I'm building muscle, keeping lean, you know,
performing.
I don't have any sportspersonally that I'm into, but
um, you know, I have kids, justwant to be healthy.

Yeah, what I would do for you is give you
something to stimulate yoursystem's ability to make a
little bit more testosterone,and then see how that works for
you, see what kind of changesyou have, and then add on a
couple of peptides, you know,because the performance aspect
of testosterone is significant,and you don't have to jump to
using testosterone replacement.

(47:22):
There are plenty of ways tooptimize what your body can do
as long as it's stillfunctioning, and yours is.
So every cell in your body,except for your sperm, responds
to testosterone.
There's a reason for that, anduh, and so that's why I feel
like that is a usefulfoundational tool.

(47:43):
And we don't have to sacrificeyour ability to make
testosterone.
We can actually just amplify ita little bit and then see if
that gets you a little moremuscle, gets you some PRs.
And if it does, great.
And you don't have to do itpermanently, you can do it in
cycles.
See how you do for threemonths.
You know, somebody that's isalready an athlete will respond

(48:03):
pretty quickly to it.

So now the listener's like, what the heck
is he talking about?
What stimulates testosterone?
Because there, there again, isanother area rife for taking
advantage of people, right?
Because there's beentestosterone boosters for years
that are that are BS.
Let's be honest.
Um, what are you talking about?

I'm talking about uh enclomebe, talking
about HCG, I'm talking about uhthe ones that are over the
counter that are that aresupplement-based or herb-based,
you're at best gonna get maybe a150-point increase in your
total testosterone, and thatdoesn't guarantee that it's uh
it's increasing your free.

(48:39):
So marginal benefits withthose.
Mostly what you get you what ifyou're gonna do that, you've
got to work with you with uhpharmaceutical agents.
Yep.
Okay.
HCG is injectable andclomophene is oral, but uh and
that's a uh second generation ofClomid.
But these are used by fertilityfertility clinics and they help
improve sperm count as well astestosterone production.

(49:02):
So interesting.

Yeah, yeah, clomid.
Uh that that that takes me backto some some dark days uh my
wife and I with on on her end,but anyway.
Okay, no, that's good that'sgood for people to know, and
that's why we're talking throughall this because there are a
lot of options I think peoplearen't uh familiar with, and
also you guys need to seek outprofessionals who understand
this and who do this in acontrolled, like you said,

(49:24):
there's sterile methods that arenecessary, there's some medical
knowledge that's necessary insome cases.
Obviously, we're gonna I'mgonna pump you up as we end the
show in a bit and have see wherepeople can reach you, Dr.
Hussein.
But a couple other things on mynotes that people were
wondering about.
Yeah, one was the calciumscoring, because I had one of
those years ago.
It costs like a hundred bucksat an imaging place.

(49:45):
My wife was told to get one,and I I even told her, I said, I
don't know, we're in our 40s.
I've heard that like it's notgonna tell you anything unless
it's, I guess, really bad.
Like if it's a non-zero highscore when you're that young,
maybe it's not worth it.
But what's the deal?

Yeah.
So if we take this back to thebeginning of our conversation
and talk about what I would doin addition to or what needs to
happen in addition to those labmarkers, you need to get
imaging.
You need to get some sort ofassessment of your
atherosclerotic burden and thecoronary arteries.
Why is that?
Because cardiovascular diseaseis still the number one killer

(50:20):
globally, cardiovascular diseasemeaning atherosclerosis.
And of that, the subpopulationthat dies the most is the sudden
cardiac death portion of it.
That's 50% of the populationthat dies of heart disease, of
atherosclerosis, never makes itto the hospital because they
didn't know they had dangerousplaque and they died before they

(50:41):
could get help.
So, keeping that in mind, whenyou're getting an assessment of
risk, blood tests will only goso far because even though it's
2025, we are still in a barbaricage of medicine.
We don't have all the pieces,we don't know how to connect it
all together, we have an idea ofwhat's going on, but we can't

(51:04):
get a definitive marker, youknow, a definitive pass-through,
like line through of theprocess.
So that's why you got to takepictures.
We got to see what's at the endof the line.
The two options right now arecalcium score and a CT coronary
angiogram.
If you told me 10 years ago,you were if you asked me 10

(51:25):
years ago, should I get acalcium score?
The answer unequivocally wasyes.
Get a calcium score because atleast we get some information.
We can see if you have a lot ofcalcium, then you are a
high-risk person and we need totreat you aggressively.
Calcium scores look at only thecalcium portion of plaque.
There is that whole otherportion of plaque that's not

(51:46):
that's being missed, and that'sthe cholesterol portion.
What's in the plaque that'scholesterol is what causes heart
attacks, and that's what'sbeing missed when you get a
calcium score.
So if you have a high calciumscore, you probably have a lot
of cholesterol, you're at risk.
If you have a low calciumscore, yeah, you don't know.

You don't know.

You don't know.
So that's why right now wehave, you know, and and this has
taken years for the CAT scantechnology to come to speed up
to speed.
It is now up to speed, and ontop of that, we can do we can
take those images and processthem with AI software.
There's multiple companies thatdo it now to really get

(52:29):
specific granular details aboutthe plaque composition and the
severity.
That is so that CCTA, and andthen the one that is used very
commonly is called Clearly.
There's other ones that aregoing to be available, Carrie
Heart, Heartflow.
All of these companies do anAI-based processing that looks
at plaque and tells us exactlyhow much calcium, cholesterol,

(52:53):
and inflamed cholesterol thereis.
So uh, and that's where it'simportant because when we see
cholesterol and inflamedcholesterol, if I see that, I
know that's a person at risk,and I can correlate that with
lab data and say, okay, this iswhere I'm connecting the dots.
I can start these therapies andthen track the lab data as time

(53:16):
goes on, repeat the scan in ayear, two years, what have you,
depending on the severity.
So if you have a choice, getthe CCTA because it gives us a
much more uh uh robustassessment, it gives us a global
assessment, and it tells us ifyou are one of those people

(53:37):
that's at risk for a suddenevent.

So is that uh something anybody at just about
any age should get a baseline,or is there a minimum that you
would do it, or if you're atrisk, like who should do that
baseline?

I think at uh if there's family history or
risk, I would say do that as abaseline and probably do it
before your 40s.
Because if you get anassessment before your 40s, and
and that will be probably beforeyou there, it's severe, but
it'll tell us that stuff isbuilding up.
We need to do it early.
If you don't have uh risks, ifyou you know, like a family

(54:11):
history or no no and and yourlifestyle is pretty well
managed, ideally I'd say in the40s, but I like everyone to get
it by 40.

Okay, well, I missed that window, but still.
Yeah.
No, no, that's good, that'sgood.
Yeah, I've done I've doneepisodes where it's like, when
should you think about menopausein your 30s?
And all the women are like, I'malready it's okay.
It's okay.
We're just talking about youknow what you can do when give
it starting where you're at.
Yeah.

All right.
So one thing I will add,there's there are some concerns
about radiation with the withthis CAT scan.
Done in the right hands, it'sthe equivalent of two
mammograms.
And if you don't have to do it,you know, once every what five
to ten years, then it's minimaloverall.
But the information isimportant.

Good.
No, that's good to know.
Is that done with contrasts?

Yes.

Yeah, okay.
Is that the galadium contrastor the one that people are
concerned about?
More iodine-based iodine.
Okay.
All right, cool.
All right.
So, really to tie this up, theone thing we didn't get much
into, but is really important tothe audience here is the
lifestyle versus thetherapeutic.
We've talked a lot about uhpeptides and hormones, and you

(55:21):
mentioned briefly somemedications, right, like
statins.
Where is the balance betweenall of this and lifestyle?
And from a medicalprofessional's perspective, you
know, we know that the vastmajority of the population is
just does not live a healthylifestyle.
Sadly, that's just the case.
Where what's the escalationprocess?
People who are listening whoare trying to clean their life

(55:42):
up a little bit right now, whereshould they, what should they
prioritize, in your opinion?

I would prioritize movement and I would
prioritize the quality of food.
Okay.
All right.
If you can start with those twothings, that will take you very
far.
Adding to that would be stressmanagement and stress management
and emotional well-being.
I think that uh that gets underunderrepresented and it has a
significant uh effect on ouroverall health.

(56:08):
The movement aspect of it isgoing to improve not that's one
of the most powerful tools wehave because improving muscle
health will improve glucosemanagement.
The muscle itself releases ahost of anti-inflammatory
myocines.
You know, I think the audiencehere knows enough about this.
I don't have to go into that.

(56:28):
Um, but muscle is the currencyof health.
So movement is gonna developthat.
We need to develop that, andthen it also helps with energy
management.
So moving, say, after you havea meal, just light movement, you
know, it helps to digest thefood, helps to reduce the
glucose spikes, uh, and helpmanage energy a little bit

(56:49):
better.
And it's gonna keep you moreresilient as you get older.

Yeah, let's sit on that for a bit because the
audience has heard I've talkedtheir year off about muscle mass
and strength training and allthat.
So we don't have to go intomasterclass about that.
It's super, super, superimportant.
The movement side, I've beenkind of surprised the more I've
learned about that, not just thewalking after meals being so
powerful for like blood sugarregulation and insulin
sensitivity, like compared toeven diabetes medication.

(57:14):
I wish my dogs weren't barkingright now.
Um, but then the uh the thingthat I learned about like
movement snacks, you know, notsitting, like not sitting as an
independent risk bearable.
And I'm telling people all thetime, get up every half hour,
not even every hour, get upevery half hour, walk for two
minutes.
Yep.
And because there was an actualstudy that looked at that
specific intervention and showedjust a whole swing in

(57:36):
everything muscle proteinsynthesis, you know, how you use
glucose, nutrient partitioning,insulin sensitivity, and then
even uh the myokines and theinflammatory markers kind of
inverting when you just move alittle bit.
So I mean, tell us about allthat because people need to
understand how it's easy andpowerful to do.

Yeah, yeah.
The you know, it's it when youaccess the muscoskeletal system,
when you just start moving andengage the ability to pull
glucose in, reduce your glucosespikes, and then improve uh your
I mean you're improving bloodflow.
There in every aspect, you'reimproving your your global

(58:15):
metabolic health.
It's from multiple systems.
So, like you said, it's it'sfrom your muscle functioning
better.
It's giving your because whenthe muscle is uh and when your
system is sedentary, then atbaseline, uh you're going to
potentially develop you know thetoxins may build up, you may
get infl some inflammatoryburden.

(58:37):
The idea of sitting and uh andjust sort of uh being in and
being inactive, it's not whatour system is meant to do.
And so by just amping it upslightly, we get these little
pulses of activity that don'tcause any breakdown of tissue,
but help manage, say,inflammatory load, stress, you

(58:58):
know, all of these littleburdens that occur while we, and
especially in this in in themodern era where when we're
sitting, we're probably lookingat something, we're doing
something, engaging our emotion,our our sensory system that is
creating some sort of stress,work, some sort of burden.
You know, these little exercisesnacks serve as a like a

(59:20):
pop-off valve to purge some ofthis and allow our
parasympathetic nervous systemto be more regulated, heart rate
variability to go up, to getblood flow to the muscles,
improve nitric oxide withouthaving to do a you know a
high-intensity interval workout.
You know, these help maintainbaseline health more than just

(59:41):
you know the high intensity hourthat we get from working out.
Because going back to what wetalked about in the beginning,
that's the performance aspect ofit.
That hour of pushing ourselvesimproves our performance.
The exercise snacks improve, itlifts the baseline so that our
General health is better.

Philip Pape (01:00:01):
Yeah, I love that.
I love the baseline of healthand longevity.
Built on that is theperformance.
And then you could even widenthat baseline of performance
because your health is better.
And it's kind of a nicecyclical, or you know what I'm
trying to say, thing.
So, okay, let why don't we endon there's so many topics we
could get into.
I've enjoyed this conversation.
End on the emotional well-beingbecause people know I can be

(01:00:22):
like almost delusionallyoptimistic.
I have an optimism bias, but Iown it.
And I actually encourage peopleto try to be like optimistic
about things to a fault becauseI think I think there's better
health outcomes for well-beingbetween that and having social
connection.
Totally.
And of course, the physicalhealth leads to the mental
health as well.
There's so many things.
So tell us about that.

(01:00:43):
And again, cardiovascularhealth and emotional well-being
and what the connection is tofinish here.

Dr. Abid Husain (01:00:49):
Direct correlation between stress
management, emotional health,and cardiovascular health.
If I want to draw an easythrough line, think about it
this way.
Every time you think aboutsomething bad, you get stressed,
you get depressed, you're goingto release epinephrine and
norepinephrine.
Epinephrine and norepinephrineare stress hormones that make

(01:01:09):
your blood vessels contract.
They are pro-inflammatory andthey will reduce your heart rate
variability, increase yourheart rate, increase your blood
pressure.
I mean, the idea is that theyare designed to be used during
stress situations so we canperform better for short periods
of time and heal if we need to.

(01:01:29):
All right.
In our current society, in ourcurrent lifestyle, it's
constantly being activated.
And by doing that, we create anoverall higher inflammatory
burden that then trickles downto our vascular system, our
brain health, cortisol, becauseif we release enough epinephrine

(01:01:52):
constantly, then we're going torelease cortisol that goes
along with these stresshormones, and that will affect
our brain health as well.
So it's a it's a cascade.
And we have the ability tomanage that on some level by
understanding, okay, I don'tneed to get worked up about
this.
I can have a positive attitudeabout this.
I can reframe this thing thathappened into looking at the

(01:02:15):
positive things that have comeout of it.
You know, in and these arereally powerful tools.
I I can I can go and spend timewith people I love because that
calms me down and it reducesthe sympathetic burden.
So, you know, there there aretherapies that you can do to
help get you to that place.
There's neurotherapies, there'sinjectables, there's

(01:02:36):
psychedelics, there's, you know,there's so much that you can
do.
But at home, every day, I thinkkeeping a positive attitude,
regulating your emotions, andknowing that that really helps
your your overall health is sopowerful because that lifts the
baseline, makes you moreresilient, and I mean, it just

(01:02:57):
makes life better.

I love that.
It makes life better, it givesyou meaning and purpose and
physically allows you tofunction.
And honestly, anybody out therewho who has family and others
they depend on, because we don'tlive in a vacuum.
Yeah, that's part of the socialfabric that allows us to be
there for others and live a longlife and not be a burden to
others as well, if that's a goalof yours.
So uh, Dr.
Hussein, this has beenincredible.

(01:03:19):
I think we got it.
There's so many topics we coulddive into like as separate
episodes practically, but uh,where do you want folks to reach
out to you for either educationor to contact you or anything
else?

Yeah.
Um let's see.
I'm at Boulder LongevityInstitute.
So um I see patients therethree days a week.
You can email me there and uhlook for me if you want to
connect.
Uh, I also do a lot ofeducation in uh different
lectures with the organizations.
Uh there's uh New BioAge andthen um Vibrant Health.

(01:03:52):
And so look for me there if youwant to get some some other
ways to connect with me.

All right, cool.
We'll we'll definitely includethat stuff in the show notes for
listeners to find you, and andanybody who wants to reach out
to uh Dr.
Sane can also let me know andI'll connect to with them.
Yeah.
Thank you so much for comingon.
I mean, this is importantinformation.

Hey, thank you.
This has been a real pleasure.
I appreciate it.

It's been awesome.
Thank you.

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A Cardiologist's Guide to Hormones, Peptides, and Labs for Lifters Over 40 (Dr. Abid Husain) | Ep 406

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.css-14f5ked{margin:0;word-break:break-word;display:-webkit-box;-webkit-box-orient:vertical;box-orient:vertical;-webkit-line-clamp:2;overflow:hidden;}A Cardiologist's Guide to Hormones, Peptides, and Labs for Lifters Over 40 (Dr. Abid Husain) | Ep 406