December 7, 2025 • 10 mins
We flip health planning by backcasting from the final decade of life and engineering the strength, fitness, and biomarkers needed today. From APOB and Lp(a) to DEXA priorities, strength standards, and hormone clarity, we build a practical roadmap for longer, better years.
• defining the marginal decade and backcasting
• VO2 max decay and fitness as strongest risk modifier
• strength and muscle as metabolic armor
• bloodwork that matters: APOB and Lp(a)
• lipid strategy: diet limits and effective medications
• DEXA focus on bone density, visceral fat, lean mass
• fracture risk and heavy strength interventions
• menopausal therapy reappraised after WHI
• men’s hormones, free testosterone, and fertility
• provocative frontier: rapamycin and ovarian lifespan
This podcast is created by Ai for educational and entertainment purposes only and does not constitute professional medical or health advice. Please talk to your healthcare team for medical advice.
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
SPEAKER_02 (00:00):
Welcome.
Thanks for sharing this stack ofsource material with us.
Today's deep dive is really foryou, the person who wants to get
way ahead of the curve, not justreact to things.
SPEAKER_00 (00:10):
That's right.
SPEAKER_02 (00:11):
We're going to try and cut through some of the
noise and find the uh objectivemarkers and the philosophy that
really drive health span andlifespan.
SPEAKER_00 (00:20):
And it's all about being systematic.
The sources really champion thisidea of an engineering-based
approach.
We're looking at everything: exercise, nutrition, hormones, (00:26):
undefined
even pharmacology.
SPEAKER_02 (00:32):
Trevor Burrus, Jr.: So the mission today is to
figure out how to define yourhealth trajectory right now.
SPEAKER_00 (00:37):
Aaron Powell Exactly.
To define it against a futurethat you actually want.
SPEAKER_02 (00:40):
Okay, let's unpack that because we're starting with
a concept that sort of flips howyou think about long-term health
on its head.
It's called backcasting.
SPEAKER_00 (00:47):
Right.
And it's all about somethingcalled the marginal decade.
SPEAKER_02 (00:50):
We all forecast, you know, we plan for next year,
maybe five years out.
But this is about starting fromthe end and working backwards.
SPEAKER_00 (00:56):
Aaron Powell It's essential because we have to
know what we're aiming for.
Longevity isn't just one thing,it has two vectors.
Life span, which is, you know,binary, you're live or you're
not.
SPEAKER_02 (01:08):
Simple enough.
SPEAKER_00 (01:09):
And then there's health span.
That's the quality of that life,your physical abilities, your
cognitive function, youremotional well-being.
SPEAKER_02 (01:15):
And the marginal decade is just the last 10 years
of your life.
SPEAKER_00 (01:19):
That's it.
And the backcasting exercise isto define in like exquisite
detail what you want to be ableto do during that decade.
SPEAKER_02 (01:27):
So not just be alive, but like specific
actions.
SPEAKER_00 (01:31):
Exactly.
Do you want to be able to pickup a great grandchild from the
floor, play with them withoutassistance?
Do you want to be able to get upon your own?
SPEAKER_02 (01:37):
I love that because that sets the goal.
It's not this vague, I want tobe healthy.
It's an engineering problem.
SPEAKER_00 (01:43):
It is an engineering problem.
You've established the objectivefunction.
SPEAKER_02 (01:47):
Yeah.
If you want to run a five-minutemile, you train for that.
If you want to be a fullycapable 90-year-old, you have to
train for that.
SPEAKER_00 (01:53):
And you have to start training now.
Because backgasting forces youto quantify what's needed today
to fight what the sources callthe gravity of aging.
SPEAKER_01 (02:03):
The gravity of aging, I like that.
It's this constant pulldownwards.
SPEAKER_00 (02:08):
It is.
Your VO2 max, for example, yourbody's ability to use oxygen, it
declines by about 8 to 10% perdecade.
Every decade, starting in your30s.
SPEAKER_02 (02:17):
So wait, if I want to be functional at 90, say I
need a VO2 max of 30 just to beindependent.
What does that mean for me at50?
SPEAKER_00 (02:26):
Well, you have to do the math backwards.
SPEAKER_02 (02:27):
Yeah.
SPEAKER_00 (02:28):
You might need to be at, say, 42 or even higher at 50
just to have a buffer for thatpredictable decay.
SPEAKER_02 (02:33):
So if you're not fit now, you're basically taking out
a loan against your futureself's mobility.
SPEAKER_00 (02:39):
You are mortgaging your future physical
capabilities.
That's a perfect way to put it.
SPEAKER_02 (02:42):
Okay.
That makes so much sense.
So if we're going to engineerthis, we need data.
Let's talk metrics.
Blood work, how often, and whatare we looking for beyond the
basics?
SPEAKER_00 (02:51):
Everyone should get a baseline early.
I mean, even in your 20s.
You need to know if you have anygenetic landmines waiting for
you.
SPEAKER_02 (02:56):
And after that baseline.
SPEAKER_00 (02:58):
For someone who's already optimizing, maybe two to
four times a year, mostly totrack an intervention or just
confirm you're stable.
SPEAKER_02 (03:06):
Yeah.
SPEAKER_00 (03:06):
But the standard lipid panel, it's just not
enough.
SPEAKER_02 (03:10):
Right.
Everyone's fixated on their LDL,their bad cholesterol.
Why is that an incompletepicture?
SPEAKER_00 (03:15):
It's incomplete because it measures the mass of
the cholesterol, not the numberof particles carrying it.
The real culprit is the particlenumber.
SPEAKER_02 (03:23):
Ah, so it's not the weight of the cars, it's the
number of cars on the roadcausing traffic jams in your
arteries.
SPEAKER_00 (03:28):
Perfect analogy.
SPEAKER_02 (03:29):
Yeah.
SPEAKER_00 (03:30):
And the metric that measures that is ACOB or
apolepoprotein B.
It is the single best predictorof your risk.
SPEAKER_02 (03:37):
APOB.
Got it.
And there was another one youhave to check once.
SPEAKER_00 (03:40):
Yes.
LPA, luboprotein, little A.
It's the most common geneticdriver of atherosclerosis.
It affects like 8 to 20% ofpeople.
You just check it once to knowif you have that risk factor.
SPEAKER_02 (03:50):
And all this ties into the four horsemen of
disease, right?
SPEAKER_00 (03:52):
Yes, exactly.
Atherosclerotic disease, soheart attacks and strokes
cancer, neurodegenerativedisease like Alzheimer's, and
metabolic disease.
SPEAKER_02 (04:00):
And those four account for what, 80% of death
in nonsmokers?
SPEAKER_00 (04:05):
Aaron Powell About that, yeah.
And blood work is our bestweapon against the
atherosclerotic and metabolichorsemen.
And metabolic health fuels theother two, so we start there.
SPEAKER_02 (04:14):
Okay, let's move to functional testing.
Blood work can't tell you aboutyour bones or muscles.
We need a DEXIS scan.
SPEAKER_00 (04:21):
Right.
And most people think DEX isjust for body fat percentage.
Trevor Burrus, Jr.
SPEAKER_02 (04:24):
Which you're saying is the least important metric
from that scam.
SPEAKER_00 (04:27):
It is.
It's number four on the list.
Yeah.
The big three are one, bonemineral density or BMD, two,
visceral fat.
That's the dangerous fat aroundyour organs.
SPEAKER_02 (04:37):
And number three.
SPEAKER_00 (04:38):
Appendicular lean mass index.
Basically, how much muscle youhave in your arms and legs.
It's your strength reserve.
SPEAKER_02 (04:44):
Aaron Powell, let's talk about bone density for a
second because the risk there asyou age is it's terrifying.
SPEAKER_00 (04:50):
You're catastrophic.
If you're over 65 and you breaka hip from a simple fall, your
one-year mortality rate isbetween 30 and 40 percent.
SPEAKER_02 (04:57):
30 to 40 percent from a broken bone.
SPEAKER_00 (04:59):
It's the cascade.
Yeah, immobility, thecomplications, that's what gets
you.
SPEAKER_02 (05:03):
And our peak bone mass is set by our mid-20s.
So what's the intervention now?
How do we protect ourselves?
SPEAKER_00 (05:10):
Heavy strength training.
Things that put sheer force onthe bone, power lifting, heavy
farmer carries.
You have to stress the bone tomake it stronger.
SPEAKER_02 (05:18):
That morbidity risk is a huge motivator.
But let's shift because the dataon cardiovascular fitness, it's
even more powerful.
I mean, the numbers are juststaggering.
SPEAKER_00 (05:29):
They really are.
To put it in context, we allknow smoking is bad.
It increases your all-causemortality risk by what, about
40%?
SPEAKER_02 (05:37):
40%.
Okay.
That's our baseline for verybad.
SPEAKER_00 (05:39):
Right.
Now, VO2 max.
If you compare people in thebottom 25% of fitness to those
in the top 2.5%, the differencein mortality risk is fivefold.
SPEAKER_02 (05:50):
Wait, fivefold as in 400%.
SPEAKER_00 (05:52):
A 400% difference.
The sources are crystal clear.
It's the single strongestpredictor for any modifiable
behavior we know of.
SPEAKER_02 (05:59):
That is just, it's unbelievable.
And strength is right up there,too, isn't it?
SPEAKER_00 (06:03):
Absolutely.
Low muscle mass versus highmuscle mass is associated with a
threefold, a 200% greater riskof dying from anything.
SPEAKER_02 (06:10):
So muscle is your metabolic armor.
SPEAKER_00 (06:12):
This is your metabolic sink.
It's crucial for insulinsignaling, glucose control.
And exercise is probably thebest thing you can do to prevent
Alzheimer's.
SPEAKER_02 (06:22):
This basically proves what you could call a
Tia's rule.
Until your exercise house is inorder, maybe don't waste time
debating niche supplements.
SPEAKER_00 (06:31):
I mean, it's about priorities.
Nail the big rocks first.
SPEAKER_02 (06:34):
Okay, so let's give people some tangible goals for,
say, a 40-year-old.
SPEAKER_00 (06:39):
Yeah, some objective metrics.
You should be able to do a deadhang for two minutes if you're a
man, one and a half for a woman.
SPEAKER_02 (06:46):
Okay.
SPEAKER_00 (06:46):
You should be able to hold a deep air squat, like a
wall sit, for two minutes, and afarmer carry with your body
weight for men, or 75% forwomen, for two minutes.
SPEAKER_02 (06:55):
If you can hit those, you're building that
reserve capacity for the future.
SPEAKER_00 (06:59):
You're building that buffer against the decline.
SPEAKER_02 (07:02):
Okay.
We have to talk aboutcholesterol.
There's so much confusion.
Let's start with what we eat.
SPEAKER_00 (07:06):
Right.
Let's get some cholesterolclarity.
The cholesterol you eat in eggsor whatever has almost no impact
on the cholesterol in yourblood.
SPEAKER_02 (07:14):
It's not the dietary cholesterol.
SPEAKER_00 (07:16):
No.
It's saturated fat that for manypeople raises those dangerous
APOB particles.
SPEAKER_02 (07:21):
So if APOB is the target, what's the goal?
I mean, average isn't goodenough if average people get
heart disease.
SPEAKER_00 (07:28):
That is the key insight.
To be essentially immune toheart disease, you'd need to
keep your APOB incredibly low.
Ideally, below 30 milligdl.
SPEAKER_02 (07:37):
30.
The lab reports say under 100 isgood.
SPEAKER_00 (07:39):
Right, but under a hundred just means you'll
probably get heart disease inyour 70s instead of your 50s.
30 is the level you see innewborn babies in populations
that don't get heart disease.
SPEAKER_02 (07:49):
And there is no way you can get that low with diet
alone.
SPEAKER_00 (07:52):
For almost everyone, no.
Diet won't get you there.
This is where pharmacologicintervention often becomes
necessary if you're seriousabout prevention.
SPEAKER_02 (08:00):
So what are the tools?
SPEAKER_00 (08:02):
The main ones are statins, which slow down
production in the liver,azetamebe, which blocks
reabsorption in the gut, andthen the big guns, PCS canine
inhibitors, which basicallysupercharge your liver's ability
to clear apopey out of yourblood.
SPEAKER_02 (08:14):
That clarifies the lipid landscape a lot.
Now hormones.
This is another area of massiveconfusion, largely thanks to one
study.
SPEAKER_00 (08:22):
The Women's Health Initiative, or WHI, probably the
biggest screw up in modernmedical history.
It turned an entire generationof doctors and women off of
hormone therapy.
SPEAKER_01 (08:31):
And it was flawed, how so?
SPEAKER_00 (08:33):
Deeply flawed.
They started women 10 yearsafter menopause.
The women were already lesshealthy, many were smokers, and
crucially they use synthetichormones.
SPEAKER_02 (08:42):
Not the bioidentical ones used today.
SPEAKER_00 (08:45):
Not at all.
They use CEE, which is estrogenfrom horses, and MPA, a
synthetic progestin.
And that MPA is likely whatcaused the slight negative
signals.
SPEAKER_02 (08:54):
And the headlines about breast cancer risk were
terrifying.
SPEAKER_00 (08:58):
They were, but they were about relative risk.
The absolute risk increase wastiny, like one extra case per
thousand women per year.
The benefits for bone health andquality of life were huge.
SPEAKER_02 (09:09):
So the lesson isn't HRT is bad, it's the right
molecule at the right time iscritical.
SPEAKER_00 (09:15):
Exactly.
Start it as you enter menopause,not decade later, and use
bioidentical hormones.
It's a totally differentrisk-benefit conversation.
SPEAKER_02 (09:22):
Okay, let's shift to men in TRT.
The focus is always on totaltestosterone.
SPEAKER_00 (09:27):
Which is almost meaningless on its own.
The number you have to focus onis free testosterone or free T.
That's the portion that'sbiologically active.
SPEAKER_02 (09:35):
And the goal is to get that into the upper end of
the normal range.
SPEAKER_00 (09:38):
The upper end of the physiologic normal range?
Yes.
Usually with a low doseapproach, like 100 milligrams a
week, split into two shots, tomimic the body's natural rhythm.
SPEAKER_02 (09:47):
Aaron Powell What about men who want to preserve
their fertility?
SPEAKER_00 (09:50):
That's a huge consideration.
Exogenous testosterone shutsdown your own production.
So for those men, you'd usesomething like HCG, which
stimulates the testes directlyto produce their own
testosterone, keeping everythingonline.
SPEAKER_02 (10:05):
We've covered a ton of ground here.
From uh backcasting your90-year-old self to measuring
APOB, clarifying the WHI study,and hitting those really tough
strength metrics.
SPEAKER_00 (10:16):
It really provides an objective, actionable roadmap
you can use to influence yourown health span.
SPEAKER_02 (10:21):
Absolutely.
We've laid out the tools basedon what's proven, but the
frontiers are always moving,which leads to a really
provocative final thought foryou to consider.
SPEAKER_00 (10:30):
Right.
So there is compelling animaldata that a molecule called
rapamycin can preserve and evenextend ovarian life
dramatically.
So the question is what mightthe future of female fertility
look like if that researchtranslates to humans?
SPEAKER_02 (10:45):
Just think about the implications of that.
Keep measuring, keep training,and above all, keep learning.
Thank you for joining us forthis deep dive.
Welcome.
Thanks for sharing this stack ofsource material with us.
Today's deep dive is really foryou, the person who wants to get
way ahead of the curve, not justreact to things.
SPEAKER_00 (00:10):
That's right.
SPEAKER_02 (00:11):
We're going to try and cut through some of the
noise and find the uh objectivemarkers and the philosophy that
really drive health span andlifespan.
SPEAKER_00 (00:20):
And it's all about being systematic.
The sources really champion thisidea of an engineering-based
approach.
We're looking at everything: exercise, nutrition, hormones, (00:26):
undefined
even pharmacology.
SPEAKER_02 (00:32):
Trevor Burrus, Jr.: So the mission today is to
figure out how to define yourhealth trajectory right now.
SPEAKER_00 (00:37):
Aaron Powell Exactly.
To define it against a futurethat you actually want.
SPEAKER_02 (00:40):
Okay, let's unpack that because we're starting with
a concept that sort of flips howyou think about long-term health
on its head.
It's called backcasting.
SPEAKER_00 (00:47):
Right.
And it's all about somethingcalled the marginal decade.
SPEAKER_02 (00:50):
We all forecast, you know, we plan for next year,
maybe five years out.
But this is about starting fromthe end and working backwards.
SPEAKER_00 (00:56):
Aaron Powell It's essential because we have to
know what we're aiming for.
Longevity isn't just one thing,it has two vectors.
Life span, which is, you know,binary, you're live or you're
not.
SPEAKER_02 (01:08):
Simple enough.
SPEAKER_00 (01:09):
And then there's health span.
That's the quality of that life,your physical abilities, your
cognitive function, youremotional well-being.
SPEAKER_02 (01:15):
And the marginal decade is just the last 10 years
of your life.
SPEAKER_00 (01:19):
That's it.
And the backcasting exercise isto define in like exquisite
detail what you want to be ableto do during that decade.
SPEAKER_02 (01:27):
So not just be alive, but like specific
actions.
SPEAKER_00 (01:31):
Exactly.
Do you want to be able to pickup a great grandchild from the
floor, play with them withoutassistance?
Do you want to be able to get upon your own?
SPEAKER_02 (01:37):
I love that because that sets the goal.
It's not this vague, I want tobe healthy.
It's an engineering problem.
SPEAKER_00 (01:43):
It is an engineering problem.
You've established the objectivefunction.
SPEAKER_02 (01:47):
Yeah.
If you want to run a five-minutemile, you train for that.
If you want to be a fullycapable 90-year-old, you have to
train for that.
SPEAKER_00 (01:53):
And you have to start training now.
Because backgasting forces youto quantify what's needed today
to fight what the sources callthe gravity of aging.
SPEAKER_01 (02:03):
The gravity of aging, I like that.
It's this constant pulldownwards.
SPEAKER_00 (02:08):
It is.
Your VO2 max, for example, yourbody's ability to use oxygen, it
declines by about 8 to 10% perdecade.
Every decade, starting in your30s.
SPEAKER_02 (02:17):
So wait, if I want to be functional at 90, say I
need a VO2 max of 30 just to beindependent.
What does that mean for me at50?
SPEAKER_00 (02:26):
Well, you have to do the math backwards.
SPEAKER_02 (02:27):
Yeah.
SPEAKER_00 (02:28):
You might need to be at, say, 42 or even higher at 50
just to have a buffer for thatpredictable decay.
SPEAKER_02 (02:33):
So if you're not fit now, you're basically taking out
a loan against your futureself's mobility.
SPEAKER_00 (02:39):
You are mortgaging your future physical
capabilities.
That's a perfect way to put it.
SPEAKER_02 (02:42):
Okay.
That makes so much sense.
So if we're going to engineerthis, we need data.
Let's talk metrics.
Blood work, how often, and whatare we looking for beyond the
basics?
SPEAKER_00 (02:51):
Everyone should get a baseline early.
I mean, even in your 20s.
You need to know if you have anygenetic landmines waiting for
you.
SPEAKER_02 (02:56):
And after that baseline.
SPEAKER_00 (02:58):
For someone who's already optimizing, maybe two to
four times a year, mostly totrack an intervention or just
confirm you're stable.
SPEAKER_02 (03:06):
Yeah.
SPEAKER_00 (03:06):
But the standard lipid panel, it's just not
enough.
SPEAKER_02 (03:10):
Right.
Everyone's fixated on their LDL,their bad cholesterol.
Why is that an incompletepicture?
SPEAKER_00 (03:15):
It's incomplete because it measures the mass of
the cholesterol, not the numberof particles carrying it.
The real culprit is the particlenumber.
SPEAKER_02 (03:23):
Ah, so it's not the weight of the cars, it's the
number of cars on the roadcausing traffic jams in your
arteries.
SPEAKER_00 (03:28):
Perfect analogy.
SPEAKER_02 (03:29):
Yeah.
SPEAKER_00 (03:30):
And the metric that measures that is ACOB or
apolepoprotein B.
It is the single best predictorof your risk.
SPEAKER_02 (03:37):
APOB.
Got it.
And there was another one youhave to check once.
SPEAKER_00 (03:40):
Yes.
LPA, luboprotein, little A.
It's the most common geneticdriver of atherosclerosis.
It affects like 8 to 20% ofpeople.
You just check it once to knowif you have that risk factor.
SPEAKER_02 (03:50):
And all this ties into the four horsemen of
disease, right?
SPEAKER_00 (03:52):
Yes, exactly.
Atherosclerotic disease, soheart attacks and strokes
cancer, neurodegenerativedisease like Alzheimer's, and
metabolic disease.
SPEAKER_02 (04:00):
And those four account for what, 80% of death
in nonsmokers?
SPEAKER_00 (04:05):
Aaron Powell About that, yeah.
And blood work is our bestweapon against the
atherosclerotic and metabolichorsemen.
And metabolic health fuels theother two, so we start there.
SPEAKER_02 (04:14):
Okay, let's move to functional testing.
Blood work can't tell you aboutyour bones or muscles.
We need a DEXIS scan.
SPEAKER_00 (04:21):
Right.
And most people think DEX isjust for body fat percentage.
Trevor Burrus, Jr.
SPEAKER_02 (04:24):
Which you're saying is the least important metric
from that scam.
SPEAKER_00 (04:27):
It is.
It's number four on the list.
Yeah.
The big three are one, bonemineral density or BMD, two,
visceral fat.
That's the dangerous fat aroundyour organs.
SPEAKER_02 (04:37):
And number three.
SPEAKER_00 (04:38):
Appendicular lean mass index.
Basically, how much muscle youhave in your arms and legs.
It's your strength reserve.
SPEAKER_02 (04:44):
Aaron Powell, let's talk about bone density for a
second because the risk there asyou age is it's terrifying.
SPEAKER_00 (04:50):
You're catastrophic.
If you're over 65 and you breaka hip from a simple fall, your
one-year mortality rate isbetween 30 and 40 percent.
SPEAKER_02 (04:57):
30 to 40 percent from a broken bone.
SPEAKER_00 (04:59):
It's the cascade.
Yeah, immobility, thecomplications, that's what gets
you.
SPEAKER_02 (05:03):
And our peak bone mass is set by our mid-20s.
So what's the intervention now?
How do we protect ourselves?
SPEAKER_00 (05:10):
Heavy strength training.
Things that put sheer force onthe bone, power lifting, heavy
farmer carries.
You have to stress the bone tomake it stronger.
SPEAKER_02 (05:18):
That morbidity risk is a huge motivator.
But let's shift because the dataon cardiovascular fitness, it's
even more powerful.
I mean, the numbers are juststaggering.
SPEAKER_00 (05:29):
They really are.
To put it in context, we allknow smoking is bad.
It increases your all-causemortality risk by what, about
40%?
SPEAKER_02 (05:37):
40%.
Okay.
That's our baseline for verybad.
SPEAKER_00 (05:39):
Right.
Now, VO2 max.
If you compare people in thebottom 25% of fitness to those
in the top 2.5%, the differencein mortality risk is fivefold.
SPEAKER_02 (05:50):
Wait, fivefold as in 400%.
SPEAKER_00 (05:52):
A 400% difference.
The sources are crystal clear.
It's the single strongestpredictor for any modifiable
behavior we know of.
SPEAKER_02 (05:59):
That is just, it's unbelievable.
And strength is right up there,too, isn't it?
SPEAKER_00 (06:03):
Absolutely.
Low muscle mass versus highmuscle mass is associated with a
threefold, a 200% greater riskof dying from anything.
SPEAKER_02 (06:10):
So muscle is your metabolic armor.
SPEAKER_00 (06:12):
This is your metabolic sink.
It's crucial for insulinsignaling, glucose control.
And exercise is probably thebest thing you can do to prevent
Alzheimer's.
SPEAKER_02 (06:22):
This basically proves what you could call a
Tia's rule.
Until your exercise house is inorder, maybe don't waste time
debating niche supplements.
SPEAKER_00 (06:31):
I mean, it's about priorities.
Nail the big rocks first.
SPEAKER_02 (06:34):
Okay, so let's give people some tangible goals for,
say, a 40-year-old.
SPEAKER_00 (06:39):
Yeah, some objective metrics.
You should be able to do a deadhang for two minutes if you're a
man, one and a half for a woman.
SPEAKER_02 (06:46):
Okay.
SPEAKER_00 (06:46):
You should be able to hold a deep air squat, like a
wall sit, for two minutes, and afarmer carry with your body
weight for men, or 75% forwomen, for two minutes.
SPEAKER_02 (06:55):
If you can hit those, you're building that
reserve capacity for the future.
SPEAKER_00 (06:59):
You're building that buffer against the decline.
SPEAKER_02 (07:02):
Okay.
We have to talk aboutcholesterol.
There's so much confusion.
Let's start with what we eat.
SPEAKER_00 (07:06):
Right.
Let's get some cholesterolclarity.
The cholesterol you eat in eggsor whatever has almost no impact
on the cholesterol in yourblood.
SPEAKER_02 (07:14):
It's not the dietary cholesterol.
SPEAKER_00 (07:16):
No.
It's saturated fat that for manypeople raises those dangerous
APOB particles.
SPEAKER_02 (07:21):
So if APOB is the target, what's the goal?
I mean, average isn't goodenough if average people get
heart disease.
SPEAKER_00 (07:28):
That is the key insight.
To be essentially immune toheart disease, you'd need to
keep your APOB incredibly low.
Ideally, below 30 milligdl.
SPEAKER_02 (07:37):
30.
The lab reports say under 100 isgood.
SPEAKER_00 (07:39):
Right, but under a hundred just means you'll
probably get heart disease inyour 70s instead of your 50s.
30 is the level you see innewborn babies in populations
that don't get heart disease.
SPEAKER_02 (07:49):
And there is no way you can get that low with diet
alone.
SPEAKER_00 (07:52):
For almost everyone, no.
Diet won't get you there.
This is where pharmacologicintervention often becomes
necessary if you're seriousabout prevention.
SPEAKER_02 (08:00):
So what are the tools?
SPEAKER_00 (08:02):
The main ones are statins, which slow down
production in the liver,azetamebe, which blocks
reabsorption in the gut, andthen the big guns, PCS canine
inhibitors, which basicallysupercharge your liver's ability
to clear apopey out of yourblood.
SPEAKER_02 (08:14):
That clarifies the lipid landscape a lot.
Now hormones.
This is another area of massiveconfusion, largely thanks to one
study.
SPEAKER_00 (08:22):
The Women's Health Initiative, or WHI, probably the
biggest screw up in modernmedical history.
It turned an entire generationof doctors and women off of
hormone therapy.
SPEAKER_01 (08:31):
And it was flawed, how so?
SPEAKER_00 (08:33):
Deeply flawed.
They started women 10 yearsafter menopause.
The women were already lesshealthy, many were smokers, and
crucially they use synthetichormones.
SPEAKER_02 (08:42):
Not the bioidentical ones used today.
SPEAKER_00 (08:45):
Not at all.
They use CEE, which is estrogenfrom horses, and MPA, a
synthetic progestin.
And that MPA is likely whatcaused the slight negative
signals.
SPEAKER_02 (08:54):
And the headlines about breast cancer risk were
terrifying.
SPEAKER_00 (08:58):
They were, but they were about relative risk.
The absolute risk increase wastiny, like one extra case per
thousand women per year.
The benefits for bone health andquality of life were huge.
SPEAKER_02 (09:09):
So the lesson isn't HRT is bad, it's the right
molecule at the right time iscritical.
SPEAKER_00 (09:15):
Exactly.
Start it as you enter menopause,not decade later, and use
bioidentical hormones.
It's a totally differentrisk-benefit conversation.
SPEAKER_02 (09:22):
Okay, let's shift to men in TRT.
The focus is always on totaltestosterone.
SPEAKER_00 (09:27):
Which is almost meaningless on its own.
The number you have to focus onis free testosterone or free T.
That's the portion that'sbiologically active.
SPEAKER_02 (09:35):
And the goal is to get that into the upper end of
the normal range.
SPEAKER_00 (09:38):
The upper end of the physiologic normal range?
Yes.
Usually with a low doseapproach, like 100 milligrams a
week, split into two shots, tomimic the body's natural rhythm.
SPEAKER_02 (09:47):
Aaron Powell What about men who want to preserve
their fertility?
SPEAKER_00 (09:50):
That's a huge consideration.
Exogenous testosterone shutsdown your own production.
So for those men, you'd usesomething like HCG, which
stimulates the testes directlyto produce their own
testosterone, keeping everythingonline.
SPEAKER_02 (10:05):
We've covered a ton of ground here.
From uh backcasting your90-year-old self to measuring
APOB, clarifying the WHI study,and hitting those really tough
strength metrics.
SPEAKER_00 (10:16):
It really provides an objective, actionable roadmap
you can use to influence yourown health span.
SPEAKER_02 (10:21):
Absolutely.
We've laid out the tools basedon what's proven, but the
frontiers are always moving,which leads to a really
provocative final thought foryou to consider.
SPEAKER_00 (10:30):
Right.
So there is compelling animaldata that a molecule called
rapamycin can preserve and evenextend ovarian life
dramatically.
So the question is what mightthe future of female fertility
look like if that researchtranslates to humans?
SPEAKER_02 (10:45):
Just think about the implications of that.
Keep measuring, keep training,and above all, keep learning.
Thank you for joining us forthis deep dive.
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