May 6, 2025 • 21 mins
In this episode of The Health Pulse Podcast, we break down what your cholesterol panel is really telling you—not just about your heart, but about your liver health and overall metabolism. Inspired by Dr. Robert Lustig’s insights, we cut through the confusion around total cholesterol, LDL particle size, and triglyceride-to-HDL ratios to help you better interpret your lab results.
Learn why small dense LDL particles, not LDL alone, are the real problem, how high triglycerides often reflect liver and sugar issues, and why your ALT levels may quietly signal fatty liver disease even within the so-called normal range.
🎧 Tune in to understand how cholesterol, insulin resistance, and liver function are deeply connected—and how improving your metabolic health can transform your lipid profile.
📞 Need lab work done from the comfort of home? QLM offers fast, reliable mobile phlebotomy services—no clinic visit required.
📅 Book your appointment or learn more at:
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Disclaimer: The information provided in this podcast is for informational purposes only and should not be considered medical advice. The content discussed is based on research, expert insights, and reputable sources, but it does not replace professional medical consultation, diagnosis, or treatment. We strive to present accurate and up-to-date information, medical research is constantly evolving. Listeners should always verify details with trusted health organizations, before making any health-related decisions. If you are experiencing a medical emergency, such as severe pain, difficulty breathing, or other urgent symptoms, call your local emergency services immediately. By listening to this podcast, you acknowledge that The Health Pulse and its creators are not responsible for any actions taken based on the content of this episode. Your health and well-being should always be guided by the advice of qualified medical professionals.
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Nicolette (00:01):
Welcome to the Health Pulse, your go-to source for
quick, actionable insights onhealth, wellness and diagnostics
.
Whether you're looking tooptimize your well-being or stay
informed about the latest inmedical testing, we've got you
covered.
Join us as we break down keyhealth topics in just minutes.
Let's dive in.
Mark (00:24):
Welcome to the Deep Dive.
Today we're getting intosomething really vital for your
long-term health.
It's all about understandingyour cholesterol panel.
Rachel (00:34):
And not just the numbers but the bigger picture, right
your metabolic well-being.
Mark (00:37):
Exactly.
We're using insights from DrRobert Lustig, specifically from
a YouTube video he did.
You might have seen it it's onthe Levels channel.
Rachel (00:46):
Yeah, the one called Understand your Cholesterol
Panel and Metabolic Health Tests, the Ultimate Guide.
We're working off thetranscript from that.
Mark (00:53):
Right, and our mission today is pretty straightforward
Cut through all the you know theconfusion around these lab
results.
Rachel (00:59):
So you can actually get some actionable knowledge,
understand what's reallyhappening inside your body.
Mark (01:04):
It's fascinating, isn't it , how these tests.
They seem routine, but they'reall connected.
Rachel (01:09):
Totally.
We just see this list, maybesome red flags, green check
marks.
But Dr Lustig really shows howit's like a dynamic story, your
metabolic story.
Mark (01:19):
Okay, let's jump right in Total cholesterol.
Dr Lustig basically says throwit out, ignore it.
Why so strong?
Rachel (01:26):
Well, the thing is total cholesterol.
By itself it doesn't tell youmuch about your actual heart
disease risk.
It's kind of like knowing thetotal cars on a highway.
Nicolette (01:36):
OK.
Rachel (01:37):
But you don't know if they're like safe minivans or
you know a bunch of Ferrarispeeding.
Mark (01:42):
Right, so the total number could be high because of the
good stuff, exactly.
Rachel (01:46):
It can be misleading.
So the main point is don'tobsess over total cholesterol.
It's the types of cholesterolthat really count for
understanding your risk.
Mark (01:55):
That makes perfect sense.
Okay, so let's zoom in LDLcholesterol.
This is the one everyone callsthe bad cholesterol, the one
people worry about.
Rachel (02:02):
Yeah, and look, there's a reason.
Big population studies do showa link, right, higher LDL, more
heart disease risk.
But the, let's say, intensefocus on LDL in medicine.
It's been heavily influenced bythe history of statins, ah, the
(02:23):
drugs that lower it veryeffectively, right.
And Dr Lustig points out, theactual hazard risk ratio for
high LDL is about 1.3.
So there's an association, sure, but maybe it's not the whole
story people think it is.
Mark (02:30):
OK, and this is where it gets.
I think really, reallyinteresting.
Dr Lustig says there isn't justone type of LDL.
Rachel (02:38):
Exactly that's crucial.
You basically got two mainkinds large buoyant LDL
particles and small dense LDLparticles.
Mark (02:48):
Small and dense versus large and buoyant.
What's the difference?
Rachel (02:51):
Well, the standard LDL test.
It just measures the totalamount.
It lumps them both together,but the evidence strongly
suggests it's mainly the small,dense LDL that's linked to heart
disease developing.
The large buoy type seems muchless concerning, maybe even
neutral.
Mark (03:07):
Wow, okay, so you could have a high LDL number on your
report, but maybe, just maybe,it's mostly the less harmful
large kind.
Rachel (03:17):
That's the possibility.
Mark (03:18):
Yes, a key distinction.
But then the million-dollarquestion is how do you know
which type is dominating yourresults if the standard test
doesn't tell you?
Rachel (03:26):
And that question leads us straight to another number on
that panel triglycerides.
Now, these have had a bit of acheckered history.
Mark (03:32):
Why is that?
Rachel (03:32):
Because non-fasting samples can really mess up the
results.
Mark (03:35):
Right, like if you just had I don't know a big glass of
orange juice or something sugarybefore the test.
Rachel (03:39):
Precisely.
It skews things badly.
But and this is key when youmeasure triglycerides after a
proper fast, they actuallybecome a more significant
predictor of heart attack riskthan LDL is.
Mark (03:51):
Really More significant.
Rachel (03:52):
Yeah, the hazard risk ratio is around 1.8 for
triglycerides, compared to that1.3 for LDL we mentioned.
Mark (03:58):
Huh, so why haven't we heard as much focus on
triglycerides then?
Rachel (04:02):
Well, dr Lustig suggests one possible reason is
historically there just haven'tbeen as many blockbuster widely
used drugs specificallytargeting high triglycerides
compared to statins for LDL.
Mark (04:14):
Interesting point.
Okay, so fasting triglyceridesvery important.
How do they connect back tothose different LDL types, the
small, dense versus large,buoyant?
Rachel (04:24):
This is the critical link.
High fasting triglyceridesoften mean you have a higher
proportion of those harmfulsmall dense LDL particles.
Mark (04:33):
Okay, how does that work?
Rachel (04:34):
Think of it like this when you eat excess sugar or
carbs that break down quicklyinto sugar, your liver takes
that sugar and converts it intosomething called VLDL, very low
density lipoprotein.
Mark (04:46):
VLDL Got it.
Rachel (04:47):
And in a fasting state, your triglyceride level
basically is your VLDL level.
They're measuring the samething essentially.
Then these VLDL particles goout into your bloodstream, they
get processed, lipids getdropped off and what's left
eventually becomes that smalldense LDL.
Mark (05:05):
Ah, so high triglycerides are like an upstream indicator
for more small dense LDLdownstream.
Rachel (05:11):
Exactly.
It's a very strong clue thatmore of your LDL is likely the
problematic type.
Mark (05:16):
Got it so.
Too much sugar drives uptriglycerides.
High triglycerides suggest moreof the bad LDL.
What about HDL, the goodcholesterol?
Rachel (05:24):
Right HDL High-density lipoprotein.
Its main job is reallyimportant.
It acts like a scavenger.
Mark (05:29):
How so.
Rachel (05:29):
It helps transport fats, lipids, away from your tissues
like fat cells and back towardsthe liver for processing, maybe
removal.
Mark (05:36):
And it's high-density.
Rachel (05:37):
It's packed with protein relative to the fat it carries,
makes it denser.
Okay, and general, higher HDLis good.
Generally, yes, higher HDLlevels are linked with a
protective effect against heartdisease because of that reverse
transport rule.
There are some rare exceptions,like HDL Milano, but for most
people, yeah, you want healthy,robust HDL levels.
Mark (05:56):
Now Dr Lustig puts a lot of emphasis on a specific
calculation the triglyceride toHDL ratio.
Why look at that ratiospecifically?
Rachel (06:05):
This ratio.
It really gained tractionthanks to Dr Jerry Riven's work
on metabolic syndrome.
It's just a really powerfulsnapshot of your heart disease
risk.
Mark (06:14):
Why does it do that?
Rachel (06:15):
Well, think about it.
It directly compares the badguy, triglycerides, which we now
know are a proxy for smalldense LDL, with the good guy,
hdl, the protective cholesterol.
Mark (06:25):
So it's like a balance scale for those key lipid
players.
Rachel (06:28):
Exactly, and interestingly this ratio can
also serve as a sort of poorman's marker for insulin
resistance.
We'll definitely circle back tothat.
Mark (06:36):
Okay, good.
So this ratio gives a sense ofbalance.
What numbers should people belooking for?
What's a good target?
Rachel (06:42):
Generally speaking, you want that ratio to be 1.5 or
less.
That's considered prettyfavorable.
Mark (06:47):
Okay, 1.5 or less.
Rachel (06:48):
If it starts creeping up .
A ratio of 2.5 or greatersuggests there might be a
problem.
Higher risk.
Mark (06:55):
And you mentioned race differences.
Rachel (06:57):
Yeah, there's some data suggesting that for
African-Americans the idealtarget might be a bit lower,
closer to 1.5 or even below that, but the general principle
holds lower is better.
It's a snapshot of your lipiddynamics, right then?
Mark (07:11):
It really sounds like this ratio tells a much richer story
than just you know, looking atthe LDL number and see if it's
got a green check or a red flagnext to it.
Rachel (07:19):
Absolutely.
It's a shame really, the commonpractice of just glancing at
individual numbers within thenormal range.
It often misses these crucialrelationships, these patterns.
Mark (07:29):
You miss the interaction between them.
Rachel (07:30):
Precisely.
Mark (07:31):
Okay, let's dig back into that small dense LDL.
We know it's the one we're moreworried about, the one linked
to plaque.
What else is important here?
Rachel (07:39):
Well, first, a practical point Dr Lustig makes To
interpret your lipid profileaccurately, you need to be, you
know, generally healthy at thetime of the test, meaning no
acute illness like a bad cold orinfection which would show up
in your white blood cell countthat can affect lipids Okay.
And also your thyroid functionneeds to be stable, specifically
(08:00):
your free T4 level.
Mark (08:02):
Why thyroid?
Rachel (08:03):
Because hypothyroidism an underactive thyroid can
actually falsely increase yourtriglyceride levels.
Ah, good to know.
He even gives a quick mentionto Hashimoto's thyroiditis as a
common cause and notes you cansometimes use, you know,
holistic or complementaryapproaches alongside medication.
Mark (08:20):
Right.
Important context these numbersdon't exist in a vacuum.
Ok, back to the LDL particlesthemselves Large versus small.
Rachel (08:27):
So, as we said, the large boyan LDL that's most of
it, maybe 80 percent Seemspretty neutral cardiovascularly,
Like bigger, fluffier beachballs maybe.
Mark (08:37):
OK.
Rachel (08:37):
The small, dense LDL.
That's a smaller fraction,maybe 20 percent, but that's the
type that can wiggle its wayunder the lining of your
arteries, the endothelium.
Mark (08:45):
And start causing trouble.
Rachel (08:47):
Yeah, that's how plaque formation begins.
They're smaller, denser, theysink in lab tests and they tend
to be more inflammatory.
And again, your standard LDLtest doesn't separate these two.
Mark (08:58):
So how do we get a clue about whether we have more of
this problematic small dense LDL?
We're back to triglyceridesagain.
Rachel (09:06):
We are indeed High.
Triglycerides are yourstrongest indirect indicator
that you likely have more smalldense LDL floating around.
Mark (09:14):
Because remind us of that link again.
Rachel (09:15):
Because VLDL, which is what your fasting triglyceride
level is, is the precursorparticle.
It gets processed by the liverand fat cells, lipids are
removed and what's left overeventually becomes that small
dense LDL.
Mark (09:27):
Okay, let's really hammer home this VLDL and sugar
connection.
It seems so central.
Rachel (09:31):
It is absolutely central In that fasting state.
Remember, triglyceride levelequals VLDL level.
Mark (09:36):
Got it.
Rachel (09:36):
And here's the kicker your liver makes VLDL primarily
in response to sugar.
Mark (09:43):
Not fat.
I thought cholesterol came fromfat.
Rachel (09:45):
Well, dietary fat leads to different particles called
chylomicrons, which clear prettyquickly after a meal and don't
really affect your fastingtriglyceride number, unless you
have a very rare genetic issuelike type 5 hyperlipoproteinemia
.
Mark (09:58):
Okay, so chylomicrons are from dietary fat, short term
VLDL is from VLDL reflected inyour fasting.
Rachel (10:06):
Triglyceridesides is the liver's response to excess
carbohydrates, especiallyrefined sugars and things that
digest quickly into sugar.
Mark (10:13):
So the sugar you eat gets turned into fat triglycerides,
VLDL, by your liver.
Rachel (10:19):
That's the key takeaway.
Mark (10:24):
Fasting triglyceride.
Vldl equals liver processingsugar.
This explains so much like whyDr Lustig sees triglycerides
drop dramatically when peoplecut back on sugar.
Rachel (10:31):
Exactly, it happens quite quickly sometimes.
Mark (10:33):
And it also highlights, like you said, the missed
opportunities in standardinterpretation.
Rachel (10:37):
Totally.
Someone might have LDL.
That's just a bit high.
Maybe HDL is a bit low.
Triglycerides are borderline.
Mark (10:42):
And individually.
The doctor says you're fine.
Rachel (10:45):
Right.
But when you look at thosenumbers together, especially
with that triglyceride HDL ratio, it can scream metabolic issues
brewing, even if nothing istechnically in the red zone.
Mark (10:55):
It's about the pattern, not just the isolated dots.
Rachel (10:57):
Precisely, and these numbers aren't set in stone,
they're dynamic, you can changethem with lifestyle.
Reducing sugar is a huge leverthere.
Mark (11:05):
Which brings up a bigger point Dr Lustig touches on.
Maybe the training doctors getneeds adjusting.
Rachel (11:12):
Well, he notes that primary care physicians often
don't get super deep training inlipidology, the specifics of
lipid metabolism.
Mark (11:19):
So the approach becomes a bit simplistic.
Rachel (11:23):
It can be.
Sometimes it's just LEL, highstatin, triglycerides, high
maybe a fibrate, without alwaysdigging into the why, the
underlying metabolic enginedriving those numbers.
Mark (11:33):
And he also pushes back against the idea that metabolic
health is just about weightright.
Rachel (11:38):
Absolutely.
He debunks that myth prettyfirmly.
You can be thin butmetabolically unhealthy to a
five.
Thin on the outside, fat on theinside.
Mark (11:45):
With a terrible lipid profile.
Rachel (11:47):
Exactly, and, conversely , someone who carries more
weight might actually bemetabolically quite healthy.
It's not about the subcutaneousfat, the fat under your skin.
Mark (11:56):
It's the visceral fat.
Rachel (11:57):
Yes, especially fat in the liver.
That's the real metabolictroublemaker and it's largely
driven by excess sugar, not justoverall calories or visible
body fat.
Mark (12:06):
Okay, this is all incredibly insightful.
Rachel (12:08):
Yeah.
Mark (12:09):
So for people listening wanting to understand their own
results, what's the practicalgame plan?
Rachel (12:14):
Okay, first step, you get your results.
If your LDL is a little high,don't freak out immediately.
Okay, breathe.
Look straight at yourtriglyceride number and your HDL
number.
Calculate that triglyceride toHDL ratio.
Mark (12:30):
What's a good triglyceride ?
Rachel (12:30):
number on its own.
Generally, if yourtriglycerides are under 100
milligdl, that's usually a goodsign.
It suggests you probably don'thave a ton of that small dense
LDL.
Mark (12:38):
Below 100 is good.
What if it's higher?
Rachel (12:40):
If it's higher, then you really need to look at it in
relation to your HDL.
Using that ratio, Remember theconnection Triglycerides become
small dense LDL.
Mark (12:48):
While HDL is trying to clean things up.
Rachel (12:52):
Right, and that ratio, the triglyceride HDL, as we
mentioned, is also a decentproxy for insulin resistance.
Mark (12:58):
OK, insulin resistance we hear that term constantly.
Now let's unpack its role here.
Rachel (13:02):
It's absolutely central to this whole metabolic picture.
People think of insulin as justthe diabetes hormone regulating
blood sugar.
Mark (13:10):
But it's more than that.
Rachel (13:11):
Oh yeah, its primary job is actually being the energy
storage hormone.
It tells your body what to dowith the energy you consume,
store it.
Primarily store it.
Yes, Especially excess energy.
It pushes it into fat cellsunder the skin, around organs
and, crucially, into the liver.
Mark (13:29):
And insulin resistance is when.
Rachel (13:31):
It's when your cells, particularly your liver cells,
become kind of numb to insulinsignal, often because they're
already stuffed with fat.
Mark (13:38):
So they don't respond properly.
Rachel (13:40):
Right, and because the signal isn't getting through
effectively, your pancreasthinks, uh-oh, need to shout
louder, and it pumps out moreinsulin to try and force the
message through.
Mark (13:49):
And the liver is ground zero for this.
You mentioned the portal vein.
Rachel (13:52):
Exactly right.
The blood leaving your pancreasloaded with freshly made
insulin goes straight into theportal vein which leads directly
to the liver, gets the highestconcentration.
Mark (14:02):
So the liver's health is paramount for insulin signaling.
Rachel (14:06):
Absolutely.
And when the liver gets fatty,which is incredibly common now,
maybe affecting 45% of US adults.
Some estimates say Wow 45%.
Yeah, it's epidemic.
When the liver's fatty, itresists insulin, making the
pancreas work overtime, leadingto chronically high insulin
levels.
Mark (14:23):
And high insulin isn't just about blood sugar.
Rachel (14:25):
No High insulin itself that hyperinsulinemia is linked
to a whole host of chronicdiseases Heart disease, yes, but
also certain cancers, dementia,pcos, the list goes on.
Insulin is essential, but toomuch for too long due to
resistance is bad news.
Mark (14:41):
Okay, so clearly understanding our insulin
sensitivity is key.
How can we measure that,besides just looking at blood
sugar?
Rachel (14:47):
Well, in research they use a calculation called
OCHIONEIR sure homeostatic modelassessment for insulin
resistance.
Mark (14:53):
Sounds complicated.
Rachel (14:54):
It uses your fasting insulin level and your fasting
glucose level.
You can actually findcalculators online for it, like
on MDCalc, if you have those twonumbers.
Okay, h-o-a-i-r, but you alsosaid I also said that
triglyceride to HDL ratio wekeep talking about is a
surprisingly good, readilyavailable proxy for insulin
sensitivity Much easier to get.
Mark (15:13):
And what about directly measuring the small dense LDL?
Rachel (15:17):
You can get tests for LDL, particle size or number,
but they're often not standard,might not be covered by
insurance, cost more, so theyaren't routine for most people
yet.
Mark (15:26):
Right, which brings us back to insulin.
Could you just ask for afasting insulin test?
Rachel (15:31):
You can, and it's a really valuable test for
metabolic health.
It's a separate blood draw,usually not part of the standard
chemistry panel.
Mark (15:37):
But there's some controversy, isn't there?
The American DiabetesAssociation advises against it.
Rachel (15:42):
Yes, they do, somewhat controversially, dr Lustig
discusses their reasons andpushes back.
Mark (15:47):
What are their reasons?
Rachel (15:48):
Okay.
Reason one lack ofstandardization, meaning the lab
methods, the assays formeasuring insulin can vary a bit
, lab to lab giving slightlydifferent numbers.
Mark (15:59):
OK, that sounds like a potential issue.
Rachel (16:00):
It is to a degree.
But Dr Lustig's point is, evenwith that variability, if your
level is consistently high, itstill means something is wrong.
It indicates your pancreas isunder stress.
Mark (16:12):
Even if the exact number is slightly fuzzy.
Rachel (16:14):
Right, and some assays might also pick up pro-insulin,
which is like a precursor toactive insulin.
But again, high levels of thatalso indicate the pancreas is
working too hard.
So it doesn't invalidate thetest's usefulness in signaling a
problem.
Mark (16:29):
Okay, what's the ADA's second argument against routine
testing?
Rachel (16:33):
They say insulin levels don't correlate perfectly with
obesity.
Mark (16:37):
And Dr Lusdy's response.
Rachel (16:38):
He agrees, but he says that's precisely why you should
measure it.
It tells you about metabolichealth independent of weight.
Mark (16:44):
Ah, like the TOFI, concept again.
Rachel (16:46):
Exactly, you can be lean with high insulin,
metabolically unhealthy or obese.
With normal insulin,metabolically healthier.
Mark (16:57):
The insulin level reflects the underlying metabolic
function, not just the number onthe scale, so it seems like a
really useful test that's maybeunderutilized.
If someone does get a fastinginsulin test, what are they
hoping to see?
What are good levels?
Rachel (17:06):
Well, generally, the lower the better.
Truly Elite marathon runnersmight be down around two micro
IU per ml.
Mark (17:13):
Wow, okay, for the rest of us.
Rachel (17:15):
Generally under 6 or 7 is considered quite good.
Under 10 is probably still okay.
Mark (17:20):
And when do you start getting concerned?
Rachel (17:22):
When levels are consistently creeping above 10,
that raises a flag for insulinresistance and if you're seeing
levels of 15 or higher, thatstrongly suggests significant
insulin resistance is present.
Mark (17:33):
And that high level points towards.
Rachel (17:35):
It points towards litter dysfunction, liver fat usually,
and a pancreas that's reallystraining to keep up.
Mark (17:41):
This keeps coming back to liver, doesn't it?
Its health seems critical.
Rachel (17:45):
Absolutely critical, and liver function tests, or LFTs,
are often glanced over unlesssomething is wildly abnormal
like high bilirubin causingjaundice.
Mark (17:53):
But there's more subtle information there.
Rachel (17:55):
Definitely Specifically look at the ALT level alanine
aminotransferase it used to becalled SGPT.
Mark (18:02):
ALT.
What does that tell us?
Rachel (18:04):
ALT is a really good indicator of liver fat.
When liver cells are damaged orstressed, often by excess fat,
they leak ALT into thebloodstream.
Mark (18:12):
And what's considered a normal ALT level, because those
ranges on lab reports can bewide.
Rachel (18:17):
They can.
And Dr Lustig points outsomething crucial the upper
limit of normal for ALT hasactually crept up over the years
.
It used to be maybe 25.
Now it's often 40 or evenhigher on lab reports.
Mark (18:29):
Why'd it go up?
Rachel (18:30):
Because the average population has gotten
unhealthier, specifically withmore fatty liver disease, the
normal range shifted to reflectthe less healthy average not
necessarily what's optimal, sousing that higher range might
mask problems.
What ALT levels should make uspay attention?
Dr Lessig argues prettystrongly that an ALT level
consistently above 25, maybeeven above 20 for
(18:51):
African-Americans should beconsidered suspicious for liver
fat until proven otherwise.
Mark (18:56):
Above 25, that's much lower than the usual cutoff.
Rachel (18:59):
It is.
His point is don't wait for itto hit 40 or 50.
An ALT creeping above 25suggests something's going on in
the liver that needs addressing.
The goal is to get the fat outof the liver.
Mark (19:10):
Because clearing liver fat improves liver function.
Rachel (19:12):
Improves liver function, which helps lower insulin
levels, which helps prevent allthose downstream metabolic
diseases we talked about.
It's all connected.
Mark (19:20):
Okay, wow, we've covered a lot of ground.
Let's try and quickly recap themain takeaways for everyone
listening.
Rachel (19:25):
Sounds good.
Okay, number one totalcholesterol.
Not that useful on its own,don't fixate on it.
Mark (19:31):
Right Number two LDL alone isn't enough either.
You have to look attriglycerides and HDL too.
Rachel (19:37):
Absolutely Number three.
That triglyceride to HDL ratiois key.
Aim for under 2.5, ideallyunder 1.5, especially for
African-Americans.
Lower is better.
Mark (19:48):
Okay, four triglycerides themselves under 100 is
generally a good sign.
Suggests less of the harmfulsmall dense LDL.
Rachel (19:56):
Yep Five aim for higher HDL, well above those minimums
on the lab report.
Genetics plays a role, butlifestyle helps.
Mark (20:02):
Six remember the sugar connection.
Excess sugar dries liver fat.
Rachel (20:06):
Which leads to insulin resistance and the production of
that bad small dense LDL.
It's a chain reaction.
Mark (20:14):
Seven pay attention to your ALT liver enzyme.
If it's consistently over 25,investigate for liver fat.
Rachel (20:20):
Don't wait for to be sky-high right and finally eight
, consider asking your doctorabout a fasting insulin test.
Mark (20:26):
Aim for under six or seven , ideally and if you can't get
the insulin test, really focuson that triglyceride to HDL
ratio as your next bestindicator.
Rachel (20:36):
Exactly that ratio gives you a lot of insight.
Mark (20:39):
This deep dive.
Hopefully it's giving you, thelistener, a much clearer, more
nuanced way to look at yourcholesterol panel.
It's not just numbers.
Rachel (20:47):
Not at all.
They really do tell a story,don't they?
A story about how your body ishandling energy, day in and day
out.
Mark (20:53):
So here's maybe a final thought to leave you with.
We've seen how powerfully sugarimpacts.
These numbers impacts yourmetabolic health.
Rachel (20:59):
Yeah, it's profound when you connect the dots from the
diet to the liver, to the lipids, to insulin.
Mark (21:03):
So the question for you is knowing this, what small, maybe
seemingly insignificant, changecould you make, starting today,
to begin shifting these markersto protect your health
long-term?
Rachel (21:14):
The answers might actually be simpler than you
think, and just understandingthese connections we've talked
about that's a huge, powerfulfirst step.
Nicolette (21:29):
Thanks for tuning into the Health Pulse.
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Welcome to the Health Pulse, your go-to source for
quick, actionable insights onhealth, wellness and diagnostics
.
Whether you're looking tooptimize your well-being or stay
informed about the latest inmedical testing, we've got you
covered.
Join us as we break down keyhealth topics in just minutes.
Let's dive in.
Mark (00:24):
Welcome to the Deep Dive.
Today we're getting intosomething really vital for your
long-term health.
It's all about understandingyour cholesterol panel.
Rachel (00:34):
And not just the numbers but the bigger picture, right
your metabolic well-being.
Mark (00:37):
Exactly.
We're using insights from DrRobert Lustig, specifically from
a YouTube video he did.
You might have seen it it's onthe Levels channel.
Rachel (00:46):
Yeah, the one called Understand your Cholesterol
Panel and Metabolic Health Tests, the Ultimate Guide.
We're working off thetranscript from that.
Mark (00:53):
Right, and our mission today is pretty straightforward
Cut through all the you know theconfusion around these lab
results.
Rachel (00:59):
So you can actually get some actionable knowledge,
understand what's reallyhappening inside your body.
Mark (01:04):
It's fascinating, isn't it , how these tests.
They seem routine, but they'reall connected.
Rachel (01:09):
Totally.
We just see this list, maybesome red flags, green check
marks.
But Dr Lustig really shows howit's like a dynamic story, your
metabolic story.
Mark (01:19):
Okay, let's jump right in Total cholesterol.
Dr Lustig basically says throwit out, ignore it.
Why so strong?
Rachel (01:26):
Well, the thing is total cholesterol.
By itself it doesn't tell youmuch about your actual heart
disease risk.
It's kind of like knowing thetotal cars on a highway.
Nicolette (01:36):
OK.
Rachel (01:37):
But you don't know if they're like safe minivans or
you know a bunch of Ferrarispeeding.
Mark (01:42):
Right, so the total number could be high because of the
good stuff, exactly.
Rachel (01:46):
It can be misleading.
So the main point is don'tobsess over total cholesterol.
It's the types of cholesterolthat really count for
understanding your risk.
Mark (01:55):
That makes perfect sense.
Okay, so let's zoom in LDLcholesterol.
This is the one everyone callsthe bad cholesterol, the one
people worry about.
Rachel (02:02):
Yeah, and look, there's a reason.
Big population studies do showa link, right, higher LDL, more
heart disease risk.
But the, let's say, intensefocus on LDL in medicine.
It's been heavily influenced bythe history of statins, ah, the
(02:23):
drugs that lower it veryeffectively, right.
And Dr Lustig points out, theactual hazard risk ratio for
high LDL is about 1.3.
So there's an association, sure, but maybe it's not the whole
story people think it is.
Mark (02:30):
OK, and this is where it gets.
I think really, reallyinteresting.
Dr Lustig says there isn't justone type of LDL.
Rachel (02:38):
Exactly that's crucial.
You basically got two mainkinds large buoyant LDL
particles and small dense LDLparticles.
Mark (02:48):
Small and dense versus large and buoyant.
What's the difference?
Rachel (02:51):
Well, the standard LDL test.
It just measures the totalamount.
It lumps them both together,but the evidence strongly
suggests it's mainly the small,dense LDL that's linked to heart
disease developing.
The large buoy type seems muchless concerning, maybe even
neutral.
Mark (03:07):
Wow, okay, so you could have a high LDL number on your
report, but maybe, just maybe,it's mostly the less harmful
large kind.
Rachel (03:17):
That's the possibility.
Mark (03:18):
Yes, a key distinction.
But then the million-dollarquestion is how do you know
which type is dominating yourresults if the standard test
doesn't tell you?
Rachel (03:26):
And that question leads us straight to another number on
that panel triglycerides.
Now, these have had a bit of acheckered history.
Mark (03:32):
Why is that?
Rachel (03:32):
Because non-fasting samples can really mess up the
results.
Mark (03:35):
Right, like if you just had I don't know a big glass of
orange juice or something sugarybefore the test.
Rachel (03:39):
Precisely.
It skews things badly.
But and this is key when youmeasure triglycerides after a
proper fast, they actuallybecome a more significant
predictor of heart attack riskthan LDL is.
Mark (03:51):
Really More significant.
Rachel (03:52):
Yeah, the hazard risk ratio is around 1.8 for
triglycerides, compared to that1.3 for LDL we mentioned.
Mark (03:58):
Huh, so why haven't we heard as much focus on
triglycerides then?
Rachel (04:02):
Well, dr Lustig suggests one possible reason is
historically there just haven'tbeen as many blockbuster widely
used drugs specificallytargeting high triglycerides
compared to statins for LDL.
Mark (04:14):
Interesting point.
Okay, so fasting triglyceridesvery important.
How do they connect back tothose different LDL types, the
small, dense versus large,buoyant?
Rachel (04:24):
This is the critical link.
High fasting triglyceridesoften mean you have a higher
proportion of those harmfulsmall dense LDL particles.
Mark (04:33):
Okay, how does that work?
Rachel (04:34):
Think of it like this when you eat excess sugar or
carbs that break down quicklyinto sugar, your liver takes
that sugar and converts it intosomething called VLDL, very low
density lipoprotein.
Mark (04:46):
VLDL Got it.
Rachel (04:47):
And in a fasting state, your triglyceride level
basically is your VLDL level.
They're measuring the samething essentially.
Then these VLDL particles goout into your bloodstream, they
get processed, lipids getdropped off and what's left
eventually becomes that smalldense LDL.
Mark (05:05):
Ah, so high triglycerides are like an upstream indicator
for more small dense LDLdownstream.
Rachel (05:11):
Exactly.
It's a very strong clue thatmore of your LDL is likely the
problematic type.
Mark (05:16):
Got it so.
Too much sugar drives uptriglycerides.
High triglycerides suggest moreof the bad LDL.
What about HDL, the goodcholesterol?
Rachel (05:24):
Right HDL High-density lipoprotein.
Its main job is reallyimportant.
It acts like a scavenger.
Mark (05:29):
How so.
Rachel (05:29):
It helps transport fats, lipids, away from your tissues
like fat cells and back towardsthe liver for processing, maybe
removal.
Mark (05:36):
And it's high-density.
Rachel (05:37):
It's packed with protein relative to the fat it carries,
makes it denser.
Okay, and general, higher HDLis good.
Generally, yes, higher HDLlevels are linked with a
protective effect against heartdisease because of that reverse
transport rule.
There are some rare exceptions,like HDL Milano, but for most
people, yeah, you want healthy,robust HDL levels.
Mark (05:56):
Now Dr Lustig puts a lot of emphasis on a specific
calculation the triglyceride toHDL ratio.
Why look at that ratiospecifically?
Rachel (06:05):
This ratio.
It really gained tractionthanks to Dr Jerry Riven's work
on metabolic syndrome.
It's just a really powerfulsnapshot of your heart disease
risk.
Mark (06:14):
Why does it do that?
Rachel (06:15):
Well, think about it.
It directly compares the badguy, triglycerides, which we now
know are a proxy for smalldense LDL, with the good guy,
hdl, the protective cholesterol.
Mark (06:25):
So it's like a balance scale for those key lipid
players.
Rachel (06:28):
Exactly, and interestingly this ratio can
also serve as a sort of poorman's marker for insulin
resistance.
We'll definitely circle back tothat.
Mark (06:36):
Okay, good.
So this ratio gives a sense ofbalance.
What numbers should people belooking for?
What's a good target?
Rachel (06:42):
Generally speaking, you want that ratio to be 1.5 or
less.
That's considered prettyfavorable.
Mark (06:47):
Okay, 1.5 or less.
Rachel (06:48):
If it starts creeping up .
A ratio of 2.5 or greatersuggests there might be a
problem.
Higher risk.
Mark (06:55):
And you mentioned race differences.
Rachel (06:57):
Yeah, there's some data suggesting that for
African-Americans the idealtarget might be a bit lower,
closer to 1.5 or even below that, but the general principle
holds lower is better.
It's a snapshot of your lipiddynamics, right then?
Mark (07:11):
It really sounds like this ratio tells a much richer story
than just you know, looking atthe LDL number and see if it's
got a green check or a red flagnext to it.
Rachel (07:19):
Absolutely.
It's a shame really, the commonpractice of just glancing at
individual numbers within thenormal range.
It often misses these crucialrelationships, these patterns.
Mark (07:29):
You miss the interaction between them.
Rachel (07:30):
Precisely.
Mark (07:31):
Okay, let's dig back into that small dense LDL.
We know it's the one we're moreworried about, the one linked
to plaque.
What else is important here?
Rachel (07:39):
Well, first, a practical point Dr Lustig makes To
interpret your lipid profileaccurately, you need to be, you
know, generally healthy at thetime of the test, meaning no
acute illness like a bad cold orinfection which would show up
in your white blood cell countthat can affect lipids Okay.
And also your thyroid functionneeds to be stable, specifically
(08:00):
your free T4 level.
Mark (08:02):
Why thyroid?
Rachel (08:03):
Because hypothyroidism an underactive thyroid can
actually falsely increase yourtriglyceride levels.
Ah, good to know.
He even gives a quick mentionto Hashimoto's thyroiditis as a
common cause and notes you cansometimes use, you know,
holistic or complementaryapproaches alongside medication.
Mark (08:20):
Right.
Important context these numbersdon't exist in a vacuum.
Ok, back to the LDL particlesthemselves Large versus small.
Rachel (08:27):
So, as we said, the large boyan LDL that's most of
it, maybe 80 percent Seemspretty neutral cardiovascularly,
Like bigger, fluffier beachballs maybe.
Mark (08:37):
OK.
Rachel (08:37):
The small, dense LDL.
That's a smaller fraction,maybe 20 percent, but that's the
type that can wiggle its wayunder the lining of your
arteries, the endothelium.
Mark (08:45):
And start causing trouble.
Rachel (08:47):
Yeah, that's how plaque formation begins.
They're smaller, denser, theysink in lab tests and they tend
to be more inflammatory.
And again, your standard LDLtest doesn't separate these two.
Mark (08:58):
So how do we get a clue about whether we have more of
this problematic small dense LDL?
We're back to triglyceridesagain.
Rachel (09:06):
We are indeed High.
Triglycerides are yourstrongest indirect indicator
that you likely have more smalldense LDL floating around.
Mark (09:14):
Because remind us of that link again.
Rachel (09:15):
Because VLDL, which is what your fasting triglyceride
level is, is the precursorparticle.
It gets processed by the liverand fat cells, lipids are
removed and what's left overeventually becomes that small
dense LDL.
Mark (09:27):
Okay, let's really hammer home this VLDL and sugar
connection.
It seems so central.
Rachel (09:31):
It is absolutely central In that fasting state.
Remember, triglyceride levelequals VLDL level.
Mark (09:36):
Got it.
Rachel (09:36):
And here's the kicker your liver makes VLDL primarily
in response to sugar.
Mark (09:43):
Not fat.
I thought cholesterol came fromfat.
Rachel (09:45):
Well, dietary fat leads to different particles called
chylomicrons, which clear prettyquickly after a meal and don't
really affect your fastingtriglyceride number, unless you
have a very rare genetic issuelike type 5 hyperlipoproteinemia
.
Mark (09:58):
Okay, so chylomicrons are from dietary fat, short term
VLDL is from VLDL reflected inyour fasting.
Rachel (10:06):
Triglyceridesides is the liver's response to excess
carbohydrates, especiallyrefined sugars and things that
digest quickly into sugar.
Mark (10:13):
So the sugar you eat gets turned into fat triglycerides,
VLDL, by your liver.
Rachel (10:19):
That's the key takeaway.
Mark (10:24):
Fasting triglyceride.
Vldl equals liver processingsugar.
This explains so much like whyDr Lustig sees triglycerides
drop dramatically when peoplecut back on sugar.
Rachel (10:31):
Exactly, it happens quite quickly sometimes.
Mark (10:33):
And it also highlights, like you said, the missed
opportunities in standardinterpretation.
Rachel (10:37):
Totally.
Someone might have LDL.
That's just a bit high.
Maybe HDL is a bit low.
Triglycerides are borderline.
Mark (10:42):
And individually.
The doctor says you're fine.
Rachel (10:45):
Right.
But when you look at thosenumbers together, especially
with that triglyceride HDL ratio, it can scream metabolic issues
brewing, even if nothing istechnically in the red zone.
Mark (10:55):
It's about the pattern, not just the isolated dots.
Rachel (10:57):
Precisely, and these numbers aren't set in stone,
they're dynamic, you can changethem with lifestyle.
Reducing sugar is a huge leverthere.
Mark (11:05):
Which brings up a bigger point Dr Lustig touches on.
Maybe the training doctors getneeds adjusting.
Rachel (11:12):
Well, he notes that primary care physicians often
don't get super deep training inlipidology, the specifics of
lipid metabolism.
Mark (11:19):
So the approach becomes a bit simplistic.
Rachel (11:23):
It can be.
Sometimes it's just LEL, highstatin, triglycerides, high
maybe a fibrate, without alwaysdigging into the why, the
underlying metabolic enginedriving those numbers.
Mark (11:33):
And he also pushes back against the idea that metabolic
health is just about weightright.
Rachel (11:38):
Absolutely.
He debunks that myth prettyfirmly.
You can be thin butmetabolically unhealthy to a
five.
Thin on the outside, fat on theinside.
Mark (11:45):
With a terrible lipid profile.
Rachel (11:47):
Exactly, and, conversely , someone who carries more
weight might actually bemetabolically quite healthy.
It's not about the subcutaneousfat, the fat under your skin.
Mark (11:56):
It's the visceral fat.
Rachel (11:57):
Yes, especially fat in the liver.
That's the real metabolictroublemaker and it's largely
driven by excess sugar, not justoverall calories or visible
body fat.
Mark (12:06):
Okay, this is all incredibly insightful.
Rachel (12:08):
Yeah.
Mark (12:09):
So for people listening wanting to understand their own
results, what's the practicalgame plan?
Rachel (12:14):
Okay, first step, you get your results.
If your LDL is a little high,don't freak out immediately.
Okay, breathe.
Look straight at yourtriglyceride number and your HDL
number.
Calculate that triglyceride toHDL ratio.
Mark (12:30):
What's a good triglyceride ?
Rachel (12:30):
number on its own.
Generally, if yourtriglycerides are under 100
milligdl, that's usually a goodsign.
It suggests you probably don'thave a ton of that small dense
LDL.
Mark (12:38):
Below 100 is good.
What if it's higher?
Rachel (12:40):
If it's higher, then you really need to look at it in
relation to your HDL.
Using that ratio, Remember theconnection Triglycerides become
small dense LDL.
Mark (12:48):
While HDL is trying to clean things up.
Rachel (12:52):
Right, and that ratio, the triglyceride HDL, as we
mentioned, is also a decentproxy for insulin resistance.
Mark (12:58):
OK, insulin resistance we hear that term constantly.
Now let's unpack its role here.
Rachel (13:02):
It's absolutely central to this whole metabolic picture.
People think of insulin as justthe diabetes hormone regulating
blood sugar.
Mark (13:10):
But it's more than that.
Rachel (13:11):
Oh yeah, its primary job is actually being the energy
storage hormone.
It tells your body what to dowith the energy you consume,
store it.
Primarily store it.
Yes, Especially excess energy.
It pushes it into fat cellsunder the skin, around organs
and, crucially, into the liver.
Mark (13:29):
And insulin resistance is when.
Rachel (13:31):
It's when your cells, particularly your liver cells,
become kind of numb to insulinsignal, often because they're
already stuffed with fat.
Mark (13:38):
So they don't respond properly.
Rachel (13:40):
Right, and because the signal isn't getting through
effectively, your pancreasthinks, uh-oh, need to shout
louder, and it pumps out moreinsulin to try and force the
message through.
Mark (13:49):
And the liver is ground zero for this.
You mentioned the portal vein.
Rachel (13:52):
Exactly right.
The blood leaving your pancreasloaded with freshly made
insulin goes straight into theportal vein which leads directly
to the liver, gets the highestconcentration.
Mark (14:02):
So the liver's health is paramount for insulin signaling.
Rachel (14:06):
Absolutely.
And when the liver gets fatty,which is incredibly common now,
maybe affecting 45% of US adults.
Some estimates say Wow 45%.
Yeah, it's epidemic.
When the liver's fatty, itresists insulin, making the
pancreas work overtime, leadingto chronically high insulin
levels.
Mark (14:23):
And high insulin isn't just about blood sugar.
Rachel (14:25):
No High insulin itself that hyperinsulinemia is linked
to a whole host of chronicdiseases Heart disease, yes, but
also certain cancers, dementia,pcos, the list goes on.
Insulin is essential, but toomuch for too long due to
resistance is bad news.
Mark (14:41):
Okay, so clearly understanding our insulin
sensitivity is key.
How can we measure that,besides just looking at blood
sugar?
Rachel (14:47):
Well, in research they use a calculation called
OCHIONEIR sure homeostatic modelassessment for insulin
resistance.
Mark (14:53):
Sounds complicated.
Rachel (14:54):
It uses your fasting insulin level and your fasting
glucose level.
You can actually findcalculators online for it, like
on MDCalc, if you have those twonumbers.
Okay, h-o-a-i-r, but you alsosaid I also said that
triglyceride to HDL ratio wekeep talking about is a
surprisingly good, readilyavailable proxy for insulin
sensitivity Much easier to get.
Mark (15:13):
And what about directly measuring the small dense LDL?
Rachel (15:17):
You can get tests for LDL, particle size or number,
but they're often not standard,might not be covered by
insurance, cost more, so theyaren't routine for most people
yet.
Mark (15:26):
Right, which brings us back to insulin.
Could you just ask for afasting insulin test?
Rachel (15:31):
You can, and it's a really valuable test for
metabolic health.
It's a separate blood draw,usually not part of the standard
chemistry panel.
Mark (15:37):
But there's some controversy, isn't there?
The American DiabetesAssociation advises against it.
Rachel (15:42):
Yes, they do, somewhat controversially, dr Lustig
discusses their reasons andpushes back.
Mark (15:47):
What are their reasons?
Rachel (15:48):
Okay.
Reason one lack ofstandardization, meaning the lab
methods, the assays formeasuring insulin can vary a bit
, lab to lab giving slightlydifferent numbers.
Mark (15:59):
OK, that sounds like a potential issue.
Rachel (16:00):
It is to a degree.
But Dr Lustig's point is, evenwith that variability, if your
level is consistently high, itstill means something is wrong.
It indicates your pancreas isunder stress.
Mark (16:12):
Even if the exact number is slightly fuzzy.
Rachel (16:14):
Right, and some assays might also pick up pro-insulin,
which is like a precursor toactive insulin.
But again, high levels of thatalso indicate the pancreas is
working too hard.
So it doesn't invalidate thetest's usefulness in signaling a
problem.
Mark (16:29):
Okay, what's the ADA's second argument against routine
testing?
Rachel (16:33):
They say insulin levels don't correlate perfectly with
obesity.
Mark (16:37):
And Dr Lusdy's response.
Rachel (16:38):
He agrees, but he says that's precisely why you should
measure it.
It tells you about metabolichealth independent of weight.
Mark (16:44):
Ah, like the TOFI, concept again.
Rachel (16:46):
Exactly, you can be lean with high insulin,
metabolically unhealthy or obese.
With normal insulin,metabolically healthier.
Mark (16:57):
The insulin level reflects the underlying metabolic
function, not just the number onthe scale, so it seems like a
really useful test that's maybeunderutilized.
If someone does get a fastinginsulin test, what are they
hoping to see?
What are good levels?
Rachel (17:06):
Well, generally, the lower the better.
Truly Elite marathon runnersmight be down around two micro
IU per ml.
Mark (17:13):
Wow, okay, for the rest of us.
Rachel (17:15):
Generally under 6 or 7 is considered quite good.
Under 10 is probably still okay.
Mark (17:20):
And when do you start getting concerned?
Rachel (17:22):
When levels are consistently creeping above 10,
that raises a flag for insulinresistance and if you're seeing
levels of 15 or higher, thatstrongly suggests significant
insulin resistance is present.
Mark (17:33):
And that high level points towards.
Rachel (17:35):
It points towards litter dysfunction, liver fat usually,
and a pancreas that's reallystraining to keep up.
Mark (17:41):
This keeps coming back to liver, doesn't it?
Its health seems critical.
Rachel (17:45):
Absolutely critical, and liver function tests, or LFTs,
are often glanced over unlesssomething is wildly abnormal
like high bilirubin causingjaundice.
Mark (17:53):
But there's more subtle information there.
Rachel (17:55):
Definitely Specifically look at the ALT level alanine
aminotransferase it used to becalled SGPT.
Mark (18:02):
ALT.
What does that tell us?
Rachel (18:04):
ALT is a really good indicator of liver fat.
When liver cells are damaged orstressed, often by excess fat,
they leak ALT into thebloodstream.
Mark (18:12):
And what's considered a normal ALT level, because those
ranges on lab reports can bewide.
Rachel (18:17):
They can.
And Dr Lustig points outsomething crucial the upper
limit of normal for ALT hasactually crept up over the years
.
It used to be maybe 25.
Now it's often 40 or evenhigher on lab reports.
Mark (18:29):
Why'd it go up?
Rachel (18:30):
Because the average population has gotten
unhealthier, specifically withmore fatty liver disease, the
normal range shifted to reflectthe less healthy average not
necessarily what's optimal, sousing that higher range might
mask problems.
What ALT levels should make uspay attention?
Dr Lessig argues prettystrongly that an ALT level
consistently above 25, maybeeven above 20 for
(18:51):
African-Americans should beconsidered suspicious for liver
fat until proven otherwise.
Mark (18:56):
Above 25, that's much lower than the usual cutoff.
Rachel (18:59):
It is.
His point is don't wait for itto hit 40 or 50.
An ALT creeping above 25suggests something's going on in
the liver that needs addressing.
The goal is to get the fat outof the liver.
Mark (19:10):
Because clearing liver fat improves liver function.
Rachel (19:12):
Improves liver function, which helps lower insulin
levels, which helps prevent allthose downstream metabolic
diseases we talked about.
It's all connected.
Mark (19:20):
Okay, wow, we've covered a lot of ground.
Let's try and quickly recap themain takeaways for everyone
listening.
Rachel (19:25):
Sounds good.
Okay, number one totalcholesterol.
Not that useful on its own,don't fixate on it.
Mark (19:31):
Right Number two LDL alone isn't enough either.
You have to look attriglycerides and HDL too.
Rachel (19:37):
Absolutely Number three.
That triglyceride to HDL ratiois key.
Aim for under 2.5, ideallyunder 1.5, especially for
African-Americans.
Lower is better.
Mark (19:48):
Okay, four triglycerides themselves under 100 is
generally a good sign.
Suggests less of the harmfulsmall dense LDL.
Rachel (19:56):
Yep Five aim for higher HDL, well above those minimums
on the lab report.
Genetics plays a role, butlifestyle helps.
Mark (20:02):
Six remember the sugar connection.
Excess sugar dries liver fat.
Rachel (20:06):
Which leads to insulin resistance and the production of
that bad small dense LDL.
It's a chain reaction.
Mark (20:14):
Seven pay attention to your ALT liver enzyme.
If it's consistently over 25,investigate for liver fat.
Rachel (20:20):
Don't wait for to be sky-high right and finally eight
, consider asking your doctorabout a fasting insulin test.
Mark (20:26):
Aim for under six or seven , ideally and if you can't get
the insulin test, really focuson that triglyceride to HDL
ratio as your next bestindicator.
Rachel (20:36):
Exactly that ratio gives you a lot of insight.
Mark (20:39):
This deep dive.
Hopefully it's giving you, thelistener, a much clearer, more
nuanced way to look at yourcholesterol panel.
It's not just numbers.
Rachel (20:47):
Not at all.
They really do tell a story,don't they?
A story about how your body ishandling energy, day in and day
out.
Mark (20:53):
So here's maybe a final thought to leave you with.
We've seen how powerfully sugarimpacts.
These numbers impacts yourmetabolic health.
Rachel (20:59):
Yeah, it's profound when you connect the dots from the
diet to the liver, to the lipids, to insulin.
Mark (21:03):
So the question for you is knowing this, what small, maybe
seemingly insignificant, changecould you make, starting today,
to begin shifting these markersto protect your health
long-term?
Rachel (21:14):
The answers might actually be simpler than you
think, and just understandingthese connections we've talked
about that's a huge, powerfulfirst step.
Nicolette (21:29):
Thanks for tuning into the Health Pulse.
If you found this episodehelpful, don't forget to
subscribe and share it withsomeone who might benefit.
For more health insights anddiagnostics, visit us online at
wwwquicklabmobilecom.
Stay informed, stay healthy andwe'll catch you in the next
episode.
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