August 22, 2025 • 21 mins
Pancreatic cancer has earned its reputation as a “silent killer” for good reason. In this episode of The Health Pulse, we explore why this cancer often remains hidden until late stages, and why it accounts for a disproportionate share of cancer deaths despite being relatively rare.
We break down the dual role of the pancreas in digestion and blood sugar regulation, and how cancer disrupts these vital systems. You’ll learn the subtle warning signs—like unexplained weight loss, fatigue, or sudden-onset diabetes without risk factors—that may point to early disease.
We also dive into the diagnostic tools doctors use today, from advanced imaging and blood biomarkers to biopsies and molecular profiling. Treatment options include surgery, chemotherapy, and radiation, alongside promising new therapies that target genetic mutations and metabolic vulnerabilities. We even discuss how ketogenic dietary strategies are being studied as potential adjuncts to standard care.
If you or someone you love is concerned about pancreatic cancer, this episode delivers the insights you need to understand risks, recognize warning signs, and learn what modern science is uncovering about this elusive disease.
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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 (00:26):
Welcome to the Deep Dive.
Today we're plunging into atopic that touches so many lives
, yet often remains shrouded insilence.
Rachel (00:37):
Pancreatic cancer yeah, it's a tough one.
Mark (00:39):
It's frequently called a silent killer, and for good
reason.
The central question for ourDeep Dive today is this why is
it so incredibly challenging todetect?
And for good reason.
The central question for ourdeep dive today is this why is
it so incredibly challenging todetect and treat Right and
importantly, what are thecrucial advancements that are
(00:59):
truly changing the landscape?
Rachel (01:00):
for, you know, both early detection and personalized
care.
That's basically our missiontoday to unravel the complex
realities of pancreatic cancer.
We'll be drawing from some keysources, like the American
Cancer Society and the NationalCancer Institute, and we want to
provide you with insights intoits risk factors, symptoms, how
it's diagnosed and the evolvingstrategies for treatment.
Mark (01:16):
And our goal for you, our listener, is to gain a thorough
understanding of this criticalhealth topic without getting
bogged down in like supertechnical medical jargon.
Rachel (01:25):
Exactly.
Mark (01:25):
You'll walk away well-informed, ready to ask
better questions and hopefullywith a fresh perspective.
Okay, let's dive in.
Let's do it.
So you mentioned, pancreaticcancer is often called a silent
killer.
What does that actually mean inpractical terms?
Why is it so insidious?
Rachel (01:40):
Well, the real issue, the core problem, is that it can
progress for months, sometimeseven years, without any obvious
symptoms showing up.
Mark (01:49):
Wow Years.
Rachel (01:50):
Yeah, and the American Cancer Society highlights a
really stark reality Whilepancreatic cancer accounts for
only about 3 percent of allcancers in the US, which sounds
relatively small.
Right, it sounds small, butit's tragically responsible for
about 7% of all cancer-relateddeaths.
Mark (02:06):
That 3% versus 7% statistic really jumps out,
doesn't?
Rachel (02:09):
it, it does.
Mark (02:10):
It isn't just about late diagnosis.
It speaks to the, I guess, theinherent aggression and rapid
progression of this specificcancer.
Rachel (02:17):
Exactly, it's like a brutal race against time.
It makes the window foreffective intervention
incredibly narrow, much more sothan many other cancers window
for effective interventionincredibly narrow, much more so
than many other cancers andthose early tumors.
They often produce really mild,non-specific symptoms, things
like fatigue, maybe someindigestion or subtle weight
loss.
Mark (02:34):
Things you could easily brush off, totally, easily
mistaken for much less seriouseveryday conditions, which is
precisely the challenge, right?
But despite that inherentstealth, are we seeing any
progress?
Is there hope there?
Rachel (02:48):
We are actually Advances in lab testing, more
sophisticated imaging techniquesand genetic screening.
They're all steadily improvingour ability to identify it
earlier than we could before.
Mark (03:00):
Okay, that's good to hear.
Before we go deeper into thedisease itself, maybe it helps
to zoom out a bit and reallyappreciate the pancreas.
Rachel (03:07):
Yeah, good idea.
Mark (03:08):
This small but incredibly vital organ, sort of tucked away
deep behind your stomach?
What exactly makes its functionso critical?
Rachel (03:16):
It has this dual role, which is part of what makes
things complicated when cancerstrikes.
First, it produces digestiveenzymes.
These are absolutely essentialfor breaking down the food we
eat.
Mark (03:26):
Okay, digestion.
Rachel (03:27):
And second, equally vital, it releases hormones like
insulin and glucagon.
These are basically the masterregulators of our blood sugar.
Mark (03:34):
Okay.
So when cancer develops, it'sbecause normal cells undergo
these genetic mutations, theystart growing uncontrollably and
form tumors, and because thesetumors interfere with both
digestion and glucose metabolism.
That's why the symptoms oftenoverlap with things like
diabetes or chronic pancreatitis.
Rachel (03:54):
That's a great way to put it.
It's almost like the cancer ishijacking the pancreas' natural
functions.
Mark (03:59):
Okay.
Rachel (04:00):
And according to the National Cancer Institute,
pancreatic cancer is primarilycategorized into two major types
.
About 90 to 95 percent of casesare what we call exocrine
pancreatic cancers.
Mark (04:12):
Exocrine.
Rachel (04:13):
Got it.
These arise from those cellsthat produce the digestive
enzymes, and the most commonsubtype here is pancreatic
ductal adenocarcinoma, or PDACfor short.
Mark (04:23):
PDAC.
That's the main one we hearabout.
So that covers the most commontype.
What about the rarer forms?
How do they differ?
Rachel (04:29):
So the rarer form, making up about 5 to 10 percent
of cases, are neuroendocrinetumors or NETs.
Mark (04:34):
NETs.
Rachel (04:35):
These actually arise from the hormone-producing cells
.
Now, while they're often slowergrowing than PDFs, some types
can be quite aggressive inproducing excess hormones.
Mark (04:44):
Ah, so they cause different symptoms then?
Rachel (04:46):
Exactly.
They can lead to uniquesymptoms related to those
specific hormonal imbalances,think low blood sugar or severe
diarrhea, depending on thehormone.
Mark (04:55):
It's striking how that deep location in the abdomen
really plays such a big rolehere you mentioned earlier.
It's hard to spot.
Rachel (05:02):
It's huge.
More than half of cases arediagnosed after the cancer has
already spread, which justunderscores that critical need
for earlier detection methods.
Mark (05:10):
Yeah, definitely.
Okay, we've called it thesilent killer, but you mentioned
there are these subtle whispersof the disease, things easily
missed.
What exactly are those earlynonspecific signs that maybe we
should be a bit more alert to?
Rachel (05:26):
Okay.
So when we look at early signsto watch for, they include
things like unexplained weightloss.
This is often due to impaireddigestion or metabolic changes
the tumor itself is causing.
Mark (05:36):
Makes sense.
Rachel (05:37):
Then there's loss of appetite Sometimes tumor-related
inflammation can just disruptnormal hunger signals and, of
course, general fatigue andweakness may be caused by
nutrient malabsorption or evenanemia.
Mark (05:48):
Those sound pretty vague though.
Rachel (05:49):
It is, but here's where it gets really interesting,
potentially a bit more specificNew onset diabetes.
Mark (05:56):
Oh, okay, tell me more.
Rachel (05:58):
Imagine someone suddenly developing type 2 diabetes, but
they don't really have theusual risk factors.
Or maybe someone with diabetesfinds it suddenly worsening
significantly for no clearreason.
In some cases, these pancreatictumors are directly messing
with insulin production.
That leads to these sudden,unexplained blood sugar
(06:19):
imbalances.
It's a clue that'sunfortunately, often missed.
Mark (06:23):
Wow, that's a really important connection.
So those are the subtle earlysigns.
But what happens as the diseaseprogresses or in more advanced
stages?
What are the clearer, morepronounced symptoms that
typically emerge then?
Rachel (06:34):
Yeah, as the disease advances, the symptoms usually
become more insistent, harder toignore.
We're talking persistentabdominal or back pain.
This is often because thetumors are literally pressing on
nearby nerves and organs.
Mark (06:46):
Okay, that sounds more noticeable, Definitely, and
jaundice.
Rachel (06:49):
You know the yellowing of the skin and eyes.
That's a common sign.
It often happens because tumorsare blocking the bile ducts.
Mark (06:55):
Right, I've heard of that one.
Rachel (06:56):
Other progressive symptoms can include changes in
stool.
It might become greasy and paleagain due to reduced pancreatic
enzyme secretion, and nauseaand vomiting, often related to
some kind of digestiveobstruction caused by the tumor.
Mark (07:11):
It's really sobering to realize how easily these
nonspecific symptoms, even thelater ones, sometimes get
misattributed to other commonconditions.
Rachel (07:20):
It is.
It really highlights thechallenge.
Mark (07:22):
And underscores the critical need for advanced
testing, doesn't it.
Rachel (07:25):
It absolutely does.
This is precisely why labtesting and imaging are so
utterly essential for trying tocatch it earlier.
Mark (07:32):
So let's talk about risk.
Who's most at risk?
You hear it's not just onesingle cause, right?
It's more like a complexinterplay of genetic stuff,
metabolic factors, lifestyle.
Rachel (07:41):
That's exactly right.
It's multifactorial.
Understanding these differentpieces helps us identify
individuals who might benefitfrom earlier or perhaps more
frequent screening.
Mark (07:50):
OK, so break that down for us why, what about?
Rachel (07:54):
the metabolic and hormonal factors.
Sure On the metabolic andhormonal front, people with
longstanding type 2 diabetes andinsulin resistance seem to have
an increased risk.
The NCI suggests this might bedue to chronic high insulin
levels, hyperinsulinemia andinflammation.
Mark (08:10):
Okay, diabetes is a link.
What else?
Rachel (08:12):
Obesity, particularly excess visceral fat that belly
fat also contributes.
It tends to drive systemicinflammation and insulin
resistance, both of which arelinked to higher risk and,
importantly, chronicpancreatitis, that's, repeated
inflammation of the pancreasitself, often triggered by
things like heavy alcohol use,very high triglycerides or even
(08:33):
gallstones.
That significantly raises therisk.
Mark (08:36):
Wow, okay, so those are metabolic issues.
What about lifestyle Things wecan potentially change?
Rachel (08:40):
Lifestyle plays a huge role, a very significant one,
actually.
Tobacco use is one of thestrongest modifiable risk
factors.
Mark (08:46):
Really how strong.
Rachel (08:47):
According to the American Cancer Society, it's
responsible for about 25 percentof cases one in four.
Mark (08:53):
That's huge.
Rachel (08:54):
It is Also diets high in refined carbohydrates and added
sugars can contribute, probablyby promoting that insulin
resistance and inflammation wetalked about.
And of course, heavy alcoholconsumption is a known factor
because it chronically damagesthe pancreas and promotes
inflammation.
Mark (09:10):
And then, inevitably, there are the factors.
We can't change our genes andfamily history.
Rachel (09:14):
Exactly.
We know that inherited genemutations, specifically in genes
like BRCA1, BRCA2, PALB2, andATM.
Mark (09:22):
The BOCA genes often link to breast and ovarian cancer too
right.
Rachel (09:26):
Very same ones.
Mutations in these cansignificantly elevate lifetime
risk for pancreatic cancer aswell.
And then there's family history.
Having relatives, especiallyfirst-degree relatives like a
parent or sibling, withpancreatic cancer increases
personal risk.
If you have two or morefirst-degree relatives, the risk
can go up substantially, maybeeven up to six-fold.
Mark (09:46):
Okay, so quite a few factors to consider there.
Given all these challenges injust recognizing the symptoms,
how has the diagnostic processimproved?
You mentioned advances in labtesting, imaging genetic
screening.
How does that diagnostictoolkit actually work to move us
beyond just symptoms?
Rachel (10:04):
Well, blood tests and biomarkers are definitely key
pieces of the puzzle.
The most commonly used one isCA-19-9.
That stands for carbohydrateantigen 19-9.
Mark (10:14):
CA-19-9.
Okay.
Rachel (10:16):
It's found to be elevated in about 70-80% of
patients who have pancreaticcancer.
Now the NCI points out it's notspecific enough to use for
general population screening.
Mark (10:25):
Meaning other things can make it go up too.
Rachel (10:27):
Exactly, but once someone is diagnosed, it's
crucial for tracking how thedisease is progressing and how
well treatment is working.
Mark (10:33):
Okay, so it's more for monitoring.
Rachel (10:35):
Primarily yes.
Another marker that might beelevated, especially in more
advanced stages, is CEA,carcinoembryonic antigen.
Mark (10:42):
CEA got it.
Rachel (10:43):
And, of course, because pancreatic tumors often disrupt
glucose metabolism.
Like we discussed with thediabetes link, sudden new onset
diabetes or just unexplained bigswings in blood sugar can
definitely prompt doctors toorder further testing, looking
at blood sugar and insulinlevels more closely.
Mark (10:59):
It really sounds like we're leveraging the body's own
chemistry to try and get theseearly clues.
But often seeing is believingright.
What role do the advancedimaging techniques play in this
whole diagnostic puzzle?
Rachel (11:12):
Oh, they're critical.
Imaging studies like CT scansand MRIs provide these really
high-resolution pictures.
They help doctors locate tumorsand assess if and where they
might have spread.
Mark (11:21):
Okay.
Rachel (11:22):
Then there's something called endoscopic ultrasound or
EUS.
This is pretty sophisticated ituses an endoscope to get an
ultrasound probe right up closeto the pancreas from inside the
body.
Wow yeah, it offers incrediblydetailed imaging and, crucially,
it allows for a guided biopsyof any suspicious areas they see
.
Pete scans are also usefulsometimes, especially for
detecting cancer spreadelsewhere in the body and
(11:44):
helping plan treatment.
Mark (11:45):
So, after all these advanced scans and blood tests,
what's the sort of gold standardfor a definitive diagnosis,
what truly confirms, yes, thisis cancer?
Rachel (11:53):
That's where the biopsy comes in.
Usually through that EOSprocedure or sometimes guided by
CT, they perform a fine needleaspiration or FNA.
Nicolette (12:03):
FNA.
Rachel (12:03):
That collects actual tissue samples which are then
examined under a microscope forcancer cells.
That gives the definitivehistological confirmation.
And increasingly important nowis molecular profiling of that
biopsy tissue.
Mark (12:17):
What does that tell you?
Rachel (12:18):
It identifies specific genetic mutations within the
tumor cells, like those BRCA1 orBRCA2 mutations we mentioned
earlier.
Knowing about these mutationscan directly influence treatment
choices, opening the door fortargeted therapies.
Mark (12:31):
That makes sense.
Rachel (12:32):
And it's worth noting here, you know the practical
side of getting these tests done.
The emergence of convenientmobile lab services is actually
making a difference.
How so lab services is actuallymaking a difference.
How so Well they can bringcritical tests like CA-19-9,
fasting glucose, hba1c lipidpanels right to a patient's home
.
This cuts down on logisticalhurdles, especially for people
who aren't feeling well, andensures the care teams get
(12:53):
timely data, which is reallyimportant for monitoring.
Mark (12:56):
That convenience factor sounds like a big deal,
especially for ongoing care.
Okay, so once someone isdiagnosed, what are the
treatment options?
It sounds like a challengingdisease to treat, but you
mentioned advancements areimproving outcomes.
Rachel (13:10):
That's right.
It is challenging, but thereare options and they're getting
better.
For early-stage disease, whenthe cancer hasn't spread,
surgery currently offers thebest chance of long-term
survival, potentially even acure.
Mark (13:23):
Okay, Surgery first.
It's possible.
What kind?
Rachel (13:26):
The most common operation, especially for tumors
in the head of the pancreas, isthe Whipple procedure.
It's technically called apancreaticoduodenectomy.
It's a major operation.
Mark (13:37):
Whipple Heard of that.
Rachel (13:38):
If the tumor is in the tail or body of the pancreas,
they might do a distalpancreatectomy, which often
involves removing the scline aswell, and very rarely a total
pancreatectomy removes theentire pancreas.
Mark (13:50):
But you said early stage.
What's the catch?
Rachel (13:52):
The crucial limitation, unfortunately, is that, because
it's often caught late, onlyabout 15, 20 percent of patients
are actually eligible forsurgery when they're diagnosed.
That's according to data fromplaces like Johns Hopkins
Medicine.
Mark (14:04):
Only 15, 20 percent.
Wow.
So for the other 80, 85 percent.
What are the mainstays?
Rachel (14:09):
For those patients, or sometimes in addition to surgery
, chemotherapy and radiationtherapy are frequently used.
Chemo drugs like fulfironox orgemcitabine are common.
Mark (14:18):
How are they used Before surgery after?
Rachel (14:21):
Both.
Actually, it can be givenbefore surgery, which we call
neoadjuvant therapy, the goalbeing to shrink the tumor to
make surgery possible or moreeffective.
Or it can be given aftersurgery, that's adjuvant therapy
, to try and kill any remainingcancer cells and prevent
recurrence.
Mark (14:36):
And radiation.
Rachel (14:37):
Radiation therapy is often combined with chemo.
It can be used to control localtumor growth target areas
surgery couldn't reach, orsometimes just to help relieve
symptoms like pain.
Mark (14:46):
Okay, so surgery, chemo, radiation, those are the
established approaches.
Are there any truly cuttingedge, or say experimental
therapies emerging that arechanging the treatment landscape
?
Rachel (14:59):
Absolutely.
Yeah, this is where things aregetting more personalized.
For patients whose tumors havethose BRCA1 or BRCA2 mutations
we talked about, there aretargeted drugs called PRP
inhibitors.
These interfere with the cancercell's ability to repair their
DNA, making them more vulnerable.
Mark (15:17):
Interesting.
Rachel (15:18):
Immunotherapies like checkpoint inhibitors are also
being explored.
These are designed to basicallytake the brakes off the
patient's own immune system soit can better attack the cancer
cells.
They're still largelyexperimental for most pancreatic
cancers, but showing promise incertain subsets.
Mark (15:34):
Okay.
Rachel (15:35):
And for some of those rarer pancreatic neuroendocrine
tumors, the NETs.
Mark (15:39):
Right the hormone-producing ones.
Rachel (15:41):
There's a novel therapy called peptide receptor
radionuclide therapy, or PRRT,that targets specific receptors
on those tumor cells.
It's showing good results forsome patients.
Mark (15:50):
Okay, prp inhibitors, immunotherapy, prrt a lot's
happening Now.
Here's where you said earlier.
It gets really interesting theemerging metabolic approaches.
Rachel (15:59):
Yes.
Mark (16:00):
This sounds like a completely different angle than
just attacking the tumordirectly.
Rachel (16:04):
It is, and it really represents a fascinating
potential paradigm shift.
Imagine if we could not onlyattack cancer cells with chemo
or radiation, but also kind ofstarve them by manipulating
their preferred fuel source.
Mark (16:18):
Starve the cancer.
Rachel (16:19):
By making them uniquely vulnerable metabolically.
That's the revolutionary ideabehind these metabolic
approaches.
Research, for instance, from DrThomas Seyfried at Boston
College is exploring howaltering cancer cell metabolism.
How do you?
Do that, for instance, throughthings like very low
carbohydrate or ketogenicdietary strategies, how these
(16:41):
might actually enhance theeffectiveness of traditional
treatments like chemo.
Mark (16:45):
So using diet to make chemo work better.
Rachel (16:47):
Potentially.
Yes, it's an exciting area ofresearch.
But and this is reallyimportant to clarify these are
currently considered adjunctivestrategies, meaning they're
meant to support and possiblyimprove traditional treatments,
not replace them.
They are not standalonetherapies for pancreatic cancer
at this point.
Mark (17:04):
Got it Supportive, not replacement.
That's a critical distinction.
It's clear that treatmentdoesn't just stop after the
initial diagnosis and therapyright.
Rachel (17:12):
Not at all.
Mark (17:13):
The ongoing monitoring, watching for disease progression
, checking treatment response,looking out for recurrence risk.
That seems like a criticallifelong challenge.
Rachel (17:22):
It absolutely is, and lab testing plays a crucial role
in this continuous care.
Mark (17:27):
How so?
What are you tracking?
Rachel (17:29):
Well.
Monitoring those tumor markerswe discussed, especially CA 19
to 9, after surgery or duringchemotherapy, is really
important.
It helps doctors assess if thetreatment is working.
Mark (17:40):
And if it starts rising again?
Rachel (17:41):
A rising CA 19-9 can be an early warning sign that the
cancer might be recurring,sometimes even before it shows
up on scans.
Cea levels can also be trackedalongside CA19-9 for additional
information.
Mark (17:53):
Okay, tumor markers are key for recurrence watch, and
because pancreatic cancer itselfor its treatment often affects
insulin production and glucoseregulation, evaluating metabolic
health must be a big part ofongoing care too.
Rachel (18:06):
Indeed, it's vital.
Tests like fasting, glucose andHbA1c are routinely done.
They help detect new-onsetdiabetes, which can happen after
surgery or worsening insulinresistance.
Mark (18:19):
What else metabolically?
Rachel (18:20):
Lipid panels are important, too, to assess
cardiovascular risk.
Cancer and its treatments canincrease inflammation, which
impacts cholesterol and, ofcourse, liver function tests are
essential.
Mark (18:31):
Why liver function specifically.
Rachel (18:32):
To monitor for any bile duct obstruction caused by the
tumor or spread, and just tocheck general liver health, as
the liver is a common site forpancreatic cancer to spread to.
Mark (18:42):
So this ongoing monitoring , this is where those mobile lab
services you mentioned earliercould really shine right in
supporting that long-term care.
Rachel (18:49):
Precisely Think about it .
For someone managing a chronic,serious illness like pancreatic
cancer, having to constantly goto a lab for blood draws can be
a significant burden.
Mark (18:58):
Yeah, I can imagine.
Rachel (18:59):
Convenient mobile lab services support this ongoing
care by offering at-home testingfor all these key markers CA 19
to 9, cea, glucose, hba1c, fullmetabolic profiles and they
often have fast turnaround times.
Mark (19:12):
So the doctors get the data quickly.
Rachel (19:14):
Exactly.
It ensures that the care teamshave timely data, which is just
paramount for managing a complexdisease like pancreatic cancer
effectively over the long term,makes adjustments possible
sooner.
Mark (19:25):
So we've really journeyed through the complexities of
pancreatic cancer.
Today it remains well aformidable opponent, often
dubbed the silent killer, forall the reasons we've discussed.
But what we've also seen isthat advancements in early
diagnosis tools, targetedtherapies, personalized care
they are certainly offering moreoptions and maybe more hope
(19:47):
than ever before.
Rachel (19:48):
That's really the key takeaway, I think Recognizing
those subtle early warning signswe talked about, understanding
your own personal risk factorsand leveraging comprehensive lab
testing and imaging it trulycan make a significant
difference in outcomes.
Knowledge is power here,especially with a disease that
often hides in plain sight forso long.
Imaging it truly can make asignificant difference in
outcomes.
Knowledge is power here,especially with a disease that
often hides in plain sight forso long.
Mark (20:06):
Absolutely so.
As we wrap up, what does thisall mean for you, our listener?
Given pancreatic cancer'sinsidious silent killer nature,
how might future technologiesreally push the envelope?
Rachel (20:17):
Yeah, where do we go from here?
Mark (20:19):
Could we move beyond even the current biomarkers and
imaging to truly predict riskmuch earlier, maybe through
advanced genetic profiling on awider scale, or perhaps detailed
metabolic profiling even beforeany symptoms appear?
How could we realisticallytransform early detection into
truly pre-symptomaticidentification for a much wider
(20:41):
population?
That feels like the nextfrontier, doesn't it?
Rachel (20:44):
It really does A challenging goal, but an
incredibly important one,definitely something to ponder.
Nicolette (20:56):
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.
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 (00:26):
Welcome to the Deep Dive.
Today we're plunging into atopic that touches so many lives
, yet often remains shrouded insilence.
Rachel (00:37):
Pancreatic cancer yeah, it's a tough one.
Mark (00:39):
It's frequently called a silent killer, and for good
reason.
The central question for ourDeep Dive today is this why is
it so incredibly challenging todetect?
And for good reason.
The central question for ourdeep dive today is this why is
it so incredibly challenging todetect and treat Right and
importantly, what are thecrucial advancements that are
(00:59):
truly changing the landscape?
Rachel (01:00):
for, you know, both early detection and personalized
care.
That's basically our missiontoday to unravel the complex
realities of pancreatic cancer.
We'll be drawing from some keysources, like the American
Cancer Society and the NationalCancer Institute, and we want to
provide you with insights intoits risk factors, symptoms, how
it's diagnosed and the evolvingstrategies for treatment.
Mark (01:16):
And our goal for you, our listener, is to gain a thorough
understanding of this criticalhealth topic without getting
bogged down in like supertechnical medical jargon.
Rachel (01:25):
Exactly.
Mark (01:25):
You'll walk away well-informed, ready to ask
better questions and hopefullywith a fresh perspective.
Okay, let's dive in.
Let's do it.
So you mentioned, pancreaticcancer is often called a silent
killer.
What does that actually mean inpractical terms?
Why is it so insidious?
Rachel (01:40):
Well, the real issue, the core problem, is that it can
progress for months, sometimeseven years, without any obvious
symptoms showing up.
Mark (01:49):
Wow Years.
Rachel (01:50):
Yeah, and the American Cancer Society highlights a
really stark reality Whilepancreatic cancer accounts for
only about 3 percent of allcancers in the US, which sounds
relatively small.
Right, it sounds small, butit's tragically responsible for
about 7% of all cancer-relateddeaths.
Mark (02:06):
That 3% versus 7% statistic really jumps out,
doesn't?
Rachel (02:09):
it, it does.
Mark (02:10):
It isn't just about late diagnosis.
It speaks to the, I guess, theinherent aggression and rapid
progression of this specificcancer.
Rachel (02:17):
Exactly, it's like a brutal race against time.
It makes the window foreffective intervention
incredibly narrow, much more sothan many other cancers window
for effective interventionincredibly narrow, much more so
than many other cancers andthose early tumors.
They often produce really mild,non-specific symptoms, things
like fatigue, maybe someindigestion or subtle weight
loss.
Mark (02:34):
Things you could easily brush off, totally, easily
mistaken for much less seriouseveryday conditions, which is
precisely the challenge, right?
But despite that inherentstealth, are we seeing any
progress?
Is there hope there?
Rachel (02:48):
We are actually Advances in lab testing, more
sophisticated imaging techniquesand genetic screening.
They're all steadily improvingour ability to identify it
earlier than we could before.
Mark (03:00):
Okay, that's good to hear.
Before we go deeper into thedisease itself, maybe it helps
to zoom out a bit and reallyappreciate the pancreas.
Rachel (03:07):
Yeah, good idea.
Mark (03:08):
This small but incredibly vital organ, sort of tucked away
deep behind your stomach?
What exactly makes its functionso critical?
Rachel (03:16):
It has this dual role, which is part of what makes
things complicated when cancerstrikes.
First, it produces digestiveenzymes.
These are absolutely essentialfor breaking down the food we
eat.
Mark (03:26):
Okay, digestion.
Rachel (03:27):
And second, equally vital, it releases hormones like
insulin and glucagon.
These are basically the masterregulators of our blood sugar.
Mark (03:34):
Okay.
So when cancer develops, it'sbecause normal cells undergo
these genetic mutations, theystart growing uncontrollably and
form tumors, and because thesetumors interfere with both
digestion and glucose metabolism.
That's why the symptoms oftenoverlap with things like
diabetes or chronic pancreatitis.
Rachel (03:54):
That's a great way to put it.
It's almost like the cancer ishijacking the pancreas' natural
functions.
Mark (03:59):
Okay.
Rachel (04:00):
And according to the National Cancer Institute,
pancreatic cancer is primarilycategorized into two major types
.
About 90 to 95 percent of casesare what we call exocrine
pancreatic cancers.
Mark (04:12):
Exocrine.
Rachel (04:13):
Got it.
These arise from those cellsthat produce the digestive
enzymes, and the most commonsubtype here is pancreatic
ductal adenocarcinoma, or PDACfor short.
Mark (04:23):
PDAC.
That's the main one we hearabout.
So that covers the most commontype.
What about the rarer forms?
How do they differ?
Rachel (04:29):
So the rarer form, making up about 5 to 10 percent
of cases, are neuroendocrinetumors or NETs.
Mark (04:34):
NETs.
Rachel (04:35):
These actually arise from the hormone-producing cells
.
Now, while they're often slowergrowing than PDFs, some types
can be quite aggressive inproducing excess hormones.
Mark (04:44):
Ah, so they cause different symptoms then?
Rachel (04:46):
Exactly.
They can lead to uniquesymptoms related to those
specific hormonal imbalances,think low blood sugar or severe
diarrhea, depending on thehormone.
Mark (04:55):
It's striking how that deep location in the abdomen
really plays such a big rolehere you mentioned earlier.
It's hard to spot.
Rachel (05:02):
It's huge.
More than half of cases arediagnosed after the cancer has
already spread, which justunderscores that critical need
for earlier detection methods.
Mark (05:10):
Yeah, definitely.
Okay, we've called it thesilent killer, but you mentioned
there are these subtle whispersof the disease, things easily
missed.
What exactly are those earlynonspecific signs that maybe we
should be a bit more alert to?
Rachel (05:26):
Okay.
So when we look at early signsto watch for, they include
things like unexplained weightloss.
This is often due to impaireddigestion or metabolic changes
the tumor itself is causing.
Mark (05:36):
Makes sense.
Rachel (05:37):
Then there's loss of appetite Sometimes tumor-related
inflammation can just disruptnormal hunger signals and, of
course, general fatigue andweakness may be caused by
nutrient malabsorption or evenanemia.
Mark (05:48):
Those sound pretty vague though.
Rachel (05:49):
It is, but here's where it gets really interesting,
potentially a bit more specificNew onset diabetes.
Mark (05:56):
Oh, okay, tell me more.
Rachel (05:58):
Imagine someone suddenly developing type 2 diabetes, but
they don't really have theusual risk factors.
Or maybe someone with diabetesfinds it suddenly worsening
significantly for no clearreason.
In some cases, these pancreatictumors are directly messing
with insulin production.
That leads to these sudden,unexplained blood sugar
(06:19):
imbalances.
It's a clue that'sunfortunately, often missed.
Mark (06:23):
Wow, that's a really important connection.
So those are the subtle earlysigns.
But what happens as the diseaseprogresses or in more advanced
stages?
What are the clearer, morepronounced symptoms that
typically emerge then?
Rachel (06:34):
Yeah, as the disease advances, the symptoms usually
become more insistent, harder toignore.
We're talking persistentabdominal or back pain.
This is often because thetumors are literally pressing on
nearby nerves and organs.
Mark (06:46):
Okay, that sounds more noticeable, Definitely, and
jaundice.
Rachel (06:49):
You know the yellowing of the skin and eyes.
That's a common sign.
It often happens because tumorsare blocking the bile ducts.
Mark (06:55):
Right, I've heard of that one.
Rachel (06:56):
Other progressive symptoms can include changes in
stool.
It might become greasy and paleagain due to reduced pancreatic
enzyme secretion, and nauseaand vomiting, often related to
some kind of digestiveobstruction caused by the tumor.
Mark (07:11):
It's really sobering to realize how easily these
nonspecific symptoms, even thelater ones, sometimes get
misattributed to other commonconditions.
Rachel (07:20):
It is.
It really highlights thechallenge.
Mark (07:22):
And underscores the critical need for advanced
testing, doesn't it.
Rachel (07:25):
It absolutely does.
This is precisely why labtesting and imaging are so
utterly essential for trying tocatch it earlier.
Mark (07:32):
So let's talk about risk.
Who's most at risk?
You hear it's not just onesingle cause, right?
It's more like a complexinterplay of genetic stuff,
metabolic factors, lifestyle.
Rachel (07:41):
That's exactly right.
It's multifactorial.
Understanding these differentpieces helps us identify
individuals who might benefitfrom earlier or perhaps more
frequent screening.
Mark (07:50):
OK, so break that down for us why, what about?
Rachel (07:54):
the metabolic and hormonal factors.
Sure On the metabolic andhormonal front, people with
longstanding type 2 diabetes andinsulin resistance seem to have
an increased risk.
The NCI suggests this might bedue to chronic high insulin
levels, hyperinsulinemia andinflammation.
Mark (08:10):
Okay, diabetes is a link.
What else?
Rachel (08:12):
Obesity, particularly excess visceral fat that belly
fat also contributes.
It tends to drive systemicinflammation and insulin
resistance, both of which arelinked to higher risk and,
importantly, chronicpancreatitis, that's, repeated
inflammation of the pancreasitself, often triggered by
things like heavy alcohol use,very high triglycerides or even
(08:33):
gallstones.
That significantly raises therisk.
Mark (08:36):
Wow, okay, so those are metabolic issues.
What about lifestyle Things wecan potentially change?
Rachel (08:40):
Lifestyle plays a huge role, a very significant one,
actually.
Tobacco use is one of thestrongest modifiable risk
factors.
Mark (08:46):
Really how strong.
Rachel (08:47):
According to the American Cancer Society, it's
responsible for about 25 percentof cases one in four.
Mark (08:53):
That's huge.
Rachel (08:54):
It is Also diets high in refined carbohydrates and added
sugars can contribute, probablyby promoting that insulin
resistance and inflammation wetalked about.
And of course, heavy alcoholconsumption is a known factor
because it chronically damagesthe pancreas and promotes
inflammation.
Mark (09:10):
And then, inevitably, there are the factors.
We can't change our genes andfamily history.
Rachel (09:14):
Exactly.
We know that inherited genemutations, specifically in genes
like BRCA1, BRCA2, PALB2, andATM.
Mark (09:22):
The BOCA genes often link to breast and ovarian cancer too
right.
Rachel (09:26):
Very same ones.
Mutations in these cansignificantly elevate lifetime
risk for pancreatic cancer aswell.
And then there's family history.
Having relatives, especiallyfirst-degree relatives like a
parent or sibling, withpancreatic cancer increases
personal risk.
If you have two or morefirst-degree relatives, the risk
can go up substantially, maybeeven up to six-fold.
Mark (09:46):
Okay, so quite a few factors to consider there.
Given all these challenges injust recognizing the symptoms,
how has the diagnostic processimproved?
You mentioned advances in labtesting, imaging genetic
screening.
How does that diagnostictoolkit actually work to move us
beyond just symptoms?
Rachel (10:04):
Well, blood tests and biomarkers are definitely key
pieces of the puzzle.
The most commonly used one isCA-19-9.
That stands for carbohydrateantigen 19-9.
Mark (10:14):
CA-19-9.
Okay.
Rachel (10:16):
It's found to be elevated in about 70-80% of
patients who have pancreaticcancer.
Now the NCI points out it's notspecific enough to use for
general population screening.
Mark (10:25):
Meaning other things can make it go up too.
Rachel (10:27):
Exactly, but once someone is diagnosed, it's
crucial for tracking how thedisease is progressing and how
well treatment is working.
Mark (10:33):
Okay, so it's more for monitoring.
Rachel (10:35):
Primarily yes.
Another marker that might beelevated, especially in more
advanced stages, is CEA,carcinoembryonic antigen.
Mark (10:42):
CEA got it.
Rachel (10:43):
And, of course, because pancreatic tumors often disrupt
glucose metabolism.
Like we discussed with thediabetes link, sudden new onset
diabetes or just unexplained bigswings in blood sugar can
definitely prompt doctors toorder further testing, looking
at blood sugar and insulinlevels more closely.
Mark (10:59):
It really sounds like we're leveraging the body's own
chemistry to try and get theseearly clues.
But often seeing is believingright.
What role do the advancedimaging techniques play in this
whole diagnostic puzzle?
Rachel (11:12):
Oh, they're critical.
Imaging studies like CT scansand MRIs provide these really
high-resolution pictures.
They help doctors locate tumorsand assess if and where they
might have spread.
Mark (11:21):
Okay.
Rachel (11:22):
Then there's something called endoscopic ultrasound or
EUS.
This is pretty sophisticated ituses an endoscope to get an
ultrasound probe right up closeto the pancreas from inside the
body.
Wow yeah, it offers incrediblydetailed imaging and, crucially,
it allows for a guided biopsyof any suspicious areas they see
.
Pete scans are also usefulsometimes, especially for
detecting cancer spreadelsewhere in the body and
(11:44):
helping plan treatment.
Mark (11:45):
So, after all these advanced scans and blood tests,
what's the sort of gold standardfor a definitive diagnosis,
what truly confirms, yes, thisis cancer?
Rachel (11:53):
That's where the biopsy comes in.
Usually through that EOSprocedure or sometimes guided by
CT, they perform a fine needleaspiration or FNA.
Nicolette (12:03):
FNA.
Rachel (12:03):
That collects actual tissue samples which are then
examined under a microscope forcancer cells.
That gives the definitivehistological confirmation.
And increasingly important nowis molecular profiling of that
biopsy tissue.
Mark (12:17):
What does that tell you?
Rachel (12:18):
It identifies specific genetic mutations within the
tumor cells, like those BRCA1 orBRCA2 mutations we mentioned
earlier.
Knowing about these mutationscan directly influence treatment
choices, opening the door fortargeted therapies.
Mark (12:31):
That makes sense.
Rachel (12:32):
And it's worth noting here, you know the practical
side of getting these tests done.
The emergence of convenientmobile lab services is actually
making a difference.
How so lab services is actuallymaking a difference.
How so Well they can bringcritical tests like CA-19-9,
fasting glucose, hba1c lipidpanels right to a patient's home
.
This cuts down on logisticalhurdles, especially for people
who aren't feeling well, andensures the care teams get
(12:53):
timely data, which is reallyimportant for monitoring.
Mark (12:56):
That convenience factor sounds like a big deal,
especially for ongoing care.
Okay, so once someone isdiagnosed, what are the
treatment options?
It sounds like a challengingdisease to treat, but you
mentioned advancements areimproving outcomes.
Rachel (13:10):
That's right.
It is challenging, but thereare options and they're getting
better.
For early-stage disease, whenthe cancer hasn't spread,
surgery currently offers thebest chance of long-term
survival, potentially even acure.
Mark (13:23):
Okay, Surgery first.
It's possible.
What kind?
Rachel (13:26):
The most common operation, especially for tumors
in the head of the pancreas, isthe Whipple procedure.
It's technically called apancreaticoduodenectomy.
It's a major operation.
Mark (13:37):
Whipple Heard of that.
Rachel (13:38):
If the tumor is in the tail or body of the pancreas,
they might do a distalpancreatectomy, which often
involves removing the scline aswell, and very rarely a total
pancreatectomy removes theentire pancreas.
Mark (13:50):
But you said early stage.
What's the catch?
Rachel (13:52):
The crucial limitation, unfortunately, is that, because
it's often caught late, onlyabout 15, 20 percent of patients
are actually eligible forsurgery when they're diagnosed.
That's according to data fromplaces like Johns Hopkins
Medicine.
Mark (14:04):
Only 15, 20 percent.
Wow.
So for the other 80, 85 percent.
What are the mainstays?
Rachel (14:09):
For those patients, or sometimes in addition to surgery
, chemotherapy and radiationtherapy are frequently used.
Chemo drugs like fulfironox orgemcitabine are common.
Mark (14:18):
How are they used Before surgery after?
Rachel (14:21):
Both.
Actually, it can be givenbefore surgery, which we call
neoadjuvant therapy, the goalbeing to shrink the tumor to
make surgery possible or moreeffective.
Or it can be given aftersurgery, that's adjuvant therapy
, to try and kill any remainingcancer cells and prevent
recurrence.
Mark (14:36):
And radiation.
Rachel (14:37):
Radiation therapy is often combined with chemo.
It can be used to control localtumor growth target areas
surgery couldn't reach, orsometimes just to help relieve
symptoms like pain.
Mark (14:46):
Okay, so surgery, chemo, radiation, those are the
established approaches.
Are there any truly cuttingedge, or say experimental
therapies emerging that arechanging the treatment landscape
?
Rachel (14:59):
Absolutely.
Yeah, this is where things aregetting more personalized.
For patients whose tumors havethose BRCA1 or BRCA2 mutations
we talked about, there aretargeted drugs called PRP
inhibitors.
These interfere with the cancercell's ability to repair their
DNA, making them more vulnerable.
Mark (15:17):
Interesting.
Rachel (15:18):
Immunotherapies like checkpoint inhibitors are also
being explored.
These are designed to basicallytake the brakes off the
patient's own immune system soit can better attack the cancer
cells.
They're still largelyexperimental for most pancreatic
cancers, but showing promise incertain subsets.
Mark (15:34):
Okay.
Rachel (15:35):
And for some of those rarer pancreatic neuroendocrine
tumors, the NETs.
Mark (15:39):
Right the hormone-producing ones.
Rachel (15:41):
There's a novel therapy called peptide receptor
radionuclide therapy, or PRRT,that targets specific receptors
on those tumor cells.
It's showing good results forsome patients.
Mark (15:50):
Okay, prp inhibitors, immunotherapy, prrt a lot's
happening Now.
Here's where you said earlier.
It gets really interesting theemerging metabolic approaches.
Rachel (15:59):
Yes.
Mark (16:00):
This sounds like a completely different angle than
just attacking the tumordirectly.
Rachel (16:04):
It is, and it really represents a fascinating
potential paradigm shift.
Imagine if we could not onlyattack cancer cells with chemo
or radiation, but also kind ofstarve them by manipulating
their preferred fuel source.
Mark (16:18):
Starve the cancer.
Rachel (16:19):
By making them uniquely vulnerable metabolically.
That's the revolutionary ideabehind these metabolic
approaches.
Research, for instance, from DrThomas Seyfried at Boston
College is exploring howaltering cancer cell metabolism.
How do you?
Do that, for instance, throughthings like very low
carbohydrate or ketogenicdietary strategies, how these
(16:41):
might actually enhance theeffectiveness of traditional
treatments like chemo.
Mark (16:45):
So using diet to make chemo work better.
Rachel (16:47):
Potentially.
Yes, it's an exciting area ofresearch.
But and this is reallyimportant to clarify these are
currently considered adjunctivestrategies, meaning they're
meant to support and possiblyimprove traditional treatments,
not replace them.
They are not standalonetherapies for pancreatic cancer
at this point.
Mark (17:04):
Got it Supportive, not replacement.
That's a critical distinction.
It's clear that treatmentdoesn't just stop after the
initial diagnosis and therapyright.
Rachel (17:12):
Not at all.
Mark (17:13):
The ongoing monitoring, watching for disease progression
, checking treatment response,looking out for recurrence risk.
That seems like a criticallifelong challenge.
Rachel (17:22):
It absolutely is, and lab testing plays a crucial role
in this continuous care.
Mark (17:27):
How so?
What are you tracking?
Rachel (17:29):
Well.
Monitoring those tumor markerswe discussed, especially CA 19
to 9, after surgery or duringchemotherapy, is really
important.
It helps doctors assess if thetreatment is working.
Mark (17:40):
And if it starts rising again?
Rachel (17:41):
A rising CA 19-9 can be an early warning sign that the
cancer might be recurring,sometimes even before it shows
up on scans.
Cea levels can also be trackedalongside CA19-9 for additional
information.
Mark (17:53):
Okay, tumor markers are key for recurrence watch, and
because pancreatic cancer itselfor its treatment often affects
insulin production and glucoseregulation, evaluating metabolic
health must be a big part ofongoing care too.
Rachel (18:06):
Indeed, it's vital.
Tests like fasting, glucose andHbA1c are routinely done.
They help detect new-onsetdiabetes, which can happen after
surgery or worsening insulinresistance.
Mark (18:19):
What else metabolically?
Rachel (18:20):
Lipid panels are important, too, to assess
cardiovascular risk.
Cancer and its treatments canincrease inflammation, which
impacts cholesterol and, ofcourse, liver function tests are
essential.
Mark (18:31):
Why liver function specifically.
Rachel (18:32):
To monitor for any bile duct obstruction caused by the
tumor or spread, and just tocheck general liver health, as
the liver is a common site forpancreatic cancer to spread to.
Mark (18:42):
So this ongoing monitoring , this is where those mobile lab
services you mentioned earliercould really shine right in
supporting that long-term care.
Rachel (18:49):
Precisely Think about it .
For someone managing a chronic,serious illness like pancreatic
cancer, having to constantly goto a lab for blood draws can be
a significant burden.
Mark (18:58):
Yeah, I can imagine.
Rachel (18:59):
Convenient mobile lab services support this ongoing
care by offering at-home testingfor all these key markers CA 19
to 9, cea, glucose, hba1c, fullmetabolic profiles and they
often have fast turnaround times.
Mark (19:12):
So the doctors get the data quickly.
Rachel (19:14):
Exactly.
It ensures that the care teamshave timely data, which is just
paramount for managing a complexdisease like pancreatic cancer
effectively over the long term,makes adjustments possible
sooner.
Mark (19:25):
So we've really journeyed through the complexities of
pancreatic cancer.
Today it remains well aformidable opponent, often
dubbed the silent killer, forall the reasons we've discussed.
But what we've also seen isthat advancements in early
diagnosis tools, targetedtherapies, personalized care
they are certainly offering moreoptions and maybe more hope
(19:47):
than ever before.
Rachel (19:48):
That's really the key takeaway, I think Recognizing
those subtle early warning signswe talked about, understanding
your own personal risk factorsand leveraging comprehensive lab
testing and imaging it trulycan make a significant
difference in outcomes.
Knowledge is power here,especially with a disease that
often hides in plain sight forso long.
Imaging it truly can make asignificant difference in
outcomes.
Knowledge is power here,especially with a disease that
often hides in plain sight forso long.
Mark (20:06):
Absolutely so.
As we wrap up, what does thisall mean for you, our listener?
Given pancreatic cancer'sinsidious silent killer nature,
how might future technologiesreally push the envelope?
Rachel (20:17):
Yeah, where do we go from here?
Mark (20:19):
Could we move beyond even the current biomarkers and
imaging to truly predict riskmuch earlier, maybe through
advanced genetic profiling on awider scale, or perhaps detailed
metabolic profiling even beforeany symptoms appear?
How could we realisticallytransform early detection into
truly pre-symptomaticidentification for a much wider
(20:41):
population?
That feels like the nextfrontier, doesn't it?
Rachel (20:44):
It really does A challenging goal, but an
incredibly important one,definitely something to ponder.
Nicolette (20:56):
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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