July 16, 2025 • 20 mins
Could cancer’s greatest weakness be its sweet tooth? In this episode of The Health Pulse, we explore the science behind the phrase “cancer cells love sugar,” diving into the Warburg Effect—the phenomenon where cancer cells rely heavily on glucose for energy, even when oxygen is abundant.
We discuss how the ketogenic diet creates a metabolic environment that may starve cancer cells while supporting healthy ones, shifting the body from glucose to ketones as its primary fuel source. Beyond glucose restriction, ketosis appears to reduce insulin and IGF-1, lower inflammation, and may even improve the effectiveness of conventional treatments like chemotherapy and radiation.
You’ll learn which types of cancer may benefit most, when caution is needed, and why personalized lab monitoring is key for safety and success. This episode offers an exciting glimpse into the evolving world of metabolic oncology—where diet and diagnostics converge for smarter, individualized care.
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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.
Rachel (00:25):
You hear quite a bit, maybe from oncologists, maybe
nutritionists this phrase cancercells love sugar.
It's a really common saying,yeah, and it sounds simple.
But honestly it's more thanjust catchy.
This whole idea that a lot ofcancer cells really rely on
glucose in a unique way.
It's actually driving a wholenew area of research really rely
on glucose in a unique way.
(00:45):
It's actually driving a wholenew area of research looking
into how diet, and specificallythe ketogenic diet, could you
know, play a real part inintegrated cancer care.
Mark (00:54):
It's a fascinating intersection.
Rachel (00:55):
So just quickly for anyone maybe not familiar the
ketogenic diet keto it'sbasically high fat but really
really low in carbohydrates.
Mark (01:02):
Right, Very low carb.
Rachel (01:03):
And the whole point is to shift your body's metabolism.
So instead of burning glucose,your default fuel, it starts
using something else.
Mark (01:11):
Ketone bodies.
It's your liver makes from fatwhen carbs aren't available.
Rachel (01:15):
Exactly Now you might have heard about keto for weight
loss, maybe even for epilepsy,but today our deep dive is all
about how this new research islooking at it as a potential
metabolic therapy in the cancercontext.
Mark (01:29):
Yeah, a very specific application.
Rachel (01:30):
So our mission today is to really unpack this.
How do cancer cells actuallyuse glucose differently?
What's the science behind ketoas like an anti-cancer idea?
Mark (01:42):
And, crucially, what does the research really say?
The studies, the limitations?
Rachel (01:46):
Yes, exactly, and then we'll get practical like who
might this actually be suitablefor, who needs to be really
careful and what lab tests areabsolutely essential if you or
someone you know is evenconsidering this approach
alongside other treatments.
Mark (02:00):
A lot to cover, but important stuff.
Rachel (02:01):
Think of this as maybe a shortcut to understanding some
pretty cool complex stuff abouthow your body uses fuel,
especially when it's facingsomething like cancer.
Some real aha moments,hopefully.
Mark (02:12):
Let's dive in.
Rachel (02:13):
Okay, so first things first, this unique, almost weird
relationship cancer cells havewith sugar.
It comes down to somethingcalled the Warburg effect.
Mark (02:22):
Right named after Otto Warburg, who first observed it.
Rachel (02:25):
So what is it basically?
How are cancer cells different?
Mark (02:28):
Well, your healthy cells.
They're pretty flexible.
Metabolically speaking, theygenerally prefer using their
mitochondria, the powerhouses,right Through a process called
oxidative phosphorylation.
It's slower but super efficientat making energy.
Rachel (02:43):
Okay, slow and steady wins the race for healthy cells.
Mark (02:46):
Kind of yeah, yeah, but many cancer cells?
They do something different.
Even when there's plenty ofoxygen around, which is key,
they often default to a muchfaster process called glycolysis
.
Rachel (02:58):
That's just breaking down glucose.
Mark (02:59):
Exactly Breaking down glucose directly for energy.
It's way faster but much, muchless efficient.
They burn through glucose likecrazy.
Rachel (03:06):
So they're choosing speed over efficiency.
Mark (03:08):
In many cases, yes, especially those really
aggressive, fast-growing tumors.
This makes them incrediblydependent on a steady supply of
glucose.
It's like they're constantlysprinting these short bursts
instead of running thatefficient marathon.
Rachel (03:22):
That's a great way to put it.
Mark (03:23):
And what's really fascinating, I think, is this
sort of metabolic inflexibilityyou see in many cancer cells.
Healthy cells, they can usuallyswitch fuels.
If they need to Use fats, useketones.
Rachel (03:34):
But these cancer cells are kind of stuck.
Mark (03:36):
Many seem to be yeah, Stuck on glucose.
And that raises a really,really important question for
researchers what happens if youlimit that glucose, If you take
their favorite fuel out of thepicture or at least drastically
reduce it?
Rachel (03:50):
Ah, okay, and that leads us right into ketosis, doesn't
it?
Mark (03:54):
Precisely, that's the connection.
Rachel (03:55):
So when you cut carbs way down, like usually people
say, under 20 grams a day, whichis really low, very low.
Mark (04:01):
Yes, that's the typical threshold for nutritional
ketosis.
Rachel (04:04):
Your liver starts making these ketone bodies.
You mentioned them earlierbeta-hydroxybutyrate, BHB is the
main one.
Mark (04:10):
BHB and acetoacetate.
Yeah, they're made frombreaking down fat.
Rachel (04:14):
And this whole metabolic state is ketosis.
Mark (04:16):
That's it.
Your body switches its primaryfuel source from glucose to
ketones.
Rachel (04:21):
So the main theory here, sometimes called the starvation
theory, what's the thinking?
Mark (04:32):
The core idea is that, unlike your healthy cells, which
adapt beautifully to usingketones, many cancer cells just
don't expect.
They lack the machinery or it'simpaired.
Rachel (04:36):
So they can't use ketones efficiently for energy.
Mark (04:39):
That's a hypothesis.
So if you switch the body'sfuel supply to ketones, you're
essentially nourishing yourhealthy cells but potentially
starving those glucose-dependentcancer cells.
Rachel (04:50):
Interesting, depriving them of their go-to fuel.
Mark (04:53):
Exactly, but it might be more complex than just fuel
deprivation.
Some of the early preclinicalresearch also hints that ketones
themselves might have othereffects.
Rachel (05:04):
Like what.
Mark (05:05):
Things like potentially reducing oxidative stress, maybe
lowering inflammation, evenpossibly impacting angiogenesis.
Rachel (05:12):
Angiogenesis, that's the blood vessel growth tumors need
right.
Mark (05:15):
That's the one Tumors need to build their own blood supply
to grow, so there could bemultiple mechanisms at play.
Rachel (05:21):
Okay, so this whole theoretical framework, it sounds
pretty compelling, leveragingthis metabolic weakness.
Mark (05:27):
It really is.
That's why there's so muchinterest.
But theory is one thing.
The crucial question is alwayswhat does the actual research
show?
When we look at studies, what'sthe evidence?
Rachel (05:36):
Right, that's where the rubber meets the road.
Let's get into that.
What have the studies actuallyfound?
Maybe start with animal studies.
Mark (05:43):
Sure.
The animal studies generallyhave been, I'd say, promising,
but definitely still early stage.
We see quite consistently thatketogenic diets can slow tumor
growth in various models.
Rachel (05:56):
Slow the growth.
Mark (05:57):
Yeah, and sometimes improve survival times, in mice,
for instance.
They've also shown potentialfor enhancing the effect of
other treatments like chemo orradiation in animal models.
Rachel (06:07):
Are there specific examples that stand out?
Mark (06:09):
Well, there was a meta-analysis back in 2014, I
think it was in PLOS One.
It looked at a bunch of studiesand found that keto diet
significantly prolongs survivalin mice with systemic cancers
compared to standard diet.
Okay that sounds significant,and another one, maybe 2017 in
Nature Communications thatshowed a keto diet combined with
chemo improved survival andreduced tumor burden in mice
(06:31):
with pancreatic cancer.
So you see these signalssuggesting a real biological
effect, at least in these models.
Rachel (06:37):
Okay, so promising in animals, but the big question is
always does it translate tohumans?
What about human trials?
Mark (06:44):
Right, and that's where we need to be a bit more cautious,
but still encouraged, I'd say.
The human trials are generallymuch smaller.
Rachel (06:51):
Smaller scale.
Mark (06:52):
Yes, and, very importantly , they almost always look at the
ketogenic diet alongsidestandard cancer treatments.
It's viewed as an adjunct, asupportive therapy, not a
replacement.
Rachel (07:02):
Okay, so it's part of an integrated approach.
Mark (07:05):
Exactly.
For example, there was a pilotstudy 2018, nutrition and
Metabolism just 10 patients withadvanced cancer.
It showed things like improvedquality of life, stable disease
in some and, importantly, nomajor safety issues with the
diet itself.
Rachel (07:19):
Small but positive signs .
Mark (07:22):
And there are case studies too.
I remember one in Frontiers inNutrition about a patient with a
glioblastoma, that's a toughbrain cancer, who maintained
stable disease for over a yearusing keto alongside their
standard therapy.
And more recently, a randomizedtrial 2022 in cell reports
looked at rectal cancer patientsgetting radiation.
The ones on keto had greaterfat loss, better metabolic
(07:45):
markers and, importantly,similar tumor response rates to
the standard diet group.
So it seems safe andmetabolically beneficial.
Rachel (07:52):
in that context, so even in these smaller human studies
there is a consistent sort ofsignal emerging.
Mark (07:59):
There really is.
It suggests we're tapping intosomething fundamental about
cancer metabolism.
But these are small studies,pilot studies, case reports,
small trials.
Rachel (08:08):
Right, not definitive proof yet.
Mark (08:10):
Exactly.
We absolutely need larger,well-designed randomized
controlled trials to confirm ifthis really improves long-term
outcomes like survival, and tounderstand the safety profile
across different cancers andpatient groups.
The field is moving fast,though More studies are underway
.
Rachel (08:25):
Okay, that makes sense.
So looking at the mechanisms.
Then we talked about starvingtumors of glucose, but you
mentioned other possibility.
What else might be going on?
How else could keto potentiallysupport cancer treatment?
Mark (08:37):
Right, it does seem to be more nuanced than just cutting
off the fuel line.
Rachel (08:40):
So first back to the glucose and insulin.
Lowering carbs means lowerblood sugar and, really
importantly, lower insulin right.
Mark (08:47):
Critically important.
Insulin is a growth hormone andhigh levels are linked to worse
outcomes in many cancers.
And there was that study, Ithink, in Nutrition and
Metabolism showing keto reducedIGF-1.
Rachel (09:00):
Insulin-like growth factor one yeah.
Mark (09:03):
Another potent growth signal that many tumors respond
to.
So lowering insulin and IGF-1could remove a significant
growth stimulus for some cancers.
Rachel (09:11):
Okay, so that's one major angle.
What else you mentioned?
Mitochondria.
Mark (09:15):
Yeah, this is interesting.
While cancer cells mightstruggle with ketones, your
healthy cells generally use themvery efficiently in their
mitochondria.
This might actually supportmitochondrial health in normal
tissues.
How would that help?
Well, it could reduce oxidativestress and maybe protect
healthy cells from damage, whichis particularly relevant during
harsh treatments like chemo orradiation that can cause a lot
(09:36):
of collateral damage.
Preserving healthy tissuefunction is huge.
Rachel (09:39):
Okay, protecting the good cells makes sense and
inflammation and angiogenesis?
Mark (09:44):
Right Ketones themselves, especially BHB, seem to act as
more than just fuel.
They act like signalingmolecules.
There's growing evidence theycan have anti-inflammatory
effects.
Rachel (09:55):
So dialing down systemic inflammation.
Mark (09:57):
Potentially, yes.
They act like signalingmolecules.
There's growing evidence theycan have anti-inflammatory
effects.
So dialing down systemicinflammation?
Potentially, yes.
Lowering markers like HSCRPRight, and since chronic
inflammation can fuel cancergrowth, that's a potential
benefit.
And then there's angiogenesis,that blood vessel formation.
Some preclinical work suggestsketones might interfere with
that process too.
Rachel (10:11):
Wow so multiple potential pathways.
Mark (10:15):
And one more big one enhancing standard therapies.
Rachel (10:18):
Making chemo or radiation work better.
Mark (10:20):
There's research, mostly in cell culture and animal
models, so far suggesting ketomight make cancer cells more
sensitive to chemo and radiation.
Like that 2017 study in RedoxBiology on glioma models,
combining keto and radiationseemed to boost the
tumor-killing effect.
Rachel (10:36):
So it could be like a metabolic sensitizer.
Mark (10:38):
That's the idea.
It's creating an internalenvironment that's less
hospitable for the cancer andpotentially more supportive of
the treatments workingeffectively.
Rachel (10:45):
OK, when you lay it all out like that, the potential
seems really multifaceted.
Mark (10:51):
It is, and it really underscores why it's best viewed
as a complementary approach.
It's not about ditchingconventional medicine.
It's about potentially addinganother layer of support,
metabolically speaking.
Rachel (11:02):
But tailored right.
You mentioned that.
Mark (11:04):
Absolutely critical.
It has to be individualized,based on the cancer type, the
stage, the person's overallhealth, other treatments.
It's not a one-size-fits-allprescription.
Rachel (11:14):
Which leads perfectly to the next question Given all
this potential, who might be thebest candidates for trying this
?
And, just as critical, whoreally needs to be cautious or
maybe avoid it?
Mark (11:25):
Great question.
Based on the mechanisms wediscussed, patients whose
cancers are known to beparticularly sugar-hungry,
highly glycolytic, might beprime candidates.
Rachel (11:35):
Like which ones?
Mark (11:36):
Things like glioblastoma often come up.
Some pancreatic cancers, maybecolorectal, certain types of
breast cancer, Cancers that showhigh activity on a PT span, for
instance, which usesradioactive glucose.
Rachel (11:47):
Because the PT scan literally shows glucose uptake.
Mark (11:49):
Exactly.
Also individuals who alreadyhave metabolic issues like
insulin resistance, metabolicsyndrome or obesity.
We know those conditions canworsen cancer outcomes.
Rachel (12:00):
So keto could help address the underlying metabolic
problem and potentially impactthe cancer.
Mark (12:06):
That's the hope.
Improving insulin sensitivity,reducing inflammation.
It can make them more resilientduring treatment too, and
sometimes just stabilizing bloodsugar can help with energy
levels and appetite control,which can be major quality of
life issues during therapy.
Rachel (12:21):
Okay, Now who needs to be careful?
Mark (12:23):
Definitely patients who are already experiencing
significant weight loss ormuscle wasting.
That's called cachexia.
It's common in advanced cancer.
Rachel (12:30):
Because keto can sometimes cause initial weight
loss.
Mark (12:33):
It can.
And if someone is alreadyseverely underweight or losing
muscle mass, aggressivelyrestricting food groups without
very careful planning could makemalnutrition worse.
That needs expert management.
Rachel (12:44):
Okay, so cachexia is a big red flag.
What about the liver andpancreas?
Concerns you sometimes here,like, isn't a high-fat diet hard
on those organs?
Mark (12:53):
That's a really common misconception and it mostly
stems from thinking about fat inthe context of a high-carb,
high-insulin state.
Rachel (13:00):
Ah, okay, so the context matters.
Mark (13:02):
Immensely.
Rachel (13:03):
Yeah.
Mark (13:03):
When insulin is high, usually because of lots of carbs
, yes, the liver can getburdened trying to process
everything and it starts makingand storing fat.
That's de novo lipogenesis.
But in ketosis insulin is low.
Right Dietary fat gets absorbeddifferently initially,
bypassing the liver more.
It's actually the glucose andfructose from carbs hitting the
(13:24):
liver via the portal vein.
In a high insulin state thatreally drives fat accumulation
there for many people.
Rachel (13:29):
So low insulin changes how the body handles fat.
Mark (13:32):
Completely.
In fact, that 2020 review innutrients really highlights how
liver fat is more linked to thehigh insulin and carb load, not
necessarily dietary fat in a lowcarb context.
Some research even suggestscertain saturated fats might be
protective against liver fatwhen you're in ketosis, because
they promote ketone production.
Rachel (13:50):
Fascinating.
So the old fat is bad for theliver.
Idea needs nuance.
Mark (13:54):
A lot of nuance, especially in the context of
ketosis.
However, if someone haspre-existing severe liver or
pancreatic disease, they stillneed close monitoring.
Rachel (14:04):
of course, and anyone on complex medications.
Mark (14:07):
Absolutely.
Keto changes fluid balance,electrolytes and can affect how
some drugs are metabolized.
If you're on meds for diabetes,blood pressure steroids or even
certain chemotherapies, youneed very close supervision to
adjust doses and avoid issueslike hypoglycemia or dehydration
.
It requires careful integration.
Rachel (14:27):
Okay, super important points on caution.
So let's say, someone fits thepotential profile, they're
working with their team.
What labs are absolutelyessential to track?
This isn't something you justwing right?
Mark (14:37):
Oh, definitely not.
Monitoring is crucial forsafety, for effectiveness, for
making adjustments.
You need data.
Rachel (14:43):
What's on the must-watch list.
Mark (14:50):
Start with the basics A basic metabolic panel, or BMP,
that tracks your electrolytes,sodium, potassium, etc.
Which can shift on keto, pluskidney function markers like
creatinine and your basicglucose level.
Rachel (14:55):
Okay, BMP for the fundamentals.
Mark (14:58):
Then fasting insulin and glucose together.
You want to see those numbersideally coming down, reflecting
improved insulin sensitivity.
That's a key therapeutic target.
Rachel (15:07):
What about cholesterol?
People worry about fat andcholesterol.
Mark (15:09):
Right the lipid panel Total cholesterol, ldl, hdl,
triglycerides.
Now LDL cholesterol might go upfor some people on keto, but
the context is everything.
Rachel (15:20):
What do you mean by context?
Mark (15:21):
You often see triglycerides plummeting and HDL
good cholesterol going up,which is great, and the type of
LDL often shifts towards larger,fluffier particles which are
generally thought to be lessproblematic than small, dense
LDL.
Rachel (15:36):
So just looking at the total LDL number might not tell
the whole story.
Mark (15:39):
Exactly For a deeper dive, you might consider testing APOB
, which measures the totalnumber of atherogenic particles
or even LDL particle sizedirectly.
That gives a much clearerpicture of cardiovascular risk
than just standard LDL-C alone.
Rachel (15:53):
Good to know what else.
Mark (15:54):
Inflammatory markers, things like high-sensitivity
C-reactive protein, HSCRP, maybeferritin, ESR.
Tracking these can showsystemic inflammation is
improving.
Rachel (16:03):
And liver and pancreatic enzymes, since we discussed
those organs.
Mark (16:07):
Yes, definitely monitor those, especially when starting
out ALT, ast, alp, ggt for liverfunction and lipase for the
pancreas, just to make sureeverything is adapting well.
Rachel (16:17):
And the ketones themselves.
Mark (16:18):
Of course, beta-hydroxybutyrate BHB you
measure this in blood.
Usually it confirms you'reactually in nutritional ketosis.
Bhb you measure this in blood.
Usually it confirms you'reactually in nutritional ketosis.
The therapeutic range oftencited is somewhere between 1.0
and 3.0 millimole, but it canvary.
Rachel (16:32):
So you know the diet is working metabolically.
Mark (16:39):
Precisely.
And finally, don't forget basicnutrient status.
Restrictive diets can sometimeslead to deficiencies if not
planned well.
Checking things like magnesium,selenium, b vitamins like B12
and folate.
Maybe zinc is wise.
Rachel (16:48):
OK, that's a pretty comprehensive list for standard
monitoring.
Mark (16:52):
It covers the key safety and efficacy markers, but, you
know, to get an even fullerpicture of how the whole body is
responding and balanced.
Rachel (16:58):
There's more you could look at.
Mark (16:59):
Yeah for a really optimized, personalized approach
.
Functional lab testing can beincredibly insightful Things
like a GI map stool test toassess gut health, which is
crucial.
Rachel (17:09):
The gut microbiomes role .
Mark (17:17):
Huge, or an organic acids test, the OAT test that looks at
metabolic byproducts in urineand can tell you about
mitochondrial function, nutrientneeds, detoxification pathways.
Wow, really detailed metabolicsnapshot it really is, and a
comprehensive micronutrientpanel.
Looking inside the cells cangive a much better sense of
long-term nutrient status thanjust serum levels.
These functional tests helpfine-tune the approach for
(17:38):
optimal balance.
Rachel (17:39):
So layering deeper insights onto the standard
monitoring.
Mark (17:42):
Exactly For a truly holistic view.
Rachel (17:44):
Okay, so let's try and pull all of this together as we
wrap up this deep dive.
What's the main takeaway?
Clearly, the ketogenic dietisn't some kind of magic bullet
for cancer right?
Mark (17:55):
Absolutely not, and, critically, it's not a
replacement for standard,evidence-based cancer treatments
like surgery, chemotherapy,radiation or immunotherapy.
That needs to be crystal clear.
Rachel (18:04):
The evidence we discussed does suggest it could
be something else.
Mark (18:07):
It suggests it could be a really powerful metabolic ally,
a complementary tool, especiallywhen used carefully under
qualified supervision.
Rachel (18:15):
Particularly for those glucose-hungry tumors we talked
about, or maybe for patients whoalso have things like insulin
resistance.
Mark (18:22):
Exactly.
Its potential value seems tocome from multiple angles
lowering that insulin andglucose, possibly supporting
healthy mitochondria, reducinginflammation and maybe even
starving those inflexible cancercells of their preferred fuel.
Rachel (18:37):
So I guess the key takeaway is it's not for
everyone, but for the rightpatient in the right situation,
used in the right way.
Mark (18:45):
It could significantly support their metabolic health,
maybe improve how well theytolerate their main treatments
and ultimately contribute to abetter quality of life during a
really challenging time.
Rachel (18:55):
Yeah, you know this whole deep dive.
It really highlights how fastour understanding of metabolism
is changing, how interconnectedit all is.
Mark (19:03):
It's an incredibly dynamic field.
Rachel (19:05):
It makes you wonder what else are we going to discover?
How much more couldpersonalized nutrition tailored
to our unique biochemistryreally revolutionize how we
approach complex diseases likecancer, as we keep sort of
unlocking these intricatepathways in the body?
Mark (19:19):
It's a very exciting and hopeful area of research.
There's still so much to learn.
Rachel (19:25):
So final thought for our listeners, if this conversation
has sparked interest, if you'reconsidering exploring a
ketogenic approach as part of acancer care plan, the crucial
step is to work with ahealthcare provider or a team
that really understands bothoncology and metabolic nutrition
.
Mark (19:40):
It's a specialized area.
Rachel (19:42):
And monitor those labs right.
Track the data along the way.
Mark (19:45):
Essential, absolutely essential for doing it safely
and effectively.
Nicolette (19:52):
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
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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.
Rachel (00:25):
You hear quite a bit, maybe from oncologists, maybe
nutritionists this phrase cancercells love sugar.
It's a really common saying,yeah, and it sounds simple.
But honestly it's more thanjust catchy.
This whole idea that a lot ofcancer cells really rely on
glucose in a unique way.
It's actually driving a wholenew area of research really rely
on glucose in a unique way.
(00:45):
It's actually driving a wholenew area of research looking
into how diet, and specificallythe ketogenic diet, could you
know, play a real part inintegrated cancer care.
Mark (00:54):
It's a fascinating intersection.
Rachel (00:55):
So just quickly for anyone maybe not familiar the
ketogenic diet keto it'sbasically high fat but really
really low in carbohydrates.
Mark (01:02):
Right, Very low carb.
Rachel (01:03):
And the whole point is to shift your body's metabolism.
So instead of burning glucose,your default fuel, it starts
using something else.
Mark (01:11):
Ketone bodies.
It's your liver makes from fatwhen carbs aren't available.
Rachel (01:15):
Exactly Now you might have heard about keto for weight
loss, maybe even for epilepsy,but today our deep dive is all
about how this new research islooking at it as a potential
metabolic therapy in the cancercontext.
Mark (01:29):
Yeah, a very specific application.
Rachel (01:30):
So our mission today is to really unpack this.
How do cancer cells actuallyuse glucose differently?
What's the science behind ketoas like an anti-cancer idea?
Mark (01:42):
And, crucially, what does the research really say?
The studies, the limitations?
Rachel (01:46):
Yes, exactly, and then we'll get practical like who
might this actually be suitablefor, who needs to be really
careful and what lab tests areabsolutely essential if you or
someone you know is evenconsidering this approach
alongside other treatments.
Mark (02:00):
A lot to cover, but important stuff.
Rachel (02:01):
Think of this as maybe a shortcut to understanding some
pretty cool complex stuff abouthow your body uses fuel,
especially when it's facingsomething like cancer.
Some real aha moments,hopefully.
Mark (02:12):
Let's dive in.
Rachel (02:13):
Okay, so first things first, this unique, almost weird
relationship cancer cells havewith sugar.
It comes down to somethingcalled the Warburg effect.
Mark (02:22):
Right named after Otto Warburg, who first observed it.
Rachel (02:25):
So what is it basically?
How are cancer cells different?
Mark (02:28):
Well, your healthy cells.
They're pretty flexible.
Metabolically speaking, theygenerally prefer using their
mitochondria, the powerhouses,right Through a process called
oxidative phosphorylation.
It's slower but super efficientat making energy.
Rachel (02:43):
Okay, slow and steady wins the race for healthy cells.
Mark (02:46):
Kind of yeah, yeah, but many cancer cells?
They do something different.
Even when there's plenty ofoxygen around, which is key,
they often default to a muchfaster process called glycolysis
.
Rachel (02:58):
That's just breaking down glucose.
Mark (02:59):
Exactly Breaking down glucose directly for energy.
It's way faster but much, muchless efficient.
They burn through glucose likecrazy.
Rachel (03:06):
So they're choosing speed over efficiency.
Mark (03:08):
In many cases, yes, especially those really
aggressive, fast-growing tumors.
This makes them incrediblydependent on a steady supply of
glucose.
It's like they're constantlysprinting these short bursts
instead of running thatefficient marathon.
Rachel (03:22):
That's a great way to put it.
Mark (03:23):
And what's really fascinating, I think, is this
sort of metabolic inflexibilityyou see in many cancer cells.
Healthy cells, they can usuallyswitch fuels.
If they need to Use fats, useketones.
Rachel (03:34):
But these cancer cells are kind of stuck.
Mark (03:36):
Many seem to be yeah, Stuck on glucose.
And that raises a really,really important question for
researchers what happens if youlimit that glucose, If you take
their favorite fuel out of thepicture or at least drastically
reduce it?
Rachel (03:50):
Ah, okay, and that leads us right into ketosis, doesn't
it?
Mark (03:54):
Precisely, that's the connection.
Rachel (03:55):
So when you cut carbs way down, like usually people
say, under 20 grams a day, whichis really low, very low.
Mark (04:01):
Yes, that's the typical threshold for nutritional
ketosis.
Rachel (04:04):
Your liver starts making these ketone bodies.
You mentioned them earlierbeta-hydroxybutyrate, BHB is the
main one.
Mark (04:10):
BHB and acetoacetate.
Yeah, they're made frombreaking down fat.
Rachel (04:14):
And this whole metabolic state is ketosis.
Mark (04:16):
That's it.
Your body switches its primaryfuel source from glucose to
ketones.
Rachel (04:21):
So the main theory here, sometimes called the starvation
theory, what's the thinking?
Mark (04:32):
The core idea is that, unlike your healthy cells, which
adapt beautifully to usingketones, many cancer cells just
don't expect.
They lack the machinery or it'simpaired.
Rachel (04:36):
So they can't use ketones efficiently for energy.
Mark (04:39):
That's a hypothesis.
So if you switch the body'sfuel supply to ketones, you're
essentially nourishing yourhealthy cells but potentially
starving those glucose-dependentcancer cells.
Rachel (04:50):
Interesting, depriving them of their go-to fuel.
Mark (04:53):
Exactly, but it might be more complex than just fuel
deprivation.
Some of the early preclinicalresearch also hints that ketones
themselves might have othereffects.
Rachel (05:04):
Like what.
Mark (05:05):
Things like potentially reducing oxidative stress, maybe
lowering inflammation, evenpossibly impacting angiogenesis.
Rachel (05:12):
Angiogenesis, that's the blood vessel growth tumors need
right.
Mark (05:15):
That's the one Tumors need to build their own blood supply
to grow, so there could bemultiple mechanisms at play.
Rachel (05:21):
Okay, so this whole theoretical framework, it sounds
pretty compelling, leveragingthis metabolic weakness.
Mark (05:27):
It really is.
That's why there's so muchinterest.
But theory is one thing.
The crucial question is alwayswhat does the actual research
show?
When we look at studies, what'sthe evidence?
Rachel (05:36):
Right, that's where the rubber meets the road.
Let's get into that.
What have the studies actuallyfound?
Maybe start with animal studies.
Mark (05:43):
Sure.
The animal studies generallyhave been, I'd say, promising,
but definitely still early stage.
We see quite consistently thatketogenic diets can slow tumor
growth in various models.
Rachel (05:56):
Slow the growth.
Mark (05:57):
Yeah, and sometimes improve survival times, in mice,
for instance.
They've also shown potentialfor enhancing the effect of
other treatments like chemo orradiation in animal models.
Rachel (06:07):
Are there specific examples that stand out?
Mark (06:09):
Well, there was a meta-analysis back in 2014, I
think it was in PLOS One.
It looked at a bunch of studiesand found that keto diet
significantly prolongs survivalin mice with systemic cancers
compared to standard diet.
Okay that sounds significant,and another one, maybe 2017 in
Nature Communications thatshowed a keto diet combined with
chemo improved survival andreduced tumor burden in mice
(06:31):
with pancreatic cancer.
So you see these signalssuggesting a real biological
effect, at least in these models.
Rachel (06:37):
Okay, so promising in animals, but the big question is
always does it translate tohumans?
What about human trials?
Mark (06:44):
Right, and that's where we need to be a bit more cautious,
but still encouraged, I'd say.
The human trials are generallymuch smaller.
Rachel (06:51):
Smaller scale.
Mark (06:52):
Yes, and, very importantly , they almost always look at the
ketogenic diet alongsidestandard cancer treatments.
It's viewed as an adjunct, asupportive therapy, not a
replacement.
Rachel (07:02):
Okay, so it's part of an integrated approach.
Mark (07:05):
Exactly.
For example, there was a pilotstudy 2018, nutrition and
Metabolism just 10 patients withadvanced cancer.
It showed things like improvedquality of life, stable disease
in some and, importantly, nomajor safety issues with the
diet itself.
Rachel (07:19):
Small but positive signs .
Mark (07:22):
And there are case studies too.
I remember one in Frontiers inNutrition about a patient with a
glioblastoma, that's a toughbrain cancer, who maintained
stable disease for over a yearusing keto alongside their
standard therapy.
And more recently, a randomizedtrial 2022 in cell reports
looked at rectal cancer patientsgetting radiation.
The ones on keto had greaterfat loss, better metabolic
(07:45):
markers and, importantly,similar tumor response rates to
the standard diet group.
So it seems safe andmetabolically beneficial.
Rachel (07:52):
in that context, so even in these smaller human studies
there is a consistent sort ofsignal emerging.
Mark (07:59):
There really is.
It suggests we're tapping intosomething fundamental about
cancer metabolism.
But these are small studies,pilot studies, case reports,
small trials.
Rachel (08:08):
Right, not definitive proof yet.
Mark (08:10):
Exactly.
We absolutely need larger,well-designed randomized
controlled trials to confirm ifthis really improves long-term
outcomes like survival, and tounderstand the safety profile
across different cancers andpatient groups.
The field is moving fast,though More studies are underway
.
Rachel (08:25):
Okay, that makes sense.
So looking at the mechanisms.
Then we talked about starvingtumors of glucose, but you
mentioned other possibility.
What else might be going on?
How else could keto potentiallysupport cancer treatment?
Mark (08:37):
Right, it does seem to be more nuanced than just cutting
off the fuel line.
Rachel (08:40):
So first back to the glucose and insulin.
Lowering carbs means lowerblood sugar and, really
importantly, lower insulin right.
Mark (08:47):
Critically important.
Insulin is a growth hormone andhigh levels are linked to worse
outcomes in many cancers.
And there was that study, Ithink, in Nutrition and
Metabolism showing keto reducedIGF-1.
Rachel (09:00):
Insulin-like growth factor one yeah.
Mark (09:03):
Another potent growth signal that many tumors respond
to.
So lowering insulin and IGF-1could remove a significant
growth stimulus for some cancers.
Rachel (09:11):
Okay, so that's one major angle.
What else you mentioned?
Mitochondria.
Mark (09:15):
Yeah, this is interesting.
While cancer cells mightstruggle with ketones, your
healthy cells generally use themvery efficiently in their
mitochondria.
This might actually supportmitochondrial health in normal
tissues.
How would that help?
Well, it could reduce oxidativestress and maybe protect
healthy cells from damage, whichis particularly relevant during
harsh treatments like chemo orradiation that can cause a lot
(09:36):
of collateral damage.
Preserving healthy tissuefunction is huge.
Rachel (09:39):
Okay, protecting the good cells makes sense and
inflammation and angiogenesis?
Mark (09:44):
Right Ketones themselves, especially BHB, seem to act as
more than just fuel.
They act like signalingmolecules.
There's growing evidence theycan have anti-inflammatory
effects.
Rachel (09:55):
So dialing down systemic inflammation.
Mark (09:57):
Potentially, yes.
They act like signalingmolecules.
There's growing evidence theycan have anti-inflammatory
effects.
So dialing down systemicinflammation?
Potentially, yes.
Lowering markers like HSCRPRight, and since chronic
inflammation can fuel cancergrowth, that's a potential
benefit.
And then there's angiogenesis,that blood vessel formation.
Some preclinical work suggestsketones might interfere with
that process too.
Rachel (10:11):
Wow so multiple potential pathways.
Mark (10:15):
And one more big one enhancing standard therapies.
Rachel (10:18):
Making chemo or radiation work better.
Mark (10:20):
There's research, mostly in cell culture and animal
models, so far suggesting ketomight make cancer cells more
sensitive to chemo and radiation.
Like that 2017 study in RedoxBiology on glioma models,
combining keto and radiationseemed to boost the
tumor-killing effect.
Rachel (10:36):
So it could be like a metabolic sensitizer.
Mark (10:38):
That's the idea.
It's creating an internalenvironment that's less
hospitable for the cancer andpotentially more supportive of
the treatments workingeffectively.
Rachel (10:45):
OK, when you lay it all out like that, the potential
seems really multifaceted.
Mark (10:51):
It is, and it really underscores why it's best viewed
as a complementary approach.
It's not about ditchingconventional medicine.
It's about potentially addinganother layer of support,
metabolically speaking.
Rachel (11:02):
But tailored right.
You mentioned that.
Mark (11:04):
Absolutely critical.
It has to be individualized,based on the cancer type, the
stage, the person's overallhealth, other treatments.
It's not a one-size-fits-allprescription.
Rachel (11:14):
Which leads perfectly to the next question Given all
this potential, who might be thebest candidates for trying this
?
And, just as critical, whoreally needs to be cautious or
maybe avoid it?
Mark (11:25):
Great question.
Based on the mechanisms wediscussed, patients whose
cancers are known to beparticularly sugar-hungry,
highly glycolytic, might beprime candidates.
Rachel (11:35):
Like which ones?
Mark (11:36):
Things like glioblastoma often come up.
Some pancreatic cancers, maybecolorectal, certain types of
breast cancer, Cancers that showhigh activity on a PT span, for
instance, which usesradioactive glucose.
Rachel (11:47):
Because the PT scan literally shows glucose uptake.
Mark (11:49):
Exactly.
Also individuals who alreadyhave metabolic issues like
insulin resistance, metabolicsyndrome or obesity.
We know those conditions canworsen cancer outcomes.
Rachel (12:00):
So keto could help address the underlying metabolic
problem and potentially impactthe cancer.
Mark (12:06):
That's the hope.
Improving insulin sensitivity,reducing inflammation.
It can make them more resilientduring treatment too, and
sometimes just stabilizing bloodsugar can help with energy
levels and appetite control,which can be major quality of
life issues during therapy.
Rachel (12:21):
Okay, Now who needs to be careful?
Mark (12:23):
Definitely patients who are already experiencing
significant weight loss ormuscle wasting.
That's called cachexia.
It's common in advanced cancer.
Rachel (12:30):
Because keto can sometimes cause initial weight
loss.
Mark (12:33):
It can.
And if someone is alreadyseverely underweight or losing
muscle mass, aggressivelyrestricting food groups without
very careful planning could makemalnutrition worse.
That needs expert management.
Rachel (12:44):
Okay, so cachexia is a big red flag.
What about the liver andpancreas?
Concerns you sometimes here,like, isn't a high-fat diet hard
on those organs?
Mark (12:53):
That's a really common misconception and it mostly
stems from thinking about fat inthe context of a high-carb,
high-insulin state.
Rachel (13:00):
Ah, okay, so the context matters.
Mark (13:02):
Immensely.
Rachel (13:03):
Yeah.
Mark (13:03):
When insulin is high, usually because of lots of carbs
, yes, the liver can getburdened trying to process
everything and it starts makingand storing fat.
That's de novo lipogenesis.
But in ketosis insulin is low.
Right Dietary fat gets absorbeddifferently initially,
bypassing the liver more.
It's actually the glucose andfructose from carbs hitting the
(13:24):
liver via the portal vein.
In a high insulin state thatreally drives fat accumulation
there for many people.
Rachel (13:29):
So low insulin changes how the body handles fat.
Mark (13:32):
Completely.
In fact, that 2020 review innutrients really highlights how
liver fat is more linked to thehigh insulin and carb load, not
necessarily dietary fat in a lowcarb context.
Some research even suggestscertain saturated fats might be
protective against liver fatwhen you're in ketosis, because
they promote ketone production.
Rachel (13:50):
Fascinating.
So the old fat is bad for theliver.
Idea needs nuance.
Mark (13:54):
A lot of nuance, especially in the context of
ketosis.
However, if someone haspre-existing severe liver or
pancreatic disease, they stillneed close monitoring.
Rachel (14:04):
of course, and anyone on complex medications.
Mark (14:07):
Absolutely.
Keto changes fluid balance,electrolytes and can affect how
some drugs are metabolized.
If you're on meds for diabetes,blood pressure steroids or even
certain chemotherapies, youneed very close supervision to
adjust doses and avoid issueslike hypoglycemia or dehydration
.
It requires careful integration.
Rachel (14:27):
Okay, super important points on caution.
So let's say, someone fits thepotential profile, they're
working with their team.
What labs are absolutelyessential to track?
This isn't something you justwing right?
Mark (14:37):
Oh, definitely not.
Monitoring is crucial forsafety, for effectiveness, for
making adjustments.
You need data.
Rachel (14:43):
What's on the must-watch list.
Mark (14:50):
Start with the basics A basic metabolic panel, or BMP,
that tracks your electrolytes,sodium, potassium, etc.
Which can shift on keto, pluskidney function markers like
creatinine and your basicglucose level.
Rachel (14:55):
Okay, BMP for the fundamentals.
Mark (14:58):
Then fasting insulin and glucose together.
You want to see those numbersideally coming down, reflecting
improved insulin sensitivity.
That's a key therapeutic target.
Rachel (15:07):
What about cholesterol?
People worry about fat andcholesterol.
Mark (15:09):
Right the lipid panel Total cholesterol, ldl, hdl,
triglycerides.
Now LDL cholesterol might go upfor some people on keto, but
the context is everything.
Rachel (15:20):
What do you mean by context?
Mark (15:21):
You often see triglycerides plummeting and HDL
good cholesterol going up,which is great, and the type of
LDL often shifts towards larger,fluffier particles which are
generally thought to be lessproblematic than small, dense
LDL.
Rachel (15:36):
So just looking at the total LDL number might not tell
the whole story.
Mark (15:39):
Exactly For a deeper dive, you might consider testing APOB
, which measures the totalnumber of atherogenic particles
or even LDL particle sizedirectly.
That gives a much clearerpicture of cardiovascular risk
than just standard LDL-C alone.
Rachel (15:53):
Good to know what else.
Mark (15:54):
Inflammatory markers, things like high-sensitivity
C-reactive protein, HSCRP, maybeferritin, ESR.
Tracking these can showsystemic inflammation is
improving.
Rachel (16:03):
And liver and pancreatic enzymes, since we discussed
those organs.
Mark (16:07):
Yes, definitely monitor those, especially when starting
out ALT, ast, alp, ggt for liverfunction and lipase for the
pancreas, just to make sureeverything is adapting well.
Rachel (16:17):
And the ketones themselves.
Mark (16:18):
Of course, beta-hydroxybutyrate BHB you
measure this in blood.
Usually it confirms you'reactually in nutritional ketosis.
Bhb you measure this in blood.
Usually it confirms you'reactually in nutritional ketosis.
The therapeutic range oftencited is somewhere between 1.0
and 3.0 millimole, but it canvary.
Rachel (16:32):
So you know the diet is working metabolically.
Mark (16:39):
Precisely.
And finally, don't forget basicnutrient status.
Restrictive diets can sometimeslead to deficiencies if not
planned well.
Checking things like magnesium,selenium, b vitamins like B12
and folate.
Maybe zinc is wise.
Rachel (16:48):
OK, that's a pretty comprehensive list for standard
monitoring.
Mark (16:52):
It covers the key safety and efficacy markers, but, you
know, to get an even fullerpicture of how the whole body is
responding and balanced.
Rachel (16:58):
There's more you could look at.
Mark (16:59):
Yeah for a really optimized, personalized approach
.
Functional lab testing can beincredibly insightful Things
like a GI map stool test toassess gut health, which is
crucial.
Rachel (17:09):
The gut microbiomes role .
Mark (17:17):
Huge, or an organic acids test, the OAT test that looks at
metabolic byproducts in urineand can tell you about
mitochondrial function, nutrientneeds, detoxification pathways.
Wow, really detailed metabolicsnapshot it really is, and a
comprehensive micronutrientpanel.
Looking inside the cells cangive a much better sense of
long-term nutrient status thanjust serum levels.
These functional tests helpfine-tune the approach for
(17:38):
optimal balance.
Rachel (17:39):
So layering deeper insights onto the standard
monitoring.
Mark (17:42):
Exactly For a truly holistic view.
Rachel (17:44):
Okay, so let's try and pull all of this together as we
wrap up this deep dive.
What's the main takeaway?
Clearly, the ketogenic dietisn't some kind of magic bullet
for cancer right?
Mark (17:55):
Absolutely not, and, critically, it's not a
replacement for standard,evidence-based cancer treatments
like surgery, chemotherapy,radiation or immunotherapy.
That needs to be crystal clear.
Rachel (18:04):
The evidence we discussed does suggest it could
be something else.
Mark (18:07):
It suggests it could be a really powerful metabolic ally,
a complementary tool, especiallywhen used carefully under
qualified supervision.
Rachel (18:15):
Particularly for those glucose-hungry tumors we talked
about, or maybe for patients whoalso have things like insulin
resistance.
Mark (18:22):
Exactly.
Its potential value seems tocome from multiple angles
lowering that insulin andglucose, possibly supporting
healthy mitochondria, reducinginflammation and maybe even
starving those inflexible cancercells of their preferred fuel.
Rachel (18:37):
So I guess the key takeaway is it's not for
everyone, but for the rightpatient in the right situation,
used in the right way.
Mark (18:45):
It could significantly support their metabolic health,
maybe improve how well theytolerate their main treatments
and ultimately contribute to abetter quality of life during a
really challenging time.
Rachel (18:55):
Yeah, you know this whole deep dive.
It really highlights how fastour understanding of metabolism
is changing, how interconnectedit all is.
Mark (19:03):
It's an incredibly dynamic field.
Rachel (19:05):
It makes you wonder what else are we going to discover?
How much more couldpersonalized nutrition tailored
to our unique biochemistryreally revolutionize how we
approach complex diseases likecancer, as we keep sort of
unlocking these intricatepathways in the body?
Mark (19:19):
It's a very exciting and hopeful area of research.
There's still so much to learn.
Rachel (19:25):
So final thought for our listeners, if this conversation
has sparked interest, if you'reconsidering exploring a
ketogenic approach as part of acancer care plan, the crucial
step is to work with ahealthcare provider or a team
that really understands bothoncology and metabolic nutrition
.
Mark (19:40):
It's a specialized area.
Rachel (19:42):
And monitor those labs right.
Track the data along the way.
Mark (19:45):
Essential, absolutely essential for doing it safely
and effectively.
Nicolette (19:52):
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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