April 22, 2025 • 23 mins
In this episode of The Health Pulse Podcast, we take a closer look at seed oils—highly refined oils like soybean, corn, canola, and sunflower—that have become staples in the modern diet. While often marketed as “heart-healthy,” these oils may actually be fueling chronic inflammation and metabolic dysfunction.
We explore how the dramatic rise in omega-6 linoleic acid intake has shifted our omega balance from an ancestral 1:1 ratio to modern levels as high as 20:1—creating a perfect storm for oxidative stress, inflammation, and disease. You'll also learn about oxidized linoleic acid metabolites (OxLAMs) and how they damage tissues at the cellular level.
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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 (00:20):
You know, when people think about eating healthier,
the focus is often on sugarright or maybe cutting carbs,
avoiding saturated fat.
Rachel (00:31):
Yeah, those are the usual suspects.
Mark (00:32):
But there's this other kind of fat, these
polyunsaturated fats,specifically from seed oils like
soybean, corn, sunflower oil,that have just well exploded in
our diets over the last centuryor so.
Rachel (00:44):
Exactly, and often without much fanfare or
discussion.
Really.
Mark (00:49):
So for this deep dive, we really want to unpack that for
you Understand this big shift.
Rachel (00:53):
We're going to look into these seed oils the common ones
you see in those big plasticbottles in the supermarket you
know and explore what thescience is suggesting about
their links to potential healthissues.
Mark (01:03):
Things like soybean corn canola Right.
They're very high in a type ofomega-6 fat, specifically
something called linoleic acid,and our mission here really is
to help you understand thescience.
Is there a connection betweenthese oils and things like
obesity, diabetes, fatty liver,maybe even heart problems?
Rachel (01:21):
And why might that be happening?
We'll get into the biology abit.
Mark (01:24):
Yeah, and, importantly, offer some practical ways you
can think about reducing anypotential risks without
suggesting anything too extreme.
Rachel (01:31):
It's worth asking why they became so common in the
first place.
A big part of it is cost.
They are really cheap toproduce.
Plus, they have a long shelflife and a pretty neutral taste,
which makes them very usefulfor food manufacturers.
Mark (01:45):
So they end up in tons of processed foods.
Rachel (01:48):
Tons and restaurant cooking too.
They're kind of everywhere.
Mark (01:50):
And get this statistic.
I saw in the American Journalof Clinical Nutrition that our
intake of this linoleic acid hasapparently jumped by over 200
percent since the early 1900s.
Rachel (02:01):
Wow, that's a staggering increase Really highlights how
much our food environment haschanged.
It really does, and you know,for a long time these oils were
actually promoted as hearthealthy because they can lower
LDL cholesterol, the so-calledbad cholesterol.
Mark (02:16):
Right, I remember hearing that.
Rachel (02:18):
But that might not be the full story.
We need to consider otherfactors like oxidation, damage
to the fats themselves andinflammation, and how they
affect our overall metabolichealth, especially when we're
consuming them in such hugequantities and potentially out
of balance with other fats.
Mark (02:35):
It's almost shocking when you start reading labels.
These oils pop up in places youwouldn't expect.
Rachel (02:39):
Oh, absolutely Packaged snacks, cookies, crackers.
Mark (02:43):
Salad dressings, mayonnaise, pretty much anything
fried.
Rachel (02:46):
Even things that sound healthy, like some granola bars
or breakfast cereals and a lotof those processed foods
marketed as healthy alternatives.
Mark (02:55):
They can be really hidden, can't they?
Rachel (02:56):
Very much, so you really have to look for them.
Mark (02:58):
OK, so let's define them clearly.
What exactly are we talkingabout when we say seed oils?
Rachel (03:04):
Basically, these are vegetable oils that have been
extracted from seeds.
I think soybeans, corn,cottonseed, sunflower, safflower
, grapeseed, canola or rapeseed.
Mark (03:15):
And the key is, they're refined using industrial methods
.
Rachel (03:18):
Yes, typically involving heat chemicals, bleaching,
deodorizing.
It's quite a process and, as wesaid, they're relatively new in
the human diet on this scale.
A century ago they just weren'ta major factor.
Mark (03:32):
People used more traditional fats.
Rachel (03:33):
Things like butter, lard , tallow, olive oil, fats that
have been around for much, muchlonger.
Mark (03:40):
Got it Now.
You mentioned omega-6 fats andlinoleic acid.
Let's break that down.
Are omega-6 fats bad?
Rachel (03:47):
Not inherently.
No.
Linoleic acid, the main omega-6in these oils, is actually an
essential fatty acid.
Mark (03:52):
Meaning our bodies can't make it.
Rachel (03:54):
Correct.
We need to get some from ourdiet.
It's important for things likecell membranes, skin health,
producing certain hormone-likesubstances.
We need some.
Mark (04:01):
Okay, so the problem isn't the omega-6 itself.
Rachel (04:05):
It substances.
We need some, okay.
So the problem isn't theomega-6 itself.
It's the excess, the sheerquantity we're getting now and,
crucially, the imbalance itcreates with another type of
essential fat, the omega-3s.
Mark (04:11):
Ah, the omega-3s, like from fish oil.
Rachel (04:13):
Exactly.
The problem is too much omega-6, especially linoleic acid, and
often not enough omega-3 tocounterbalance it.
Mark (04:20):
Okay, let's dive into that mechanism.
You eat linoleic acid.
What happens next?
Rachel (04:24):
Your body can convert some of that linoleic acid into
another fatty acid calledarachidonic acid, and
arachidonic acid is then used tocreate compounds called
eicosanoids.
Now, some of these eicosanoidsare pro-inflammatory.
Mark (04:38):
Pro-inflammatory, so they promote inflammation.
Rachel (04:40):
Yes, think of inflammation.
Like your body's first responseteam, it rushes to the site of
an injury or infection.
That's acute inflammation andit's good.
It's necessary for healing.
Mark (04:51):
Like when you get a cut and it gets red and swollen for
a bit.
Rachel (04:53):
Precisely, that's your immune system doing its job, but
the issue is when thatinflammatory response doesn't
switch off properly, when itbecomes chronic, simmering away
at a low level all the time.
Mark (05:06):
And that's linked to health problems.
Rachel (05:08):
That chronic low-grade inflammation is implicated in a
whole host of modern diseasesHeart disease, metabolic
syndrome, obesity, type 2diabetes, various autoimmune
conditions, even non-alcoholicfatty liver disease or NAFLD.
Mark (05:25):
And research suggests that getting too much linoleic acid
might fuel this chronicinflammation.
Rachel (05:29):
Yes, studies like those published in journals such as
Prostaglandins, leukotrinis andEssential Fatty Acids suggest
that excessive linoleic acid canincrease markers of oxidative
stress.
Mark (05:41):
Oxidative stress like internal resting.
Rachel (05:44):
That's a decent analogy.
Yeah, cellular damage it canalso disrupt signaling within
our cells and promoteinflammation, specifically
within our fat tissue, and thisseems to be particularly
problematic if omega-3 intake islow.
Mark (05:57):
Okay, that makes sense.
You also mentioned oxidation ofthe fats themselves.
Rachel (06:01):
Right, this is another key point that makes sense.
You also mentioned oxidation ofthe fats themselves, right,
this is another key point.
Polyunsaturated fats, by theirchemical nature, are less stable
than saturated ormonounsaturated fats.
They're more prone to reactingwith oxygen.
Mark (06:11):
Especially with heat, light or air.
Rachel (06:13):
Exactly During industrial processing, storage,
and particularly duringhigh-heat cooking like frying,
these oils can oxidize.
Mark (06:20):
And when they oxidize, they form.
What was it?
Ox-lams.
Rachel (06:23):
Oxidized linoleic acid metabolites yes, ox-lams for
short.
Think of things like 4-HNE or9-Hanitin.
These are specific examples.
Mark (06:30):
And these OX-LAMs?
They're not good.
Rachel (06:33):
No, they're considered quite problematic.
They can damage the lining ofour blood vessels, the
endothelium.
They're implicated in thedevelopment of atherosclerosis,
which is hardening of thearteries, and they generally
ramp up inflammation.
Mark (06:46):
Wow.
So it's not just the amount,but also the quality and
stability of these fats.
Rachel (06:51):
That's a huge part of the concern.
Yes, especially with processedoils and fried foods.
Mark (06:56):
Okay, let's circle back to that omega-6 to omega-3 ratio
you mentioned.
Rachel (07:03):
Why is that balance so important?
Because both omega and omegathree fatty acids compete for
the same enzymes and pathways inour body, particularly those
involved in managinginflammation.
Mark (07:11):
They use the same machinery.
Rachel (07:12):
Essentially yes.
When they're in a healthybalance, they work together.
Omega six derived signals canturn inflammation on when needed
, and omega three derivedsignals tend to help resolve it,
turn it off.
It's a regulated system.
Mark (07:24):
Like a thermostat for inflammation.
Rachel (07:25):
Kind of yeah, but what's happened in our modern diets?
Ancestral diets, or dietsbefore the industrial food
revolution, are estimated tohave had an omega-6 to omega-3
ratio somewhere between, say, 1to 1 and maybe 4 to 1.
Mark (07:40):
Much more balanced.
Rachel (07:41):
Absolutely Now.
The typical Western diet loadedwith seed oils often has a
ratio estimated at 15 to one, 20to one, sometimes even higher.
Mark (07:48):
That's dramatic shift.
Rachel (07:50):
It's huge, and the concern is that this massive
imbalance skews the systemheavily towards producing more
pro-inflammatory signals.
Mark (07:59):
So the on switch is jammed .
Rachel (08:01):
That's one way to think about it.
This imbalance is linked tothat increased risk of metabolic
issues.
We talked about problems withinsulin sensitivity, heart
disease and potentially makingconditions like autoimmune
diseases or even braininflammation worse.
Mark (08:14):
I remember reading a review I think it was his
biomedicine and pharmacotherapysuggesting that simply improving
this ratio, primarily bylowering omega-6 intake, could
be a key strategy for reducingchronic disease risk.
Rachel (08:27):
That's the idea by reducing the overall
inflammatory burden and allowingcells to function more
optimally.
It's a powerful concept forpeople to consider.
Mark (08:35):
And you mentioned just adding more omega-3s might not
be enough.
Rachel (08:38):
It might not be the whole solution if the omega-6
intake remains extremely high.
It might not be the wholesolution if the omega-6 intake
remains extremely high, thatlinoleic acid can accumulate in
our cell membranes and body fatover time.
Mark (08:48):
So it sticks around.
Rachel (08:49):
It can for months or even years.
So even if you add omega-3s, ifyou're constantly flooding the
system with linoleic acid,especially the oxidized forms,
you might still have issues.
It's like trying to clean up aspill while the tap is still
running full blast.
Mark (09:05):
So maybe focusing on reducing the source of the
excess omega-6, the seed oils,is a more effective starting
point for many people.
Rachel (09:13):
That seems to be a growing perspective.
Yes, address the overload first.
Mark (09:16):
This could be relevant for people whose standard blood
tests look okay.
Maybe cholesterol is fine, butthey're still struggling with,
say, visceral belly fat or haveinflammatory conditions popping
up.
Rachel (09:26):
Exactly Things like certain thyroid conditions,
lupus, sarcoidosis.
These conditions often have aninflammatory component.
Mark (09:33):
And the idea is that these dietary fats, maybe the seed
oils, could act as a trigger.
Rachel (09:38):
They could be an environmental factor.
Yes, especially in individualswho might already have a genetic
predisposition, Diet seems toplay a significant role in
modulating that underlyingsusceptibility through
inflammation.
Mark (09:50):
OK, let's talk more directly about the links to
specific chronic diseases.
You mentioned the parallel riseof seed oil consumption and
chronic illness over the lastcentury illness over the last
century?
Rachel (10:04):
Yes, specifically oils like soybean, corn, cotton seeds
, sunflower have seen massiveincreases in consumption,
coinciding with rises in obesity, diabetes, heart disease, etc.
Mark (10:11):
But correlation isn't causation right.
Rachel (10:13):
Absolutely Crucial point .
Yeah, just because two trendshappen together doesn't prove
one caused the other.
However, there is a growingamount of mechanistic research
suggesting plausible biologicallinks.
Mark (10:24):
Okay, let's start with metabolic dysfunction, things
like insulin resistance, type 2diabetes, NEFLD.
What's the proposed connection?
Rachel (10:30):
As we've touched on, excess linoleic acid is a link
to inflammation in the fattissue itself.
This can interfere with insulinsignaling, making cells less
responsive to insulin.
Mark (10:40):
Leading towards insulin resistance.
Rachel (10:42):
Potentially, yes, less responsive to insulin, leading
towards insulin resistance.
Potentially, yes, there's alsothe buildup of those OX lambs,
those oxidized byproducts.
They've been directlyimplicated in the progression of
non-alcoholic fatty liverdisease and type 2 diabetes.
They seem to be quite toxic toliver and pancreatic cells.
Mark (10:56):
And this isn't just theoretical.
Rachel (10:58):
No Animal studies have shown high linoleic acid diets
can promote adiposity fat gain,especially around the organs,
and metabolic inflexibility,meaning the body struggles to
switch between burning carbs andfats efficiently, even if the
animals aren't overeatingcalories.
Mark (11:13):
What about human studies?
Rachel (11:14):
Human observational studies have linked higher
linoleic acid intake, or higherlevels in tissues, with markers
like higher fasting insulin,higher triglycerides in the
blood and increased fataccumulation in the liver.
Mark (11:27):
Okay, what about cardiovascular disease, Heart
health you mentioned?
This story is more complex thanjust lowering LDL.
Rachel (11:34):
Right.
While replacing saturated fatswith PUFAs often lowers LDL
cholesterol, the focus isshifting.
Newer research looks at LDLoxidation.
Is that LDL becoming damaged?
And also endothelial function?
How healthy is the lining ofour blood vessels and overall
inflammation?
High omega-6 intake mightnegatively affect these aspects.
Mark (11:55):
So lower LDL might not matter if it's damaged LDL or if
your arteries aren't workingwell.
Rachel (11:59):
That's the concern.
Some studies find higher levelsof oxidized LDL and impaired
artery function in people withhigh linoleic acid consumption,
especially if their omega-3levels are low.
Mark (12:10):
And you mentioned that Minnesota Coronary Experiment
reanalysis.
Rachel (12:13):
Yes, that was quite striking.
It was a randomized controlledtrial from the late 60s and
early 70s.
They replaced saturated fatwith corn oil high in linoleic
acid and cholesterol.
They replaced saturated fatwith corn oil high in linoleic
acid.
Lean cholesterol went down.
It did LDL cholesterol levelsdecreased in the corn oil group.
But when researchers reanalyzedthe data years later, including
unpublished data, they foundthat despite lower cholesterol,
(12:33):
the corn oil group actually hada higher risk of death overall,
and specifically from coronaryheart disease, compared to the
control group eating moresaturated fat.
Mark (12:42):
Wow, that definitely challenges the simple lower
cholesterol is always betteridea.
Rachel (12:46):
It certainly adds significant nuance and raises
questions about the potentialdownsides of very high linoleic
acid intake, even if it lowersLDL.
Mark (12:55):
Okay and quickly, on autoimmune and inflammatory
conditions.
Rachel (12:59):
The connection there is mainly through that chronic
inflammation pathway.
High omega-6 intake, especiallyfrom processed oils, is linked
to higher levels ofpro-inflammatory signaling
molecules in the body, thingslike IL-6, tnf-alpha and those
pro-inflammatory eicosanoids wediscussed.
Creating a more inflammatoryinternal environment and this
(13:19):
constantly heightenedinflammatory state is thought to
potentially contribute to theinitiation or worsening of
autoimmune diseases, where theimmune system mistakenly attacks
the body's own tissues.
Mark (13:34):
Think rheumatoid arthritis , lupus, ibd, thyroiditis, so
again, well, genetics areimportant.
Rachel (13:37):
Diet and environment, particularly factors that drive
systemic inflammation likepotentially excessive seed oil
intake, are likely keymodulators in determining who
develops these conditions andhow severe they become.
Mark (13:49):
So the overall picture, while needing more human trials,
points towards high intake ofomega-6 rich seed oils,
potentially contributing tochronic inflammation and
long-term disease risk.
Rachel (13:59):
Especially within the context of the modern, often
unbalanced diet that seems to bewhere the evidence is heading.
Mark (14:05):
Let's zoom in even closer on that inflammation pathway.
How does it work at the celllevel?
How do these fats interact withour immune system and maybe
even our genes?
Rachel (14:13):
Okay, so we start with linoleic acid from the diet.
Step one, as we said, isconversion to arachidonic acid.
Nicolette (14:19):
Right.
Rachel (14:19):
This AA gets incorporated into the membranes,
the outer layers of our cells.
It's stored there Just waitingPretty much.
Then, when there's a triggerstress, injury, infection the
immune system signals for thisAA to be released from the
membrane.
Mark (14:34):
Okay.
Rachel (14:35):
Once released, enzymes act on the AA to convert it into
those signaling molecules.
The eicosanoids Examplesinclude certain prostaglandins
like PGE2, leukotrienes andthromboxanes.
Mark (14:47):
And these are the molecules that drive the acute
inflammatory response.
Rachel (14:50):
Yes, they orchestrate things like blood vessel
dilation, pain signaling,clotting, attracting immune
cells to the area, all crucialfor short-term healing.
Mark (14:58):
But the problem is the chronic oversupply.
Rachel (15:00):
Precisely when you have chronically high levels of AA in
your cell membranes due toconstant high linoleic acid
intake, this whole pathway canbecome overactive.
It's like the system is alwaysprimed to react, leading to that
low-grade systemic inflammationwhich contributes to
endothelial dysfunction, alteredimmune responses, insulin
resistance and general metabolicstress.
Mark (15:20):
Okay, that pathway makes sense.
Now bring in those AUCXLAMsagain.
How do they contribute to theinflammation?
Rachel (15:27):
Remember, these OXXLAMs like 4-HNE-9-HO, are formed when
the seed oils themselvesoxidize, during processing,
storage or especially heating,like frying Got it.
These compounds are directlytoxic and pro-inflammatory.
They are known to damage cellmembranes, impair mitochondrial
function, the energy factoriesin our cells, and they actively
(15:47):
promote atherosclerosis andliver damage.
Mark (15:50):
So they add insult to injury, basically.
Rachel (15:52):
You could say that they also activate a key genetic
switch called NFKB.
Mark (15:57):
NFKB.
Rachel (15:58):
It's a transcription factor, essentially a master
controller that turns on a widerange of inflammatory genes.
So Auk-X-LAMs directly fuel thefire at a genetic level.
Mark (16:07):
And you mentioned, they've actually been found in disease
tissues.
Rachel (16:10):
Yes, Resurfers have detected Auk-X-LAMs within
atherosclerotic plaques inarteries, in fatty liver tissue
and in inflamed adipose fattissue.
This strongly supports theirrole in the disease process
itself.
Mark (16:21):
And lastly, this idea of epigenetic activation triggering
genes.
Rachel (16:25):
Yeah, this is another layer the overall cellular
stress caused by this chronicinflammation, the oxidative
stress, the presence of AugXlambs all of this can influence
epigenetics.
Mark (16:36):
Which isn't changing the genes themselves, but how
they're expressed.
Rachel (16:39):
Exactly.
It's about turning genes on oroff or dialing their activity up
or down, without altering theunderlying DNA sequence.
So, in individuals who might begenetically susceptible to
autoimmunity, certaininflammatory disorders or even
some cancers, this chronicinflammatory environment, driven
partly by excess linoleic acidand its byproducts, might act as
(17:00):
an environmental trigger.
Mark (17:02):
Pushing a predisposition over the edge, potentially.
Rachel (17:05):
That's the hypothesis.
It could initiate or acceleratedisease processes that might
have otherwise remained dormantor developed much later or less
severely.
Mark (17:13):
Okay, that paints a pretty detailed picture of the
potential mechanisms.
It's complex, but it seems tocenter around inflammation and
oxidation.
Rachel (17:20):
Largely yes.
Mark (17:21):
So, acknowledging all this , what do we do?
It sounds like avoiding theseoils completely is really hard.
Rachel (17:27):
It is.
They're incredibly pervasive inthe modern food supply, but the
goal doesn't have to becomplete avoidance for most
people.
Mark (17:34):
Just reducing exposure.
Rachel (17:35):
Exactly Minimizing exposure, especially from the
biggest sources like heavilyprocessed foods and restaurant
meals, can significantly loweryour overall omega-6 intake and
help nudge your body backtowards a better inflammatory
balance.
Mark (17:49):
Okay, practical step number one.
Rachel (17:51):
Cut back significantly on ultra-processed foods.
This is probably the singlebiggest impact move.
Mark (17:57):
Because that's where most of it is hiding.
Rachel (17:58):
Yes, far more comes from packaged snacks, frozen dinners
, commercial baked goods, fastfoods, sauces, dressings,
margarines, than from the oilyou constantly add in your own
kitchen.
Mark (18:10):
So rule one is read the ingredients.
Yeah, Look for soybean, canola,corn, sunflower, safflower,
cottonseed or just vegetable oil.
Rachel (18:17):
Absolutely Be a detective and try to shift
towards eating more whole singleingredient foods whenever
possible.
Cooking more at home gives youcontrol.
Mark (18:26):
Right.
So step two if we are cookingat home, what should we use?
Rachel (18:30):
Opt for more stable fats .
Extra virgin olive oil is greatfor lower heat cooking and
dressings For higher heat.
Things like cold pressedavocado oil, ghee, clarified
butter, Butter itself,especially from grass fed cows,
if possible, coconut oil, ghee,clarified butter, butter itself
especially from grass fed cows,if possible, coconut oil or even
traditional animal fats likebeef, tallow or duck fat are
good options.
Mark (18:50):
Why are those better?
Rachel (18:52):
They are generally richer in monounsaturated or
saturated fats, which are morechemically stable and less prone
to oxidizing when heated,compared to the polyunsaturated
fats dominant in seed oils.
Mark (19:03):
Plus, they might help with feeling full.
Rachel (19:05):
Yes, they can contribute to satiety and potentially
support metabolic flexibilitytoo.
Mark (19:10):
Okay, any other strategies to support our bodies in
handling these fats?
Rachel (19:14):
Ensuring adequate intake of certain nutrients can help.
Magnesium is important.
Vitamin E is a key antioxidantthat protects fats, and getting
plenty of polyphenols thosecolorful compounds in fruits,
vegetables, herbs, spices canalso support healthy
inflammatory responses.
Mark (19:28):
And omega three still matter Definitely.
Rachel (19:31):
A moderate intake of omega threes from fatty fish
like salmon or sardines, or fromchia seeds, flax seeds, walnuts
or an algae oil supplement isstill beneficial for balance and
the basics still apply rightSleep, movement Absolutely.
Don't forget the foundationsGood sleep, regular physical
activity, managing stress,supporting gut health.
(19:51):
These all profoundly influenceinflammation, independent of
your fat intake.
Mark (19:56):
And it's crucial not to swing to another extreme, isn't
it Not to start fearing all fat?
Rachel (20:00):
Precisely.
The goal isn't fat phobia oreliminating every last milligram
of omega-6.
Linoleic acid is essential insmall amounts.
The focus is on reducing thechronic overexposure from highly
processed sources.
Mark (20:13):
And recognizing nuances like maybe cold-pressed
unrefined oils are differentfrom reused deep fryer oil.
Rachel (20:19):
There are likely differences.
Yes, context matters Ultimately, use your own health markers
and how you feel as guides,rather than just following rigid
dogma.
Mark (20:26):
So it's about thoughtful swaps and awareness, not a total
diet revolution overnight.
Rachel (20:31):
Exactly Small, consistent changes.
Being more mindful of processedfood ingredients, choosing more
stable cooking fats can leadcumulatively to lower
inflammation, better metabolichealth and improve long-term
prospects inflammation, bettermetabolic health and improve
long-term prospects.
Mark (20:48):
Okay, so to wrap this up, for everyone listening, the big
takeaway seems to be that thesecommon seed oils have become a
huge source of omega-6 fats inour diets, way more than our
bodies likely evolved to handlecomfortably.
Rachel (20:56):
Right, and while some linoleic acid is necessary, this
constant flood, particularlyfrom processed and fried foods,
appears to be contributingsignificantly to a
pro-inflammatory state in thebody.
Mark (21:09):
And that underlying inflammation is linked to so
many chronic health issues.
Rachel (21:12):
Yes, the research is ongoing, of course, but the
current body of evidence pointstowards excess seed oil intake
contributing to oxidative stress, immune system dysregulation
and metabolic problems,especially when combined with
other lifestyle factors.
Mark (21:25):
And the message isn't fat is bad, but rather let's
understand how modern foodprocessing has changed the types
and amounts of fats we eat andhow they interact with our
biology.
Rachel (21:34):
Well put.
It's about finding a betterbalance that aligns more closely
with our physiological needs.
Mark (21:40):
If someone listening is curious about their own status,
are there ways to check?
Rachel (21:44):
You could potentially talk to your doctor about tests.
Markers like high-sensitivityC-reactive protein, hscrp, can
give an indication of generalinflammation.
Some labs can even measure thefatty acid profile in your blood
cells, looking directly at theomega-6 to omega-3 ratio or
levels of oxidized lipids,interesting, so there are ways
to get a3 ratio or levels ofoxidized lipids.
Mark (22:04):
Interesting, so there are ways to get a more personalized
picture.
Rachel (22:07):
There can be yes.
Mark (22:08):
So a final thought for you listening, small, consistent
changes really can make adifference.
Being more aware of thosehidden seed oils in processed
foods, choosing healthier fatswhen you cook at home,
prioritizing whole, unprocessedfoods these actions can
genuinely help lower your body'sinflammatory burden and support
better health from the insideout.
Rachel (22:29):
It really empowers you to take control.
Consider how this informationfits into your own life and
eating patterns.
Maybe start by just reading afew more labels this week.
Mark (22:37):
Great advice.
It's definitely food forthought.
Nicolette (22:44):
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 (00:20):
You know, when people think about eating healthier,
the focus is often on sugarright or maybe cutting carbs,
avoiding saturated fat.
Rachel (00:31):
Yeah, those are the usual suspects.
Mark (00:32):
But there's this other kind of fat, these
polyunsaturated fats,specifically from seed oils like
soybean, corn, sunflower oil,that have just well exploded in
our diets over the last centuryor so.
Rachel (00:44):
Exactly, and often without much fanfare or
discussion.
Really.
Mark (00:49):
So for this deep dive, we really want to unpack that for
you Understand this big shift.
Rachel (00:53):
We're going to look into these seed oils the common ones
you see in those big plasticbottles in the supermarket you
know and explore what thescience is suggesting about
their links to potential healthissues.
Mark (01:03):
Things like soybean corn canola Right.
They're very high in a type ofomega-6 fat, specifically
something called linoleic acid,and our mission here really is
to help you understand thescience.
Is there a connection betweenthese oils and things like
obesity, diabetes, fatty liver,maybe even heart problems?
Rachel (01:21):
And why might that be happening?
We'll get into the biology abit.
Mark (01:24):
Yeah, and, importantly, offer some practical ways you
can think about reducing anypotential risks without
suggesting anything too extreme.
Rachel (01:31):
It's worth asking why they became so common in the
first place.
A big part of it is cost.
They are really cheap toproduce.
Plus, they have a long shelflife and a pretty neutral taste,
which makes them very usefulfor food manufacturers.
Mark (01:45):
So they end up in tons of processed foods.
Rachel (01:48):
Tons and restaurant cooking too.
They're kind of everywhere.
Mark (01:50):
And get this statistic.
I saw in the American Journalof Clinical Nutrition that our
intake of this linoleic acid hasapparently jumped by over 200
percent since the early 1900s.
Rachel (02:01):
Wow, that's a staggering increase Really highlights how
much our food environment haschanged.
It really does, and you know,for a long time these oils were
actually promoted as hearthealthy because they can lower
LDL cholesterol, the so-calledbad cholesterol.
Mark (02:16):
Right, I remember hearing that.
Rachel (02:18):
But that might not be the full story.
We need to consider otherfactors like oxidation, damage
to the fats themselves andinflammation, and how they
affect our overall metabolichealth, especially when we're
consuming them in such hugequantities and potentially out
of balance with other fats.
Mark (02:35):
It's almost shocking when you start reading labels.
These oils pop up in places youwouldn't expect.
Rachel (02:39):
Oh, absolutely Packaged snacks, cookies, crackers.
Mark (02:43):
Salad dressings, mayonnaise, pretty much anything
fried.
Rachel (02:46):
Even things that sound healthy, like some granola bars
or breakfast cereals and a lotof those processed foods
marketed as healthy alternatives.
Mark (02:55):
They can be really hidden, can't they?
Rachel (02:56):
Very much, so you really have to look for them.
Mark (02:58):
OK, so let's define them clearly.
What exactly are we talkingabout when we say seed oils?
Rachel (03:04):
Basically, these are vegetable oils that have been
extracted from seeds.
I think soybeans, corn,cottonseed, sunflower, safflower
, grapeseed, canola or rapeseed.
Mark (03:15):
And the key is, they're refined using industrial methods
.
Rachel (03:18):
Yes, typically involving heat chemicals, bleaching,
deodorizing.
It's quite a process and, as wesaid, they're relatively new in
the human diet on this scale.
A century ago they just weren'ta major factor.
Mark (03:32):
People used more traditional fats.
Rachel (03:33):
Things like butter, lard , tallow, olive oil, fats that
have been around for much, muchlonger.
Mark (03:40):
Got it Now.
You mentioned omega-6 fats andlinoleic acid.
Let's break that down.
Are omega-6 fats bad?
Rachel (03:47):
Not inherently.
No.
Linoleic acid, the main omega-6in these oils, is actually an
essential fatty acid.
Mark (03:52):
Meaning our bodies can't make it.
Rachel (03:54):
Correct.
We need to get some from ourdiet.
It's important for things likecell membranes, skin health,
producing certain hormone-likesubstances.
We need some.
Mark (04:01):
Okay, so the problem isn't the omega-6 itself.
Rachel (04:05):
It substances.
We need some, okay.
So the problem isn't theomega-6 itself.
It's the excess, the sheerquantity we're getting now and,
crucially, the imbalance itcreates with another type of
essential fat, the omega-3s.
Mark (04:11):
Ah, the omega-3s, like from fish oil.
Rachel (04:13):
Exactly.
The problem is too much omega-6, especially linoleic acid, and
often not enough omega-3 tocounterbalance it.
Mark (04:20):
Okay, let's dive into that mechanism.
You eat linoleic acid.
What happens next?
Rachel (04:24):
Your body can convert some of that linoleic acid into
another fatty acid calledarachidonic acid, and
arachidonic acid is then used tocreate compounds called
eicosanoids.
Now, some of these eicosanoidsare pro-inflammatory.
Mark (04:38):
Pro-inflammatory, so they promote inflammation.
Rachel (04:40):
Yes, think of inflammation.
Like your body's first responseteam, it rushes to the site of
an injury or infection.
That's acute inflammation andit's good.
It's necessary for healing.
Mark (04:51):
Like when you get a cut and it gets red and swollen for
a bit.
Rachel (04:53):
Precisely, that's your immune system doing its job, but
the issue is when thatinflammatory response doesn't
switch off properly, when itbecomes chronic, simmering away
at a low level all the time.
Mark (05:06):
And that's linked to health problems.
Rachel (05:08):
That chronic low-grade inflammation is implicated in a
whole host of modern diseasesHeart disease, metabolic
syndrome, obesity, type 2diabetes, various autoimmune
conditions, even non-alcoholicfatty liver disease or NAFLD.
Mark (05:25):
And research suggests that getting too much linoleic acid
might fuel this chronicinflammation.
Rachel (05:29):
Yes, studies like those published in journals such as
Prostaglandins, leukotrinis andEssential Fatty Acids suggest
that excessive linoleic acid canincrease markers of oxidative
stress.
Mark (05:41):
Oxidative stress like internal resting.
Rachel (05:44):
That's a decent analogy.
Yeah, cellular damage it canalso disrupt signaling within
our cells and promoteinflammation, specifically
within our fat tissue, and thisseems to be particularly
problematic if omega-3 intake islow.
Mark (05:57):
Okay, that makes sense.
You also mentioned oxidation ofthe fats themselves.
Rachel (06:01):
Right, this is another key point that makes sense.
You also mentioned oxidation ofthe fats themselves, right,
this is another key point.
Polyunsaturated fats, by theirchemical nature, are less stable
than saturated ormonounsaturated fats.
They're more prone to reactingwith oxygen.
Mark (06:11):
Especially with heat, light or air.
Rachel (06:13):
Exactly During industrial processing, storage,
and particularly duringhigh-heat cooking like frying,
these oils can oxidize.
Mark (06:20):
And when they oxidize, they form.
What was it?
Ox-lams.
Rachel (06:23):
Oxidized linoleic acid metabolites yes, ox-lams for
short.
Think of things like 4-HNE or9-Hanitin.
These are specific examples.
Mark (06:30):
And these OX-LAMs?
They're not good.
Rachel (06:33):
No, they're considered quite problematic.
They can damage the lining ofour blood vessels, the
endothelium.
They're implicated in thedevelopment of atherosclerosis,
which is hardening of thearteries, and they generally
ramp up inflammation.
Mark (06:46):
Wow.
So it's not just the amount,but also the quality and
stability of these fats.
Rachel (06:51):
That's a huge part of the concern.
Yes, especially with processedoils and fried foods.
Mark (06:56):
Okay, let's circle back to that omega-6 to omega-3 ratio
you mentioned.
Rachel (07:03):
Why is that balance so important?
Because both omega and omegathree fatty acids compete for
the same enzymes and pathways inour body, particularly those
involved in managinginflammation.
Mark (07:11):
They use the same machinery.
Rachel (07:12):
Essentially yes.
When they're in a healthybalance, they work together.
Omega six derived signals canturn inflammation on when needed
, and omega three derivedsignals tend to help resolve it,
turn it off.
It's a regulated system.
Mark (07:24):
Like a thermostat for inflammation.
Rachel (07:25):
Kind of yeah, but what's happened in our modern diets?
Ancestral diets, or dietsbefore the industrial food
revolution, are estimated tohave had an omega-6 to omega-3
ratio somewhere between, say, 1to 1 and maybe 4 to 1.
Mark (07:40):
Much more balanced.
Rachel (07:41):
Absolutely Now.
The typical Western diet loadedwith seed oils often has a
ratio estimated at 15 to one, 20to one, sometimes even higher.
Mark (07:48):
That's dramatic shift.
Rachel (07:50):
It's huge, and the concern is that this massive
imbalance skews the systemheavily towards producing more
pro-inflammatory signals.
Mark (07:59):
So the on switch is jammed .
Rachel (08:01):
That's one way to think about it.
This imbalance is linked tothat increased risk of metabolic
issues.
We talked about problems withinsulin sensitivity, heart
disease and potentially makingconditions like autoimmune
diseases or even braininflammation worse.
Mark (08:14):
I remember reading a review I think it was his
biomedicine and pharmacotherapysuggesting that simply improving
this ratio, primarily bylowering omega-6 intake, could
be a key strategy for reducingchronic disease risk.
Rachel (08:27):
That's the idea by reducing the overall
inflammatory burden and allowingcells to function more
optimally.
It's a powerful concept forpeople to consider.
Mark (08:35):
And you mentioned just adding more omega-3s might not
be enough.
Rachel (08:38):
It might not be the whole solution if the omega-6
intake remains extremely high.
It might not be the wholesolution if the omega-6 intake
remains extremely high, thatlinoleic acid can accumulate in
our cell membranes and body fatover time.
Mark (08:48):
So it sticks around.
Rachel (08:49):
It can for months or even years.
So even if you add omega-3s, ifyou're constantly flooding the
system with linoleic acid,especially the oxidized forms,
you might still have issues.
It's like trying to clean up aspill while the tap is still
running full blast.
Mark (09:05):
So maybe focusing on reducing the source of the
excess omega-6, the seed oils,is a more effective starting
point for many people.
Rachel (09:13):
That seems to be a growing perspective.
Yes, address the overload first.
Mark (09:16):
This could be relevant for people whose standard blood
tests look okay.
Maybe cholesterol is fine, butthey're still struggling with,
say, visceral belly fat or haveinflammatory conditions popping
up.
Rachel (09:26):
Exactly Things like certain thyroid conditions,
lupus, sarcoidosis.
These conditions often have aninflammatory component.
Mark (09:33):
And the idea is that these dietary fats, maybe the seed
oils, could act as a trigger.
Rachel (09:38):
They could be an environmental factor.
Yes, especially in individualswho might already have a genetic
predisposition, Diet seems toplay a significant role in
modulating that underlyingsusceptibility through
inflammation.
Mark (09:50):
OK, let's talk more directly about the links to
specific chronic diseases.
You mentioned the parallel riseof seed oil consumption and
chronic illness over the lastcentury illness over the last
century?
Rachel (10:04):
Yes, specifically oils like soybean, corn, cotton seeds
, sunflower have seen massiveincreases in consumption,
coinciding with rises in obesity, diabetes, heart disease, etc.
Mark (10:11):
But correlation isn't causation right.
Rachel (10:13):
Absolutely Crucial point .
Yeah, just because two trendshappen together doesn't prove
one caused the other.
However, there is a growingamount of mechanistic research
suggesting plausible biologicallinks.
Mark (10:24):
Okay, let's start with metabolic dysfunction, things
like insulin resistance, type 2diabetes, NEFLD.
What's the proposed connection?
Rachel (10:30):
As we've touched on, excess linoleic acid is a link
to inflammation in the fattissue itself.
This can interfere with insulinsignaling, making cells less
responsive to insulin.
Mark (10:40):
Leading towards insulin resistance.
Rachel (10:42):
Potentially, yes, less responsive to insulin, leading
towards insulin resistance.
Potentially, yes, there's alsothe buildup of those OX lambs,
those oxidized byproducts.
They've been directlyimplicated in the progression of
non-alcoholic fatty liverdisease and type 2 diabetes.
They seem to be quite toxic toliver and pancreatic cells.
Mark (10:56):
And this isn't just theoretical.
Rachel (10:58):
No Animal studies have shown high linoleic acid diets
can promote adiposity fat gain,especially around the organs,
and metabolic inflexibility,meaning the body struggles to
switch between burning carbs andfats efficiently, even if the
animals aren't overeatingcalories.
Mark (11:13):
What about human studies?
Rachel (11:14):
Human observational studies have linked higher
linoleic acid intake, or higherlevels in tissues, with markers
like higher fasting insulin,higher triglycerides in the
blood and increased fataccumulation in the liver.
Mark (11:27):
Okay, what about cardiovascular disease, Heart
health you mentioned?
This story is more complex thanjust lowering LDL.
Rachel (11:34):
Right.
While replacing saturated fatswith PUFAs often lowers LDL
cholesterol, the focus isshifting.
Newer research looks at LDLoxidation.
Is that LDL becoming damaged?
And also endothelial function?
How healthy is the lining ofour blood vessels and overall
inflammation?
High omega-6 intake mightnegatively affect these aspects.
Mark (11:55):
So lower LDL might not matter if it's damaged LDL or if
your arteries aren't workingwell.
Rachel (11:59):
That's the concern.
Some studies find higher levelsof oxidized LDL and impaired
artery function in people withhigh linoleic acid consumption,
especially if their omega-3levels are low.
Mark (12:10):
And you mentioned that Minnesota Coronary Experiment
reanalysis.
Rachel (12:13):
Yes, that was quite striking.
It was a randomized controlledtrial from the late 60s and
early 70s.
They replaced saturated fatwith corn oil high in linoleic
acid and cholesterol.
They replaced saturated fatwith corn oil high in linoleic
acid.
Lean cholesterol went down.
It did LDL cholesterol levelsdecreased in the corn oil group.
But when researchers reanalyzedthe data years later, including
unpublished data, they foundthat despite lower cholesterol,
(12:33):
the corn oil group actually hada higher risk of death overall,
and specifically from coronaryheart disease, compared to the
control group eating moresaturated fat.
Mark (12:42):
Wow, that definitely challenges the simple lower
cholesterol is always betteridea.
Rachel (12:46):
It certainly adds significant nuance and raises
questions about the potentialdownsides of very high linoleic
acid intake, even if it lowersLDL.
Mark (12:55):
Okay and quickly, on autoimmune and inflammatory
conditions.
Rachel (12:59):
The connection there is mainly through that chronic
inflammation pathway.
High omega-6 intake, especiallyfrom processed oils, is linked
to higher levels ofpro-inflammatory signaling
molecules in the body, thingslike IL-6, tnf-alpha and those
pro-inflammatory eicosanoids wediscussed.
Creating a more inflammatoryinternal environment and this
(13:19):
constantly heightenedinflammatory state is thought to
potentially contribute to theinitiation or worsening of
autoimmune diseases, where theimmune system mistakenly attacks
the body's own tissues.
Mark (13:34):
Think rheumatoid arthritis , lupus, ibd, thyroiditis, so
again, well, genetics areimportant.
Rachel (13:37):
Diet and environment, particularly factors that drive
systemic inflammation likepotentially excessive seed oil
intake, are likely keymodulators in determining who
develops these conditions andhow severe they become.
Mark (13:49):
So the overall picture, while needing more human trials,
points towards high intake ofomega-6 rich seed oils,
potentially contributing tochronic inflammation and
long-term disease risk.
Rachel (13:59):
Especially within the context of the modern, often
unbalanced diet that seems to bewhere the evidence is heading.
Mark (14:05):
Let's zoom in even closer on that inflammation pathway.
How does it work at the celllevel?
How do these fats interact withour immune system and maybe
even our genes?
Rachel (14:13):
Okay, so we start with linoleic acid from the diet.
Step one, as we said, isconversion to arachidonic acid.
Nicolette (14:19):
Right.
Rachel (14:19):
This AA gets incorporated into the membranes,
the outer layers of our cells.
It's stored there Just waitingPretty much.
Then, when there's a triggerstress, injury, infection the
immune system signals for thisAA to be released from the
membrane.
Mark (14:34):
Okay.
Rachel (14:35):
Once released, enzymes act on the AA to convert it into
those signaling molecules.
The eicosanoids Examplesinclude certain prostaglandins
like PGE2, leukotrienes andthromboxanes.
Mark (14:47):
And these are the molecules that drive the acute
inflammatory response.
Rachel (14:50):
Yes, they orchestrate things like blood vessel
dilation, pain signaling,clotting, attracting immune
cells to the area, all crucialfor short-term healing.
Mark (14:58):
But the problem is the chronic oversupply.
Rachel (15:00):
Precisely when you have chronically high levels of AA in
your cell membranes due toconstant high linoleic acid
intake, this whole pathway canbecome overactive.
It's like the system is alwaysprimed to react, leading to that
low-grade systemic inflammationwhich contributes to
endothelial dysfunction, alteredimmune responses, insulin
resistance and general metabolicstress.
Mark (15:20):
Okay, that pathway makes sense.
Now bring in those AUCXLAMsagain.
How do they contribute to theinflammation?
Rachel (15:27):
Remember, these OXXLAMs like 4-HNE-9-HO, are formed when
the seed oils themselvesoxidize, during processing,
storage or especially heating,like frying Got it.
These compounds are directlytoxic and pro-inflammatory.
They are known to damage cellmembranes, impair mitochondrial
function, the energy factoriesin our cells, and they actively
(15:47):
promote atherosclerosis andliver damage.
Mark (15:50):
So they add insult to injury, basically.
Rachel (15:52):
You could say that they also activate a key genetic
switch called NFKB.
Mark (15:57):
NFKB.
Rachel (15:58):
It's a transcription factor, essentially a master
controller that turns on a widerange of inflammatory genes.
So Auk-X-LAMs directly fuel thefire at a genetic level.
Mark (16:07):
And you mentioned, they've actually been found in disease
tissues.
Rachel (16:10):
Yes, Resurfers have detected Auk-X-LAMs within
atherosclerotic plaques inarteries, in fatty liver tissue
and in inflamed adipose fattissue.
This strongly supports theirrole in the disease process
itself.
Mark (16:21):
And lastly, this idea of epigenetic activation triggering
genes.
Rachel (16:25):
Yeah, this is another layer the overall cellular
stress caused by this chronicinflammation, the oxidative
stress, the presence of AugXlambs all of this can influence
epigenetics.
Mark (16:36):
Which isn't changing the genes themselves, but how
they're expressed.
Rachel (16:39):
Exactly.
It's about turning genes on oroff or dialing their activity up
or down, without altering theunderlying DNA sequence.
So, in individuals who might begenetically susceptible to
autoimmunity, certaininflammatory disorders or even
some cancers, this chronicinflammatory environment, driven
partly by excess linoleic acidand its byproducts, might act as
(17:00):
an environmental trigger.
Mark (17:02):
Pushing a predisposition over the edge, potentially.
Rachel (17:05):
That's the hypothesis.
It could initiate or acceleratedisease processes that might
have otherwise remained dormantor developed much later or less
severely.
Mark (17:13):
Okay, that paints a pretty detailed picture of the
potential mechanisms.
It's complex, but it seems tocenter around inflammation and
oxidation.
Rachel (17:20):
Largely yes.
Mark (17:21):
So, acknowledging all this , what do we do?
It sounds like avoiding theseoils completely is really hard.
Rachel (17:27):
It is.
They're incredibly pervasive inthe modern food supply, but the
goal doesn't have to becomplete avoidance for most
people.
Mark (17:34):
Just reducing exposure.
Rachel (17:35):
Exactly Minimizing exposure, especially from the
biggest sources like heavilyprocessed foods and restaurant
meals, can significantly loweryour overall omega-6 intake and
help nudge your body backtowards a better inflammatory
balance.
Mark (17:49):
Okay, practical step number one.
Rachel (17:51):
Cut back significantly on ultra-processed foods.
This is probably the singlebiggest impact move.
Mark (17:57):
Because that's where most of it is hiding.
Rachel (17:58):
Yes, far more comes from packaged snacks, frozen dinners
, commercial baked goods, fastfoods, sauces, dressings,
margarines, than from the oilyou constantly add in your own
kitchen.
Mark (18:10):
So rule one is read the ingredients.
Yeah, Look for soybean, canola,corn, sunflower, safflower,
cottonseed or just vegetable oil.
Rachel (18:17):
Absolutely Be a detective and try to shift
towards eating more whole singleingredient foods whenever
possible.
Cooking more at home gives youcontrol.
Mark (18:26):
Right.
So step two if we are cookingat home, what should we use?
Rachel (18:30):
Opt for more stable fats .
Extra virgin olive oil is greatfor lower heat cooking and
dressings For higher heat.
Things like cold pressedavocado oil, ghee, clarified
butter, Butter itself,especially from grass fed cows,
if possible, coconut oil, ghee,clarified butter, butter itself
especially from grass fed cows,if possible, coconut oil or even
traditional animal fats likebeef, tallow or duck fat are
good options.
Mark (18:50):
Why are those better?
Rachel (18:52):
They are generally richer in monounsaturated or
saturated fats, which are morechemically stable and less prone
to oxidizing when heated,compared to the polyunsaturated
fats dominant in seed oils.
Mark (19:03):
Plus, they might help with feeling full.
Rachel (19:05):
Yes, they can contribute to satiety and potentially
support metabolic flexibilitytoo.
Mark (19:10):
Okay, any other strategies to support our bodies in
handling these fats?
Rachel (19:14):
Ensuring adequate intake of certain nutrients can help.
Magnesium is important.
Vitamin E is a key antioxidantthat protects fats, and getting
plenty of polyphenols thosecolorful compounds in fruits,
vegetables, herbs, spices canalso support healthy
inflammatory responses.
Mark (19:28):
And omega three still matter Definitely.
Rachel (19:31):
A moderate intake of omega threes from fatty fish
like salmon or sardines, or fromchia seeds, flax seeds, walnuts
or an algae oil supplement isstill beneficial for balance and
the basics still apply rightSleep, movement Absolutely.
Don't forget the foundationsGood sleep, regular physical
activity, managing stress,supporting gut health.
(19:51):
These all profoundly influenceinflammation, independent of
your fat intake.
Mark (19:56):
And it's crucial not to swing to another extreme, isn't
it Not to start fearing all fat?
Rachel (20:00):
Precisely.
The goal isn't fat phobia oreliminating every last milligram
of omega-6.
Linoleic acid is essential insmall amounts.
The focus is on reducing thechronic overexposure from highly
processed sources.
Mark (20:13):
And recognizing nuances like maybe cold-pressed
unrefined oils are differentfrom reused deep fryer oil.
Rachel (20:19):
There are likely differences.
Yes, context matters Ultimately, use your own health markers
and how you feel as guides,rather than just following rigid
dogma.
Mark (20:26):
So it's about thoughtful swaps and awareness, not a total
diet revolution overnight.
Rachel (20:31):
Exactly Small, consistent changes.
Being more mindful of processedfood ingredients, choosing more
stable cooking fats can leadcumulatively to lower
inflammation, better metabolichealth and improve long-term
prospects inflammation, bettermetabolic health and improve
long-term prospects.
Mark (20:48):
Okay, so to wrap this up, for everyone listening, the big
takeaway seems to be that thesecommon seed oils have become a
huge source of omega-6 fats inour diets, way more than our
bodies likely evolved to handlecomfortably.
Rachel (20:56):
Right, and while some linoleic acid is necessary, this
constant flood, particularlyfrom processed and fried foods,
appears to be contributingsignificantly to a
pro-inflammatory state in thebody.
Mark (21:09):
And that underlying inflammation is linked to so
many chronic health issues.
Rachel (21:12):
Yes, the research is ongoing, of course, but the
current body of evidence pointstowards excess seed oil intake
contributing to oxidative stress, immune system dysregulation
and metabolic problems,especially when combined with
other lifestyle factors.
Mark (21:25):
And the message isn't fat is bad, but rather let's
understand how modern foodprocessing has changed the types
and amounts of fats we eat andhow they interact with our
biology.
Rachel (21:34):
Well put.
It's about finding a betterbalance that aligns more closely
with our physiological needs.
Mark (21:40):
If someone listening is curious about their own status,
are there ways to check?
Rachel (21:44):
You could potentially talk to your doctor about tests.
Markers like high-sensitivityC-reactive protein, hscrp, can
give an indication of generalinflammation.
Some labs can even measure thefatty acid profile in your blood
cells, looking directly at theomega-6 to omega-3 ratio or
levels of oxidized lipids,interesting, so there are ways
to get a3 ratio or levels ofoxidized lipids.
Mark (22:04):
Interesting, so there are ways to get a more personalized
picture.
Rachel (22:07):
There can be yes.
Mark (22:08):
So a final thought for you listening, small, consistent
changes really can make adifference.
Being more aware of thosehidden seed oils in processed
foods, choosing healthier fatswhen you cook at home,
prioritizing whole, unprocessedfoods these actions can
genuinely help lower your body'sinflammatory burden and support
better health from the insideout.
Rachel (22:29):
It really empowers you to take control.
Consider how this informationfits into your own life and
eating patterns.
Maybe start by just reading afew more labels this week.
Mark (22:37):
Great advice.
It's definitely food forthought.
Nicolette (22:44):
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