November 20, 2025 • 18 mins
Send us a text with a question or thought on this episode ( We cannot replay from this link)
We trace how endometriosis interacts with mast cells, connective tissue, and hormones, explaining why symptoms feel systemic and why overlap with HEDS and MCAS appears so often. We also review new data on tirzepatide and inflammation, separating promise from hype while keeping care practical and multidisciplinary.
• Mast cell activation as a shared pathway across HEDS and endometriosis
• EMT signaling via CCL2 and CCR4 and its role in lesion persistence
• Estrogen’s influence on immune activity and symptom flares
• Systemic symptom map spanning gut, bladder, fatigue and brain fog
• Antihistamines and stabilizers as volume-down tools, not cures
• Evidence on tirzepatide lowering CRP and IL‑6 with caveats
• Why correlation is not causation and why it still matters
• Multidisciplinary care to align gynecology, immunology and rheumatology
Share this episode with someone who needs validation, comment your experience so others feel less alone, and keep advocating for yourself
Mast Cell–Mediated Epithelial–Mesenchymal Transition in Endometriosis
hypermobile Ehlers-Danlos Syndrome (hEDS) and mast cells
The Role of Mast Cells in Endometriosis
Anti-inflammatory effects of tirzepatide: a systematic review and meta-analysis
Website endobattery.com
Mark as Played
Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
SPEAKER_00 (00:00):
Welcome to Indobattery Fast Charged, a
series dedicated to keeping youinformed and empowered in the
realm of endometriosis.
Teaming up with board certifiedpatient advocates, we bring you
the latest articles, research,and insights to equip you with
accurate information and adeeper understanding.
Whether you're expanding yourknowledge, staying updated, or
seeking clarity, you're in theright place.
(00:22):
I'm your host, Alana, and thisis Indobattery Fast Charged,
charging and empowering yourlife with knowledge.
Welcome back to Indobattery FastCharged, your quick hit of
clarity, validation, andgrounded science.
Today we're taking a rapid butmeaningful tour through several
(00:43):
articles that scratch out aquestion so many of us have
lived long before the researchever caught up.
Why does endometriosis seem tooverlap with so many other
conditions?
And why does it affect the wholebody, not just one organ?
Before we get into it, I need tomake something abundantly clear.
Correlation does not equalcausation.
(01:04):
These studies aren't saying onething causes another, they're
exploring patterns, biologicalpathways, and shared mechanisms
that may someday help usunderstand the lived experience
patients have been reporting fordecades.
This conversation is aboutcuriosity, connection, and
empowerment, not panic.
So without delaying this anyfurther, let's jump into it.
(01:28):
The first article we're going toexplore is titled The Potential
Connection Between HEDS andEndometriosis.
Alright, let's zoom into thissomewhat old but still
interesting 2022 study thatexplores the potential molecular
soap opera between hypermobilityEhlers-Stenlow syndrome or HEDS
(01:49):
and MAST Cell.
The same immune troublemakersthat keep popping up in
endometriosis conversations.
If this title sounds like amouthful, don't worry.
I'll unpack it in plain terms.
First, the basics.
HEDS is a connective tissuedisorder.
Think stretchy joints,hypermobile, flexible skin, and
(02:10):
ligaments that might feel alittle too floppy.
This isn't just an issue ofbeing bendy.
In HEDS, the very scaffolding ofthe body, collagen, the
extracellular matrix, is a bitdifferent, and that may change
how other cells behave.
Now, what's the study actuallyabout?
(02:30):
Well, the researchers looked athow mast cell might be
chronically overactive in peoplewith HEDS or hypermobility
spectrum disorders.
Mast cell, as you mightremember, are immune cells that
release histamine, tryptase, andcytokines.
Basically, they sound the alarmand stir up inflammation.
In HEDS, their mediators, thosemolecules mast cells release,
(02:56):
may be contributing to tissuelevel disconnects, altering how
connective tissue works andpossibly making things like pain
and stability or inflammationworse.
Here's where it gets messy orinteresting.
The authors propose that becausethe connective tissue is more
fragile or elastic in HEDS, masscell activation, the repeated
(03:19):
degranulation, could lead topersistent inflammation, which
in turn could damage tissue orat least make them more
reactive.
That could theoretically playinto how things like pelvic pain
develop.
And sure, some people with HEDSalso report endometriosis.
(03:40):
There are estimates from othersources that 6 to 23% of people
with EDS may also haveendometriosis, but huge butt.
This correlation is notcausation.
The study doesn't prove thatHEDS causes endometriosis.
What it does do is suggest aplausible biological mechanism.
(04:02):
Mast cells already being moretrigger happy in some HEDS folks
might exacerbate inflammatoryloops, influence fibroblasts,
cells that rebuild connectivetissue, and generally make
connective tissue more volatile.
There's also talk in the broaderliterature about extracellular
(04:24):
matrix or ECM remodeling, beingdysregulated in EDS, which could
affect how lesions like endolesions stick, invade, or
persist.
Though the authors of the 2022paper don't fully map that out.
So what's the takeaway?
This study doesn't drop a micwith HEDS equals endometriosis,
(04:48):
but it does supply a thoughtfulpiece of the puzzle.
It supports the idea that mastcell activation or MCAS in HEDS
could contribute to chronicinflammation, which might worsen
symptoms common in both HEDS andendometriosis like pain.
And importantly, it points outwhy multidisciplinary approach,
(05:12):
gynecologist, immunologist,rheumatologist, is so important
for people navigating bothspaces.
In plain words, we don't have asmoking gun cause and effect
yet, but we have good leads.
(05:34):
Future research could drill intowhether targeting mast cell
activation might one day easesymptoms for people with both
these conditions.
As we continue with thistrajectory of research, we're
gonna dive into an article thatis brand new but also not brand
new about mast cells andendometriosis titled Mast Cell
(05:54):
Mediated Epithelial MesenchymalTransition and Endometriosis.
That is a mouthful.
And before you panic, no, you donot need a PhD, a microscope, or
a secret decoder to bring inunderstanding this.
I'm gonna keep it simple becausescience does not need to feel
like a tax audit.
This study looks at somethingcalled the CCL2 or the CCR4
(06:19):
pathways, which, yes, absolutelysound like a droid from Star
Wars, but I promise it's just acommunication channel that mast
cells use.
So here's the deal (06:30):
the idea that mast cells are involved in
endometriosis, again, is notnew.
Mast cells are basically thedrama queens in the immune
system.
They're cells responsible forallergic reactions,
inflammation, the whole bodydoing the most experience.
We've known for a while thatpeople with endometriosis have
(06:50):
more active mast cells.
And older studies and evenanimal models have shown that
when you calm these cells,endolesions grow less.
So the concept that mast cellsplay a role, been there, seen
that, bought the t-shirt.
What the study adds though, andthis is where it gets fun, is
the mechanism.
(07:11):
Instead of just saying mastcells are here causing problems,
the researchers zoomed in andsaid, okay, how exactly are
these little immune gremlinsstirring the pot?
And what they found was thatmast cells appeared to help push
endometriosis lesions intosomething called epithelial
mesenchymal transition, alsoknown as EMT, which is much
(07:34):
easier to say.
Now, EMT is basically wherecells stop acting like
well-behaved, tidy littleepithelial cells that stay in
place and instead start behavinglike mesenchymal cells, which
are more mobile, flexible, andfrankly a bit too ambitious.
(07:54):
The cell equivalent of someonedeciding to quit their desk job
to become a traveling circusclown.
The CCL2CCR4 signaling pathwaysseem to be the walkie-talkie
connection mast cells use tonudge endometriosis cells toward
this more aggressive behavior.
So instead of just sittingquietly, these cells get the
(08:17):
message, literally, and startbecoming more invasive, harder
to remove, and more persistent.
If you've ever wondered why somelesions act like they've
unpacked their suitcases andmoved in forever, this kind of
signaling may be part of thatreason.
Now, does this change everythingwe know about endometriosis?
(08:37):
Not quite.
But it does give us a clearerpicture of what's happening on
the microscopic level.
Kind of like turning on thelights in a messy room.
The mess was always there.
Now we're just understandingwhich pile came from where.
And importantly, identifyingthese communication signals make
them potential targets forfuture treatment.
(08:58):
If we can block the mast cellmessaging or reroute them, we
might have new ways to slowlesion progression or reduce
symptoms.
So, in short, this researchdoesn't overturn the mast cell
story, but it does addmeaningful detail.
It's like adding subtitles to amovie you've watched a hundred
(09:18):
times.
You suddenly catch things youdidn't see before.
And for a disease that has beenmisunderstood or
under-researched for decades,clarity, even in small pieces,
matters.
All right, to round out the mastcell world tour, let's talk
about this article from the EDSClinic that breaks down how
(09:39):
endometriosis and the immunesystem basically get into each
other's business in messy,dramatic ways.
The article titled The Role ofMast Cells in Endometriosis
explains that endometriosisisn't just a pelvic disease.
Nope.
It's more like an overachieverof inflammatory conditions,
(09:59):
affecting hormones, immunepathways, gut function, pain
processing, and the general, whyam I like this experience?
So if you've ever felt likeendometriosis is a full body
event, congratulations, you'renot imagining it.
One of the big stars here,again, is the mast cells.
(10:20):
Think of mast cells as immunegrenades waiting for a reason to
go off.
The article explains thatendometriosis can activate these
cells, and once they'reactivated, they release
substance like histamine,prostaglandins, and cytokines
that basically screaminflammation time, and that can
(10:41):
turn up the volume on pain, gutissues, bladder dysfunction,
fatigue, and that foggy someoneunplugged my brain feeling.
This is why people with endoalso experience symptoms that
look suspiciously like histamineintolerance or mast cell
activation issues.
But the article also makesanother important point.
(11:03):
Estrogen is not helping.
Estrogen stimulates the growthof endometriosis lesions,
increasing inflammation, eveninfluencing the mast cell
behavior.
So now we've got hormones andthe immune system tag teaming
like they're auditioning for aWWE match.
This explains why flare-ups cantrack with hormonal shifts, why
(11:24):
symptoms can fluctuate, and whytreatments that touch hormone
pathways sometimes help.
And sometimes, well, they don't.
Here's where it getsinteresting.
Anthistamines and mast cellstabilizing strategies may help
some people manage symptoms,especially symptoms that don't
respond to typical endometriosistreatments.
(11:45):
The article is very clearthough.
These aren't a cure.
They're more like turning downthe volume to a very chaotic
group chat.
Think like the Secret Wives andMormon Wives group chat.
We all know how chaotic that'sgotta be.
Useful, but not a pertinentsolution.
The bigger message,endometriosis is systemic.
(12:06):
It affects the entire body, notjust reproductive organs.
That's why patients often reportgut problems, joint pain,
chronic fatigue, dizziness,bladder irritability, food
sensitivities, you name it.
And because endometriosisoverlaps with immune-related
conditions like EDS, MCAS, POTS,and autoimmune disorders, the
(12:27):
whole picture gets a bit morecomplicated.
The article basically saysyou're not imagining your
symptoms.
You're not being dramatic.
Your biology is interconnected.
So these pieces tie everythingtogether by exploring how
hormones, inflammation, and mastcells work together to create
(12:47):
systems many people withendometriosis experience.
It doesn't claim mast cellscause endometriosis, but it does
show why calming them down mighthelp some people feel better and
why the full body symptoms makefar more sense than many doctors
have realized.
(13:15):
Hi, it's me.
This article is genuinelyexciting.
Let's talk about trisepatide,the dual GLP1 GIP drug that's
been making waves for weightloss and metabolic health, but
from a slightly different angletoday.
Inflammation.
Because reducing inflammationisn't just about feeling less
(13:35):
puffy, it can also help withpain, long-term health, and
maybe even chronic illnessmanagement.
And yes, there's a systemicreview and meta-analysis on
exactly this.
A paper published in 2025 titledAnti-inflammatory effects of
trisepatide, a systemic reviewand meta-analysis, looked at
seven randomized clinicaltrials, plus an observational
(13:59):
study to see how trisepatideaffects inflammatory markers,
especially HSCRP, highsensitivity C reactive protein,
and IL6 interleukin-6.
They ran a meta-analysis, whichmeans they pooled data from
multiple studies to get aclearer picture.
The results?
Trisepatide use was associatedwith a significant drop in both
(14:22):
the HCRP and IL6, andexcitingly, this wasn't limited
to just one dose.
They saw reactions across 5milligrams, 10 milligrams, 15
milligram doses.
Why is this so cool, you mightask?
Well, lower CRP and IL6 suggestthat trisepatite might be
(14:43):
helping calm chronic low-gradeinflammation, the kind that's
often behind a lot of long-termpain, metabolic dysfunction, or
inflammatory conditions.
And because the effect showed upacross multiple studies and
doses, it's not just a fluke.
For people looking fornon-opioid ways to reduce
(15:04):
inflammation, therefore pain,this adds a promising piece to
the puzzle.
But yes, there's a but.
The majority of this data isstill from clinical trials
primarily set up for metabolicoutcomes, not inflammation or
pain.
So this isn't the same as adedicated anti-inflammatory
trial.
Reductions in biomarkers areencouraging, but they don't
(15:26):
always translate to real-worldsymptom relief like pain, joint
ache, or fatigue.
Lower markers equal good, butfeeling better, that's the real
test.
Not everyone toleratestrisepatide well.
We know from other meta-analysisthat gastrointestinal side
effects, nausea, vomiting, anddiarrhea, are common.
(15:49):
There might also be long-termsafety concerns or on-scene
effects when using trisepatidein context other than its
primary indication, especiallyif you're using it off-label for
inflammation or pain reduction.
Bottom line, trisepatide isshowing real promise as an
anti-inflammatory tool, not justa metabolic or weight loss drug.
(16:11):
For people exploring non-opioidways to manage pain, this is a
hopeful development, but it'snot a magic bullet.
More research is needed that'sspecifically designed to test
inflammation and symptomoutcomes, not just lab values.
And if someone is consideringtrisepatite for inflammation or
pain, it's absolutely worthdiscussing with a knowledgeable
(16:34):
provider to weigh the benefitsand risks of their specific
context.
If there's one message I wantyou to take from all of this,
it's that you are not toocomplicated.
Your symptoms are not random.
Your pain is not exaggerated.
Your experience is not just inyour head.
Endometriosis interacts withconnective tissue, the immune
(16:57):
system, hormones, the nervoussystem, and yes, even medication
developed for those conditions.
Your body is an ecosystem, not aset of isolated parts.
These articles collectively helpus understand the bigger
picture.
Hope isn't aboutoversimplifying.
Hope is about finally seeing thecomplexity clearly.
(17:18):
I hope this episode has broughtto light some things that could
really help you.
And if you know someone elsethat is struggling, I encourage
you to share this episode withthem as well.
Comment your own experience sothat others don't feel alone and
keep advocating for yourself.
Your symptoms deserve curiosity,not dismissal.
Here at Indobattery, you alwayshave a seat at the table, a
(17:39):
place to feel seen, and acommunity ready to recharge you.
So until next time, continueadvocating for you and for
others.
Welcome to Indobattery Fast Charged, a
series dedicated to keeping youinformed and empowered in the
realm of endometriosis.
Teaming up with board certifiedpatient advocates, we bring you
the latest articles, research,and insights to equip you with
accurate information and adeeper understanding.
Whether you're expanding yourknowledge, staying updated, or
seeking clarity, you're in theright place.
(00:22):
I'm your host, Alana, and thisis Indobattery Fast Charged,
charging and empowering yourlife with knowledge.
Welcome back to Indobattery FastCharged, your quick hit of
clarity, validation, andgrounded science.
Today we're taking a rapid butmeaningful tour through several
(00:43):
articles that scratch out aquestion so many of us have
lived long before the researchever caught up.
Why does endometriosis seem tooverlap with so many other
conditions?
And why does it affect the wholebody, not just one organ?
Before we get into it, I need tomake something abundantly clear.
Correlation does not equalcausation.
(01:04):
These studies aren't saying onething causes another, they're
exploring patterns, biologicalpathways, and shared mechanisms
that may someday help usunderstand the lived experience
patients have been reporting fordecades.
This conversation is aboutcuriosity, connection, and
empowerment, not panic.
So without delaying this anyfurther, let's jump into it.
(01:28):
The first article we're going toexplore is titled The Potential
Connection Between HEDS andEndometriosis.
Alright, let's zoom into thissomewhat old but still
interesting 2022 study thatexplores the potential molecular
soap opera between hypermobilityEhlers-Stenlow syndrome or HEDS
(01:49):
and MAST Cell.
The same immune troublemakersthat keep popping up in
endometriosis conversations.
If this title sounds like amouthful, don't worry.
I'll unpack it in plain terms.
First, the basics.
HEDS is a connective tissuedisorder.
Think stretchy joints,hypermobile, flexible skin, and
(02:10):
ligaments that might feel alittle too floppy.
This isn't just an issue ofbeing bendy.
In HEDS, the very scaffolding ofthe body, collagen, the
extracellular matrix, is a bitdifferent, and that may change
how other cells behave.
Now, what's the study actuallyabout?
(02:30):
Well, the researchers looked athow mast cell might be
chronically overactive in peoplewith HEDS or hypermobility
spectrum disorders.
Mast cell, as you mightremember, are immune cells that
release histamine, tryptase, andcytokines.
Basically, they sound the alarmand stir up inflammation.
In HEDS, their mediators, thosemolecules mast cells release,
(02:56):
may be contributing to tissuelevel disconnects, altering how
connective tissue works andpossibly making things like pain
and stability or inflammationworse.
Here's where it gets messy orinteresting.
The authors propose that becausethe connective tissue is more
fragile or elastic in HEDS, masscell activation, the repeated
(03:19):
degranulation, could lead topersistent inflammation, which
in turn could damage tissue orat least make them more
reactive.
That could theoretically playinto how things like pelvic pain
develop.
And sure, some people with HEDSalso report endometriosis.
(03:40):
There are estimates from othersources that 6 to 23% of people
with EDS may also haveendometriosis, but huge butt.
This correlation is notcausation.
The study doesn't prove thatHEDS causes endometriosis.
What it does do is suggest aplausible biological mechanism.
(04:02):
Mast cells already being moretrigger happy in some HEDS folks
might exacerbate inflammatoryloops, influence fibroblasts,
cells that rebuild connectivetissue, and generally make
connective tissue more volatile.
There's also talk in the broaderliterature about extracellular
(04:24):
matrix or ECM remodeling, beingdysregulated in EDS, which could
affect how lesions like endolesions stick, invade, or
persist.
Though the authors of the 2022paper don't fully map that out.
So what's the takeaway?
This study doesn't drop a micwith HEDS equals endometriosis,
(04:48):
but it does supply a thoughtfulpiece of the puzzle.
It supports the idea that mastcell activation or MCAS in HEDS
could contribute to chronicinflammation, which might worsen
symptoms common in both HEDS andendometriosis like pain.
And importantly, it points outwhy multidisciplinary approach,
(05:12):
gynecologist, immunologist,rheumatologist, is so important
for people navigating bothspaces.
In plain words, we don't have asmoking gun cause and effect
yet, but we have good leads.
(05:34):
Future research could drill intowhether targeting mast cell
activation might one day easesymptoms for people with both
these conditions.
As we continue with thistrajectory of research, we're
gonna dive into an article thatis brand new but also not brand
new about mast cells andendometriosis titled Mast Cell
(05:54):
Mediated Epithelial MesenchymalTransition and Endometriosis.
That is a mouthful.
And before you panic, no, you donot need a PhD, a microscope, or
a secret decoder to bring inunderstanding this.
I'm gonna keep it simple becausescience does not need to feel
like a tax audit.
This study looks at somethingcalled the CCL2 or the CCR4
(06:19):
pathways, which, yes, absolutelysound like a droid from Star
Wars, but I promise it's just acommunication channel that mast
cells use.
So here's the deal (06:30):
the idea that mast cells are involved in
endometriosis, again, is notnew.
Mast cells are basically thedrama queens in the immune
system.
They're cells responsible forallergic reactions,
inflammation, the whole bodydoing the most experience.
We've known for a while thatpeople with endometriosis have
(06:50):
more active mast cells.
And older studies and evenanimal models have shown that
when you calm these cells,endolesions grow less.
So the concept that mast cellsplay a role, been there, seen
that, bought the t-shirt.
What the study adds though, andthis is where it gets fun, is
the mechanism.
(07:11):
Instead of just saying mastcells are here causing problems,
the researchers zoomed in andsaid, okay, how exactly are
these little immune gremlinsstirring the pot?
And what they found was thatmast cells appeared to help push
endometriosis lesions intosomething called epithelial
mesenchymal transition, alsoknown as EMT, which is much
(07:34):
easier to say.
Now, EMT is basically wherecells stop acting like
well-behaved, tidy littleepithelial cells that stay in
place and instead start behavinglike mesenchymal cells, which
are more mobile, flexible, andfrankly a bit too ambitious.
(07:54):
The cell equivalent of someonedeciding to quit their desk job
to become a traveling circusclown.
The CCL2CCR4 signaling pathwaysseem to be the walkie-talkie
connection mast cells use tonudge endometriosis cells toward
this more aggressive behavior.
So instead of just sittingquietly, these cells get the
(08:17):
message, literally, and startbecoming more invasive, harder
to remove, and more persistent.
If you've ever wondered why somelesions act like they've
unpacked their suitcases andmoved in forever, this kind of
signaling may be part of thatreason.
Now, does this change everythingwe know about endometriosis?
(08:37):
Not quite.
But it does give us a clearerpicture of what's happening on
the microscopic level.
Kind of like turning on thelights in a messy room.
The mess was always there.
Now we're just understandingwhich pile came from where.
And importantly, identifyingthese communication signals make
them potential targets forfuture treatment.
(08:58):
If we can block the mast cellmessaging or reroute them, we
might have new ways to slowlesion progression or reduce
symptoms.
So, in short, this researchdoesn't overturn the mast cell
story, but it does addmeaningful detail.
It's like adding subtitles to amovie you've watched a hundred
(09:18):
times.
You suddenly catch things youdidn't see before.
And for a disease that has beenmisunderstood or
under-researched for decades,clarity, even in small pieces,
matters.
All right, to round out the mastcell world tour, let's talk
about this article from the EDSClinic that breaks down how
(09:39):
endometriosis and the immunesystem basically get into each
other's business in messy,dramatic ways.
The article titled The Role ofMast Cells in Endometriosis
explains that endometriosisisn't just a pelvic disease.
Nope.
It's more like an overachieverof inflammatory conditions,
(09:59):
affecting hormones, immunepathways, gut function, pain
processing, and the general, whyam I like this experience?
So if you've ever felt likeendometriosis is a full body
event, congratulations, you'renot imagining it.
One of the big stars here,again, is the mast cells.
(10:20):
Think of mast cells as immunegrenades waiting for a reason to
go off.
The article explains thatendometriosis can activate these
cells, and once they'reactivated, they release
substance like histamine,prostaglandins, and cytokines
that basically screaminflammation time, and that can
(10:41):
turn up the volume on pain, gutissues, bladder dysfunction,
fatigue, and that foggy someoneunplugged my brain feeling.
This is why people with endoalso experience symptoms that
look suspiciously like histamineintolerance or mast cell
activation issues.
But the article also makesanother important point.
(11:03):
Estrogen is not helping.
Estrogen stimulates the growthof endometriosis lesions,
increasing inflammation, eveninfluencing the mast cell
behavior.
So now we've got hormones andthe immune system tag teaming
like they're auditioning for aWWE match.
This explains why flare-ups cantrack with hormonal shifts, why
(11:24):
symptoms can fluctuate, and whytreatments that touch hormone
pathways sometimes help.
And sometimes, well, they don't.
Here's where it getsinteresting.
Anthistamines and mast cellstabilizing strategies may help
some people manage symptoms,especially symptoms that don't
respond to typical endometriosistreatments.
(11:45):
The article is very clearthough.
These aren't a cure.
They're more like turning downthe volume to a very chaotic
group chat.
Think like the Secret Wives andMormon Wives group chat.
We all know how chaotic that'sgotta be.
Useful, but not a pertinentsolution.
The bigger message,endometriosis is systemic.
(12:06):
It affects the entire body, notjust reproductive organs.
That's why patients often reportgut problems, joint pain,
chronic fatigue, dizziness,bladder irritability, food
sensitivities, you name it.
And because endometriosisoverlaps with immune-related
conditions like EDS, MCAS, POTS,and autoimmune disorders, the
(12:27):
whole picture gets a bit morecomplicated.
The article basically saysyou're not imagining your
symptoms.
You're not being dramatic.
Your biology is interconnected.
So these pieces tie everythingtogether by exploring how
hormones, inflammation, and mastcells work together to create
(12:47):
systems many people withendometriosis experience.
It doesn't claim mast cellscause endometriosis, but it does
show why calming them down mighthelp some people feel better and
why the full body symptoms makefar more sense than many doctors
have realized.
(13:15):
Hi, it's me.
This article is genuinelyexciting.
Let's talk about trisepatide,the dual GLP1 GIP drug that's
been making waves for weightloss and metabolic health, but
from a slightly different angletoday.
Inflammation.
Because reducing inflammationisn't just about feeling less
(13:35):
puffy, it can also help withpain, long-term health, and
maybe even chronic illnessmanagement.
And yes, there's a systemicreview and meta-analysis on
exactly this.
A paper published in 2025 titledAnti-inflammatory effects of
trisepatide, a systemic reviewand meta-analysis, looked at
seven randomized clinicaltrials, plus an observational
(13:59):
study to see how trisepatideaffects inflammatory markers,
especially HSCRP, highsensitivity C reactive protein,
and IL6 interleukin-6.
They ran a meta-analysis, whichmeans they pooled data from
multiple studies to get aclearer picture.
The results?
Trisepatide use was associatedwith a significant drop in both
(14:22):
the HCRP and IL6, andexcitingly, this wasn't limited
to just one dose.
They saw reactions across 5milligrams, 10 milligrams, 15
milligram doses.
Why is this so cool, you mightask?
Well, lower CRP and IL6 suggestthat trisepatite might be
(14:43):
helping calm chronic low-gradeinflammation, the kind that's
often behind a lot of long-termpain, metabolic dysfunction, or
inflammatory conditions.
And because the effect showed upacross multiple studies and
doses, it's not just a fluke.
For people looking fornon-opioid ways to reduce
(15:04):
inflammation, therefore pain,this adds a promising piece to
the puzzle.
But yes, there's a but.
The majority of this data isstill from clinical trials
primarily set up for metabolicoutcomes, not inflammation or
pain.
So this isn't the same as adedicated anti-inflammatory
trial.
Reductions in biomarkers areencouraging, but they don't
(15:26):
always translate to real-worldsymptom relief like pain, joint
ache, or fatigue.
Lower markers equal good, butfeeling better, that's the real
test.
Not everyone toleratestrisepatide well.
We know from other meta-analysisthat gastrointestinal side
effects, nausea, vomiting, anddiarrhea, are common.
(15:49):
There might also be long-termsafety concerns or on-scene
effects when using trisepatidein context other than its
primary indication, especiallyif you're using it off-label for
inflammation or pain reduction.
Bottom line, trisepatide isshowing real promise as an
anti-inflammatory tool, not justa metabolic or weight loss drug.
(16:11):
For people exploring non-opioidways to manage pain, this is a
hopeful development, but it'snot a magic bullet.
More research is needed that'sspecifically designed to test
inflammation and symptomoutcomes, not just lab values.
And if someone is consideringtrisepatite for inflammation or
pain, it's absolutely worthdiscussing with a knowledgeable
(16:34):
provider to weigh the benefitsand risks of their specific
context.
If there's one message I wantyou to take from all of this,
it's that you are not toocomplicated.
Your symptoms are not random.
Your pain is not exaggerated.
Your experience is not just inyour head.
Endometriosis interacts withconnective tissue, the immune
(16:57):
system, hormones, the nervoussystem, and yes, even medication
developed for those conditions.
Your body is an ecosystem, not aset of isolated parts.
These articles collectively helpus understand the bigger
picture.
Hope isn't aboutoversimplifying.
Hope is about finally seeing thecomplexity clearly.
(17:18):
I hope this episode has broughtto light some things that could
really help you.
And if you know someone elsethat is struggling, I encourage
you to share this episode withthem as well.
Comment your own experience sothat others don't feel alone and
keep advocating for yourself.
Your symptoms deserve curiosity,not dismissal.
Here at Indobattery, you alwayshave a seat at the table, a
(17:39):
place to feel seen, and acommunity ready to recharge you.
So until next time, continueadvocating for you and for
others.
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