Thyroid Shorts Episode 10: Does the Cell Danger Response Apply to Everyone?

In this episode, Dr. Eric Balcavage responds to a thoughtful viewer comment that challenges key aspects of his adaptive thyroid physiology model and Cell Danger Response theory. This deep-dive discussion addresses whether his approach applies to every hypothyroidism case, clarifies the 71% improvement statistic, and explores the role of T3 therapy in thyroid treatment.

 

Key Topics Covered:

• Does the Cell Danger Response theory apply to all hypothyroidism cases?
• Clarification of the 71% patient improvement statistic - what it really means
• Historical use of NDT (Natural Desiccated Thyroid) and treatment evolution
• Post-Graves disease thyroid management and receptor sensitivity
• Why T3 therapy works for some patients but doesn't restore physiology
• The difference between symptom management and true thyroid restoration
• When to consider alternative approaches for treatment-resistant cases

Dr. Balcavage provides nuanced responses while acknowledging the limitations of current thyroid models, emphasizing that his approach offers hope for patients who haven't found success with conventional T4, NDT, or T3 protocols.

 

Perfect for: Thyroid patients stuck in "thyroid purgatory," healthcare practitioners seeking new perspectives, and anyone interested in understanding why standard thyroid treatments sometimes fail.

Episode Transcript

Eric Balcavage (00:20):
Hello, everybody. It's Dr Eric
Balcavage. We're back foranother edition of thyroid
answers. Short and today, I wantto respond to a thoughtful and
respectful comment left on oneof my recent videos, the truth
about t3 why your thyroid isn'tbroken. And I want to say I

(00:43):
appreciate when listeners taketime to engage deeply and
critically. And this particularcomment brings up several
important challenges to theideas I present, especially
around the adaptive thyroidphysiology model and the cell
danger response as contributorsto hypothyroid physiology challenges.

(01:09):
So in this episode, I'm going tostart by reading the full
comment and then break it downpoint by point.
So the the follower says youmake a lot of good points in
your videos. For instance, youread the literature in detail
and explain many aspects ofthyroid physiology that others

(01:31):
rarely ever touch upon. However,where I start to be a little
less enthusiastic is when youinsinuate that your cell danger
response hypothyroidism theoryapplies to every single case.
I've learned over the years tobe suspicious when someone
explains every single healthproblem by one single theory,

(01:54):
which, although you believe tohave observed it indirectly, has
never been scientifically provento apply to hypothyroidism to
the extent you believe it toexist, even you yourself admit
in another video that 71% ofyour patients get better after
six months. There's also thefact that NDT used to be the

(02:17):
only treatment available formore than 70 years, and almost
everyone used to do fairly wellon it. Take, for instance,
someone who acquired tissueresistance or thyroid receptor
desensitization from years ofGraves disease due to extremely
excessive free t4 and t3 levelsin the blood creating damage,

(02:40):
and then suffers fromhypothyroidism after surgery.
I'm not convinced that in caseslike these, your theory is the
key, and there is any way tohelp such a person, but to raise
free t3 levels in the blood.
And I'm going to interject herewhen they say that the person
struggles with hypothyroidismafter thyroid surgery, if

(03:04):
somebody's getting radioactiveiodine treatment or a
thyroidectomy following Gravesdisease, there are going to be
hypothyroids because they don'thave a gland to make thyroid
hormone anymore. And I thinkwhat they're really pointing to
is persistent tissue hypothyroidsigns and symptoms on t4 only, I

(03:24):
think that's what they'rereferring to. And if the person
who wrote this it thinks I'msaying that wrong, they can feel
free to reach back out.
The person goes on to say, areyou familiar with the work of Dr
John Lowe, who is at the otherextreme from you? He did help a
lot of people with extremetissue resistance to tissue to

(03:47):
thyroid hormones and achievedurable positive results from
using large doses of t3although, like you say, the body
can deactivate it. That clearlydoesn't seem to happen in every
case. I believe that differentstrategies can help different
people, but you do offer avaluable alternative and deserve

(04:11):
to be heard.
So I appreciate the comment, andI'm going to break these, these
kind of comments down one by oneand give some information. I
think if this person who wrotethis had these thoughts and
feelings, there's probably otherpeople, even some of my

(04:34):
colleagues, that may feel thesame way. So the first big point
is, do I believe that the celldanger response in the adaptive
thyroid model apply to everysingle case of hypothyroidism?
And the answer is no, absolutelynot. There may be other things

(04:56):
that are maybe contributing todrive hypothyroidism, that maybe
aren't represented by these twocell danger response and
adaptive thyroid model. Theremay be things that I'm not
considering. So I'm not sayingthat every case of
hypothyroidism is caused by thecell danger response. There are

(05:20):
many mechanisms that can lead tohypothyroidism, hypothyroid
signs and symptoms, glandulardamage that can occur. There can
be, obviously, medications thatcan interfere. There's stress,
trauma, but these are all thingsthat are really part of that

(05:40):
cell danger response. But couldthere be something outside the
cell danger response thatpotentially triggers thyroiditis
and hypothyroidism or triggersreduced cellular transport of
thyroid hormone or or chronichypothyroid symptoms?
I'm sure there are. And what I'mnot saying is this is the only

(06:05):
model. What I'm offering this asis as a new lens for
understanding thyroidphysiology, especially in people
who have failed the conventionaland even the functional care
models. This is not a all ornone paradigm. It's not it's

(06:25):
only cell danger response or orbust. It's a framework that
helps clinicians and patientsexplore why someone might still
have symptoms despite havingnormal labs or being on what
their clinician thinks is theright dose of medication.

(06:46):
And frankly, if someone is doinggreat on their current therapy,
that's awesome, keep going. Butif they're not and they feel
stuck, this model offerspotentially a new way forward.
So I wish it was as simple, thateverything was just this is the
only way that things happen. Butwe don't know how the physiology

(07:08):
actually works in every client.We don't know the actual
triggering mechanisms.Everything, essentially is
hypothesis in theory, and thenwe we we look through a certain
lens, a certain paradigm, totreat our patients. And
sometimes that works andsometimes it doesn't. And
there's often times that we havea belief in a certain hypothesis

(07:33):
or theory. We treat based on ahypothesis in theory, we see pot
allowed to lots of people feeland function better, and then a
decade or two or three later, werealized that what we thought
was a mechanism of action forwhich we were providing
treatment wasn't actually thecase, and yet the patients still

(07:55):
seem to get better in thatmodel. So really important thing
to consider and keep in mindthat when, when I started
changing my belief process aboutwhat might be going on in a lot
of these patients who arechronically struggling in both
the allopathic and thefunctional space, where they

(08:16):
weren't doing well on t4 theyweren't doing well on NDT, they
weren't doing well on high doset3 medication. That's where I
had to start rethinking thiswhole process, like there must
be something else going on here,and that's where I found the
cell danger response, and that'swhere I started developing this

(08:38):
adaptive thyroid physiologymodel versus the model that is
generally understood inallopathic medicine, and to a
large degree in functionalmedicine, that the body's
broken, that the immune systemis just not recognized as self
tissue and destroying it, andthen it forgot how to convert t4

(08:59):
to t3 at an optimal level.
The next comment that I want totalk about is the writer says
that the comment that this wholehypothesis, the adaptive thyroid
physiology model that's kind ofbuilt on this whole hypothesis
of the cell danger response, hasnever been fully proven to be

(09:21):
the root cause of hypothyroidism.
And that's a fair point, butlet's put it in context. There
is no single proven cause ofhypothyroidism in all patients.
What we have are models,beliefs, hypothesis, all of
which try to explain what weobserve in practice. That's true

(09:41):
for conventional medicine,functional medicine and my own
mind, right? If we had a onecause mechanism and a one
treatment strategy that workedfor everybody, you know, the
discussion would be over. Theproblem is we really don't.
Know, you'll see people. You'llsee when you look at what

(10:03):
triggers immune driventhyroiditis, it's there's a
combination of factors, likegenetics are a factor, diet,
lifestyle is a factor, toxinsand organisms all factors. And
these are all the things we talkabout as things that might
trigger a cell danger responseas well. B

(10:24):
ut what I'm proposing is ahypothesis, and yes, it is just
that hypothesis. We haven't beenable to prove it yet that this
is actually the case. I thinkthe general consensus is that
it's some type of cell stress orinflammatory or defense

(10:46):
response, and it seems to impactpeople with a certain set of
genetic predisposition. But Idon't know that we have the
perfect scientific evidence tothis point, we could say this is
the only mechanism that occurs.
And even though I proposed thisas a hypothesis, I just didn't,

(11:10):
kind of wake up one day andlike, hey, I'll just throw this
out there. The hypothesis isborn from 30 years of clinical
observation of patients whofailed multiple paradigms, they
found they failed in thetraditional allopathic model,
they failed in the functionaland integrative model, and they
failed with different types ofhormone replacement therapy. T4,

(11:34):
glandulars, t3, onlycombinations of t4, t3, and
glandulars. I mean, they'vefailed trying every possible
strategy, high dose, low dose,to optimize blood levels,
assuming that optimal bloodlevels would fix all their signs
and symptoms. And it just didn'twork.
The hypothesis born on researchinto cellular stress response,

(11:56):
inflammation, mitochondrialsignaling, and a lot of time
digging into the scientificliterature. And oftentimes, what
I'm trying to do when I'mlooking in the scientific
literature is look for reasonswhy what I'm saying or this
hypothesis I'm putting out theremight not be valid in as a
general overall hypothesis for alot of these people who are

(12:19):
struggling and not doing well.
And the third way that thishypothesis came about is because
I really have a deep desire tohelp patients who feel like
they've been left behind, likethey've been told, Hey, we've
optimized you. We don't knowwhat's left, right? We've we've
optimized your t4 we'veoptimized your TSH, we've
optimized your t3 we'veoptimized your reverse t3 we've

(12:42):
optimized your TPO antibodies,thyroglobulin antibodies. We've
optimized what we can optimize.And if you still don't feel
well, we don't know what else todo, because your thyroid
physiology is now optimal.
Optimal based on what, though,is the question, is it optimal
in the blood based on what? Ifthe patient's chronically ill

(13:02):
and has chronic hypothyroidsigns and symptoms, just because
you manipulate their bloodlevels of a hormone doesn't mean
you've optimized them. It meansyou manipulated their chemistry,
but it assumes that what we sawas a low or high blood value was
the problem, versus what we sawas a low or high blood value was

(13:23):
the body's response, the body'sadaptive response to some type
of stress trigger.
And I think we want to add toothat if, if all of the models
had worked consistently, Iwouldn't have had to build a new
one. But they don't. I wish theydid. And just like any
scientific hypothesis, time andresearch will ultimately

(13:46):
validate, refine or disprovethis model, but until then, the
outcomes we see, symptom,resolution, improved conversion,
reduced medication needs supportits clinical value.
The next point I want to coveris where the person says that. I
guess the reason that the celldanger response in this adaptive

(14:10):
thyroid physio physiology modelprobably aren't valid in
everybody is because only 71% ofmy patients improve in six months.
And what I've said over and overagain is that when I look over
the last four years, because wehad to go back and do this kind

(14:31):
of tally for for a third party,say, Okay, what's this? What's
the success of your treatment?Look like we went back, took
three years. Now it's been fouryears and and looked at the
changes in patient signs andsymptoms and medication changes

(14:51):
over that time frame, and I saidthat in a six month period of
time my clients see a 71%improvement of their signs and
symptoms and measurables onaverage. Doesn't mean everybody
has 71% that means some peopleget 100% some people 90% some
people only down maybe 20 or 30%improvement in a six month time

(15:17):
frame. But that that's theaverage over four months, it
doesn't mean that only 71% of mypatients improve in in six
months. It's saying that when wetake a look at all of the
clients that I've seen over thelast four years, since we've
been actually going back andstarting to track it the the

(15:41):
average person who comes into mypractice, we typically see about
a 71% improvement of theirsigns, their symptoms and labss.
Oftentimes, as we're reducingthe amount of medication they're
needing to take.
Okay, that's pretty good. So ifthe person listening to this

(16:02):
said, Man, if I could get a 71%improvement in my symptoms in
the first six months of workingwith him, I would take that
because what is the improvementbeen in their last six months?
So I wanted to clarify thatthat's number one.
Number Two. Most of the peoplewho come to see me are not
people who've freshly beendiagnosed with hypothyroidism

(16:25):
and haven't had any thyroidmedication before. I do get
those patients that come to seeme because they're looking for a
potentially more naturalapproach to addressing what's
going on with their thyroidphysiology, or they've heard me
speak and they like they theyresonate with this adaptive
thyroid physiology model.

(16:45):
But most of the patients whocome to see me are people who've
already failed on t4 only.They've already failed an NDT or
they've already failed on t3protocols, and that what I mean
by failed is it's not that anyof these medications didn't
change their signs and symptoms,but it didn't restore their
health. It didn't get them towhere they wanted to go.

(17:06):
They're coming to see me afterseeing multiple other
practitioners because they'recaught or stuck in what I call
thyroid purgatory, the statebetween where they were before
medication and where they thinkthey should be if they're if
they were truly optimized, ortheir thyroid physiology has
truly been optimized.
So it is the model in itself isnot a failure, or it's not that

(17:30):
it doesn't work, because there'sonly a 71% improvement in
somebody's signs and symptoms insix months. I think we'd have to
say the opposite. If this model,where we're reducing excessive
stressors on somebody'sphysiology, many times, with
minimal amount ofsupplementation, is improving

(17:54):
the when people come in, there'sthe average person seeing a 71%
improvement in six months byreducing stressors using this
hypothyroid, this adaptivethyroid model, and the cell
danger response model as theparadigm, or the lens through
which we look at what's going onwith them, and then reducing

(18:18):
This excessive cell stressresponse, and we're seeing a 71%
improvement in just six months.
I don't think that means thatthe model is, is is a problem. I
think that that it actuallystarts to help validate how
important this model might befor those people who continue to
struggle, regardless of the typeof thyroid hormone replacement

(18:42):
therapy they use.
So the next point I want tocover is the person says, and I
think they're using this as ajustification for NDT, because
they were essentially talkingabout how, for greater than 70
years. NDT was the was theprimary treatment strategy

(19:04):
before Synthroid came along, andpeople did fairly well. So that
goes against what I'm saying isthat there's a reduced in these
people who struggle with signsand symptoms that reduced and
have reduced t4 to t3 conversionthat he's saying essentially

(19:27):
that t3 is the answer and thatNDT is the strategy that's been
given the longest. But I don'tknow what what that we're what
they're really trying to getfrom that, because just because
something has been used for along time doesn't mean that it's

(19:49):
the the appropriate strategy.
We do a lot of things and treatwith a lot of things, and that
doesn't mean that that strategyis the one and only answer. Um.
Um, I mean, we've been, we'vebeen treated using using aspirin
to treat conditions for over 100years, and we're still learning
that while there's risks, orwhile there's benefits, there's

(20:11):
also some risks and limitationsin using aspirin. So, you know,
does it mean that aspirin isbad? No, does it mean that it's
the only treatment strategy, orthat it has no negative
consequences. No, it doesn'tmean that at all.
And I guess the other part ofthat is when he's saying that

(20:31):
it's been used for, you know,greater than seven years, and
patients did fairly well. Youknow, what does that? What does
fairly well? Mean it's fairlywell mean that they've restored
their optimal health. Does thatmean that they've have no more
chronic hypothyroid signs andsymptoms? Is that and is fairly

(20:53):
well the goal? That may not bewhat they meant, but he may say,
hey, people took NDT thyroid fora lot of time, and they did see
and that was the only treatment,and they did pretty they seem to
do better sure any thyroidhormone is potentially going to
be better than having none. Andbut that doesn't mean it's that

(21:15):
we should stop there. Justbecause we can change some lab
values and we get some temporarysymptoms, doesn't mean we should
continue to try and consider whythe patient may still have
continual signs and symptoms,even though they've been on t4
or T, t3 or or a combination,like a like an NDT.

(21:36):
And I think the, I think thatwould cover that one I um, the
next point that the person talksabout is, I guess they're
talking about with, they'retalking where they were talking
about Graves disease, and theysaid that in cases, what about,

(21:59):
shouldn't people with who've hadGraves disease and have
potentially had receptordesensitization. They they
probably need t3 because ofwhat's happened.
So that it's interesting. Thereare some people, I guess, who've

(22:19):
had Graves disease for anextended period of time, they've
had T high t4 and t3 for years,then get surgery and now
struggle with symptoms. I seethat all the time. And what,
what the commenter is arguing isthat these people have receptor

(22:40):
desensitization,desensitization, or receptor
resistance due to having thischronic hyperthyroid state for
an extend, extremely long periodof time, and that maybe in these
people, t3 may be the onlyoption to raise Their t3 levels.

(23:01):
I don't know. I don't know ifthat we have literature and
research that shows thatsomebody who has hyperthyroidism
grades and then has theirthyroid gland remove or is going
to have persistent reduction inthyroid hormone transport, which
I think he's primarily referringto. So this is a person who
won't be able to get t4 to t3into the cells after that, and

(23:24):
that they're saying, I guessthat t3 is the only option.
Well, I don't know we have. Wehave literature that tells us
that we'll have long termthyroid receptor resistance
after the thyroid gland has beenremoved where they've had
radioactive iodine. I haven'tseen that literature yet. And if
it's out there that it la Howlong does it last for? What does

(23:46):
the science show is it how longdoes this thyroid resistance or
receptor desensitization lastfor? Does it last for six
months? Does it last for a year?Does it last for two years? 10
years into perpetuity? I don'tknow. I mean, if it that
literature is there? Pleaseshare it. I haven't seen it.
I think there's a couple keypoints that potentially might be

(24:09):
missed here. And the thing weneed to consider, or we might
ask for, somebody who's hadGraves disease or
hyperthyroidism, had theirthyroid gland removed, and
they've gone on thyroidmedication, especially t4 and
they haven't felt well, or theyhad persistently low T total, t3

(24:31):
or free t3 what we might have toask is, you know, maybe there's
still receptor desensitization,or a receptor, receptor
resistance. But maybe with theother thing we have to ask is,
what caused the Graves diseaseto begin with, right?
Is, is the thing that triggeredthis immune driven,

(24:53):
hyperthyroidism, this Gravesdisease, what triggered the
immune system to do it? Is therea stress trigger that. Still
there that at one pointactivated the immune system, and
because of that person's uniquegenetics and situation, it
triggered hyperthyroidism,Graves disease. But now that the

(25:14):
gland is gone, if that triggeris still there, could that same
trigger not only causehyperthyroidism in that patient,
but which wouldn't be possibleanymore because they don't have
a gland, but it could stillcontinue to trigger and activate
the immune response, and nowthat the immune that

(25:35):
hyperthyroid activity is gone,now we're seeing a person who's
because of this, the stressor,the trigger, is potentially
still there, or the immunesystem is still dysregulated.
Now they're having the oppositeeffect, where they can't convert
t4 to t3, is optimally becauseof the cell stress, inflammatory

(25:57):
response. We have to ask that question.
Just because we take out a glandor a radiated gland doesn't mean
we've addressed the cause. Itdoesn't mean that the peripheral
conversion of t4 to t3 isoptimal even in a hyperthyroid
state. I guess somebody couldsay, well, obviously they
converted t4 to t3 well beforebecause they were hyperthyroid

(26:20):
and they had lots of t3 butthere's other mechanisms at play
in that situation, Allostatic,just Allostatic regulatory
mechanisms that are at play totry and help manage that condition.
It doesn't mean the person isgoing to have optimal
intracellular conversion of t4to t3 there's going to be other

(26:40):
mechanisms, especially deodinaceone being highly upregulated in
that situation to do theconversion of t4 to t3 and it's
my belief that the reasonthere's a upregulation of
deiodinase one in thesehyperthyroid states is because
the half life of t4 is, youknow, somewhere around a week.

(27:01):
And too much t4 in circulation,too much free t4 being available
could also create a problem. Sothe half life of t3 to like 24
hours. So if we can convert t4to t3 and there's some cellular
resistance going on, that t3 isgoing to be metabolized much faster.
Let me see what else we gothere. Oh, the let's talk about

(27:24):
the last point I think thisperson made was that maybe I
shouldn't discount t3 let's keepin mind that I'm not discounting
t3 he's talking about how thisDr John low is that the other
extreme from from me, like Ibelieve that there's an adaptive

(27:45):
response going on where theperson has a reduced, not a
reduced, ability to convert t4to t3 and but that the body is
adaptively decreasing transportinto the cell, adaptively
decreasing Conversion of t4 tot3. Not that it is not that the

(28:05):
physiology is broken.
And what he's going on to say isthat this, Dr John low has done
a lot of work saying that thesecases where somebody is on t4
and they still have low t4 to t3conversion, their t3 is low.
Their free t3 is low. When thisguy would treat these patients,

(28:28):
he would do high dose t3 and getget some positive results. Well,
of course you would, and there'slots of people doing doing t3
mono therapy or doing high doset3 in conjunction with t4 or in
conjunction with their glandularhormone, and people get positive

(28:49):
signs and symptoms by taking t3there's no argument about that.
The issue is, does overloadingthe system with with t3
medication, does it changesymptoms? No, it can. Absolutely
it can change symptoms. Does itrestore thyroid homeostatic
regulation? In many cases, or insome cases, maybe, maybe the

(29:10):
person is truly broken, and theycan't make thyroid hormone, they
can't convert it. The receptorsare broken. The transport
mechanism is broken. Maybe, Iguess somebody can make that
argument. I don't necessarilybelieve that to be the case,
because I get patients that havebeen on high dose t3 medication

(29:30):
and still struggling withhypothyroid symptoms and hyper
thyroid symptoms, in many cases.And coming off trying to reduce
that dose as they try and reducethe dose, and especially if
they've been on higher dose, t3for an extended period of time,
it is, it is difficult and veryuncomfortable for them to try

(29:50):
and reduce the dose. They'realmost like an addict trying to
get off, you know, whatever drugit is that they're addicted to,
because it can be thatuncomfortable and that difficult
to go from high dose t3 whereyou're forcing the physiology
and suppressing the amount of t4that's in the system and
becoming highly dependent t3only, and then try to tighter it

(30:14):
down when you don't have athyroid gland that's been
working in a while, or don'thave a thyroid gland at all, or
you don't have a sufficientthyroid t4 via your thyroid
hormone replacement therapythat's available as the t3 goes
down, because as the t3 goesdown, you need to be able to
have some circulating t4 to Beable to convert to t3 and if you

(30:37):
just start tiring down t3 andyou don't have t4 in the
bloodstream, because if eitheryour glands gone, or the glands
been atrophied by taking thishigh dose t3 for a period of
time, you're not gonna feel goodright away. It's gonna be it has
to become like a really slowtighter and you'll often those
people are often gonna need t4as they go up.

(31:00):
But let's talk about the reasonswhy t3 might help somebody who's
got low total, low free t3 andpoor conversion. Well, t3 is
less tightly bound by thethyroid binding globulin. So
keep in mind that most of thethyroid hormones transported
throughout the body, bound to atransport protein because of

(31:23):
changes in pH and temperature.Typically, there may be some
other factors there that the thet3 becomes free of the binding
globulin, so gets essentiallythe binding globin is the Uber
and the hormone is essentiallythe passenger.
So when bound, hormone gets to atissue that needed needs it, and

(31:46):
it becomes free, then it's ableto get into cell. T3 is less
tightly bound, so it's easier toget t3 off of that binding
globule than it is t4 so ifthere's immune inflammatory
processes going on, t3 might beeasier to get into somebody's
cell. So they could feelpotentially better.
Once t3 gets into to the cellsand the transport mechanisms, it

(32:09):
does seem that the transportmechanisms, it's easier to get
t3 into the cell than t4 andthen once t3 is inside the cell,
it's already in its ready state,it doesn't have to go through
another step to can beconverted, and it can bind to
receptors at much higheraffinity than t4 is going to be
and you don't have this extra step.

(32:31):
So it can be helpful, but itdoesn't fix everybody, because
there's a lot of people thattake t3 and despite optimizing
their total t3 or their free t3with medication, still struggle
with signs and symptoms oftissue hypothyroidism and more,
doesn't necessarily restorethyroid physiology. Why? Because
the cells get to determine whatthe t3 state is inside the cell.

(32:55):
Many of them, some need t3 fromthe bloodstream only, and other
tissues take in t3 from thebloodstream, but also can manage
or adapt the amount of t3 in thecell via the D ID NASes, by
bringing t4 and determining howmuch of that t4 it needs to convert.
So it's not, it's it's not assimple as, hey, just give more

(33:16):
thyroid hormone as t3 and thiswill fix everything. Can it
change signs and symptoms? Absolutely.
The other thing we have to keepin mind is that it is going to
be dependent on the state of theindividual. If somebody is not
in a overly stressed state, andthey're in homeostasis, t4

(33:36):
should work, and t3 may makethem feel a little bit better,
but it should restore theirphysiology if they're in a
homeostatic regulation.
Because in a homeostatic state,the issue, the only issue, may
be that there's not enoughavailable t4 and especially if
they're fully replacing, what agland would have made with T

(33:57):
with the amount of t4 they'retaking, then they should provide
some additional t3 because ifthe if you're fully replacing
with the thyroid gland, wouldhave made from a t4 perspective,
essentially what you're doing isyou're shutting down the gland,
then you should probably givethe appropriate level of five to
10 micrograms of t3 as well.
The other thing I think that'simportant is, and I think it's

(34:20):
important for everybody, when wetalk about there's reduced t4 to
t3 conversion, or there's areduced transport, or there is,
there's a process going on. It'snot like the cell stops
converting t4 to t3 like, okay,the there's thyroid resistance
going on, so no t4 or t3 isgetting into a cell that's got,
there's where there'sinflammatory mechanisms or high

(34:43):
cortisol or anything else thatmay interfere with this thyroid receptor.
It's not on or off like that.It's not black and white. It's
shades of gray. There's there'sless transport, but not, no
transport. Okay, when we talkabout reduced conversion of T.
Four to t3 it's that thatthere's no conversion of t4, to

(35:05):
t3 it's there's a reducedconversion. When we think about
the net effect, when we saythere's an increased conversion
of t4, to T to reverse t3 or t3,to t2 it's not all or none. It's
it's a net.
So when we think about what'shappening net in the cell,
there's a net decreased level oft3 there's a net increased

(35:25):
conversion of t4 to reverse t3or a net increased deactivation
of t3 to t2 and by the way,we're not we don't measure t2 in
traditional laps, so just keepthat in mind.
So I think it's really importantto say, if you feel great on
whatever thyroid medicationyou're taking, t4 NP, thyroid

(35:45):
armor, t3 only great. I don'tcare if you feel great. I'm
happy for you, and I thinkwhatever you're doing is the
right thing to do.
But when it's not working, whenyou can't find the magic dose of
t4 so now you try adding some t3and it feels good for a bit, and
then it doesn't last. And thenyou try NDT, you know, np

(36:07):
thyroid, or armor, and it feelsbetter, but then it doesn't
last. And now you're adding,maybe you're adding t4 on top of
the armor, or you're adding t3on top of the NP thyroid, and
you're constantly searching forthe right dose, and you still
don't feel and function well.These are the people I'm trying
to speak out to. These are thepeople and that you need to

(36:28):
start to understand. There maybe another way to help you get
better by looking at what'sgoing on at the cell level
through this different model,this different hypothesis,
different lens, through theadaptive cell, through the
adaptive thyroid model and thecell danger response.
If, if this didn't work, Iprobably wouldn't. I wouldn't be
talking about it. And if itdidn't work, we wouldn't have so

(36:52):
many people resonating with thismodel and saying, Hey, I've
tried everything else. Let metry this idea, this concept,
this model, and seeing thepositive changes, the positive
results, the improvement ofsigns and symptoms and
measurables and the ability toreduce the amount of thyroid
medication they take withimproved conversion, and for

(37:13):
some people not even needing thethyroid medication in time at all.
So to the commenter, I want tothank you for raising these
points, you've helped push thisconversation forward, and I
respect that.
My goal for everybody isn't tobe right, it's to help people
think differently and giveclinicians a new lens when the

(37:34):
old one stops or isn't working.
If you're doing well, keepgoing, but if you're stuck,
maybe it's time to look at yourthyroid through a different
lens, until next time, keepasking better questions and take
care of your thyroid and overallphysiology you