T4 Conversion to T3 - A hidden cause of hypothyroid symptoms
Summary
TLDRLes patients thyroïdiens voient souvent leur état géré uniquement par des marqueurs, négligeant leurs symptômes réels. Le Dr Brad Bodle explique que la conversion de l'hormone thyroïdienne T4 en T3 est cruciale mais souvent mal comprise. Il aborde la complexité du cheminement thyroïdien et l'importance des enzymes déiodinases pour cette conversion. Même avec des niveaux normaux de TSH, une mauvaise conversion peut causer des symptômes d'hypothyroïdie. Des stratégies comme l'ajout de T3, la supplémentation en sélénium et la réduction de l'inflammation sont proposées pour améliorer la fonction thyroïdienne. Bodle encourage à consulter son médecin et à envisager des ajustements thérapeutiques.
Takeaways
- 😀 Les patients atteints de troubles thyroïdiens sont souvent mécontents des soins, car ils se basent uniquement sur les chiffres des marqueurs.
- 😀 Le cheminement thyroïdien est complexe et une défaillance à n'importe quelle étape peut entraîner des symptômes.
- 😀 La conversion de l'hormone thyroïdienne T4 en T3 est essentielle pour la fonction métabolique.
- 😀 Le cerveau régule les niveaux d'hormones thyroïdiennes en ajustant la production de TSH en fonction des besoins.
- 😀 La T4 produite par la thyroïde doit être convertie en T3, plus active, pour avoir un impact significatif sur le métabolisme.
- 😀 Les enzymes appelées désiodinases, principalement de type 2, sont responsables de cette conversion.
- 😀 Même avec des niveaux normaux de TSH, une mauvaise conversion de T4 en T3 peut entraîner des symptômes hypothyroïdiens.
- 😀 Les niveaux élevés de T4 ne garantissent pas une amélioration des symptômes en raison de la dégradation des désiodinases.
- 😀 La dégradation des désiodinases dans le cerveau est plus lente que dans le reste du corps, nécessitant des ajustements de traitement.
- 😀 Ajouter de la T3 à un traitement ou prendre des médicaments combinant T4 et T3 peut améliorer les symptômes.
- 😀 Les désiodinases étant basées sur le sélénium, des niveaux adéquats de ce minéral peuvent aider la conversion.
- 😀 Réduire l'inflammation et optimiser les nutriments peut améliorer la conversion de T4 en T3 et réduire les symptômes.
Q & A
Quel est le principal problème avec la gestion classique des patients atteints de la thyroïde?
-Le principal problème est que les médecins prennent des décisions basées uniquement sur quelques marqueurs, souvent en ignorant comment le patient se sent et fonctionne réellement.
Pourquoi est-il important de comprendre la conversion de la T4 en T3?
-Il est important car la T4 doit être convertie en T3 pour être métaboliquement active, et des problèmes à cette étape peuvent entraîner des symptômes hypothyroïdiens même si les autres marqueurs sont normaux.
Comment le cerveau régule-t-il la production d'hormones thyroïdiennes?
-Le cerveau surveille les niveaux d'hormones thyroïdiennes dans le sang et ajuste la quantité de TSH qu'il envoie à la glande thyroïde pour équilibrer les niveaux de T4 et T3.
Que se passe-t-il si la glande thyroïde ne produit pas suffisamment d'hormones?
-Le cerveau augmente la production de TSH pour stimuler la glande thyroïde à produire plus d'hormones thyroïdiennes.
Quel est le rôle des enzymes déiodinases dans la conversion des hormones thyroïdiennes?
-Les enzymes déiodinases, qui sont basées sur le sélénium, facilitent la conversion de la T4 en T3, la forme plus active métaboliquement.
Pourquoi une personne peut-elle avoir des symptômes hypothyroïdiens même avec des niveaux normaux de TSH?
-Une personne peut avoir des symptômes hypothyroïdiens si la conversion de la T4 en T3 est insuffisante, même si les niveaux globaux de TSH et de T4/T3 sont normaux.
Quelle est la différence entre la dégradation des enzymes déiodinases dans le cerveau et en périphérie?
-Les enzymes déiodinases dans le cerveau se dégradent plus lentement que celles en périphérie, ce qui signifie que moins de T4 est nécessaire pour normaliser les niveaux hormonaux dans le cerveau.
Quels facteurs peuvent influencer l'efficacité des enzymes de conversion des hormones thyroïdiennes?
-Les facteurs incluent la génétique, les carences en nutriments, et les niveaux d'inflammation.
Pourquoi la supplémentation en T3 peut-elle être bénéfique pour certains patients?
-La supplémentation en T3 peut contourner les problèmes de conversion de la T4 en T3, améliorant ainsi les symptômes hypothyroïdiens chez certains patients.
Quelles sont les recommandations pour soutenir la conversion de la T4 en T3?
-Il est recommandé d'évaluer les niveaux de T4 et de T3, de discuter avec un médecin de l'ajout de T3 si nécessaire, et de soutenir la conversion avec des nutriments comme le sélénium et en réduisant l'inflammation.
Outlines
🩺 La gestion des troubles thyroïdiens et l'importance de la conversion des hormones
Les patients atteints de troubles thyroïdiens sont souvent insatisfaits des soins reçus, car les médecins se basent uniquement sur quelques marqueurs. La vidéo aborde la complexité du système thyroïdien et la conversion de T4 en T3, une étape cruciale souvent négligée. Dr. Brad Bodle explique comment cette conversion impacte les symptômes hypothyroïdiens et invite les spectateurs à s'abonner pour plus de conseils naturels sur Hashimoto et l'hypothyroïdie.
🧠 Le rôle du cerveau dans la régulation des hormones thyroïdiennes
Le parcours des hormones thyroïdiennes commence dans le cerveau, qui surveille les niveaux de T4 et T3 dans le sang et ajuste la production de TSH par l'hypophyse. Le TSH est une commande que le cerveau envoie à la glande thyroïde pour réguler la production d'hormones. Dr. Brad Bodle utilise une métaphore pour expliquer cette relation et souligne que même si la production d'hormones est correcte, une mauvaise conversion de T4 en T3 peut toujours causer des symptômes hypothyroïdiens.
🔄 La conversion de T4 en T3 et ses défis
La conversion de T4 en T3 est essentielle car T3 est beaucoup plus actif métaboliquement. Cette conversion est médiée par des enzymes appelées désiodases, qui peuvent se dégrader plus rapidement avec des niveaux élevés de T4. Dr. Brad Bodle souligne que cette différence de conversion entre le cerveau et les cellules périphériques explique pourquoi certaines personnes ne ressentent pas d'amélioration même avec un traitement T4.
🧬 Les enzymes de conversion et leur influence sur la santé thyroïdienne
Les désiodases, en particulier de type 2, sont responsables de convertir T4 en T3 actif. Cependant, une dégradation rapide des enzymes peut limiter cette conversion. Dr. Brad Bodle explique que des niveaux élevés de T4 peuvent ne pas améliorer les symptômes en raison de la différence de dégradation entre les enzymes du cerveau et celles des cellules périphériques, ce qui justifie parfois un dosage plus élevé de T4 pour un meilleur bien-être.
💊 Stratégies pour soutenir la conversion de T4 en T3
Pour améliorer la conversion de T4 en T3, il est crucial de vérifier les niveaux de T3 et de T4 dans les analyses sanguines et de discuter avec son médecin de l'ajout possible de T3. Dr. Brad Bodle recommande également de contrôler les carences en sélénium et l'inflammation, qui peuvent affecter les enzymes de conversion. Il insiste sur l'importance d'une approche globale incluant la nutrition et le mode de vie pour optimiser la santé thyroïdienne.
📧 Contact et services personnalisés pour la santé thyroïdienne
Dr. Brad Bodle conclut en invitant les spectateurs à laisser leurs questions en commentaires et à le contacter pour un accompagnement personnalisé. Il explique les critères de sélection pour travailler avec lui et encourage les spectateurs à liker, s'abonner et partager la vidéo pour continuer à recevoir des conseils sur la gestion des troubles thyroïdiens. Il rappelle l'importance d'un suivi personnalisé pour améliorer la santé thyroïdienne.
Mindmap
Keywords
💡Thyroïde
💡TSH
💡Conversion T4 en T3
💡Déiodinases
💡Inflammation
💡Hypothyroïdie
💡Sélénium
💡Traitement combiné T4 et T3
💡Pituitaire
💡Symptômes d'hypothyroïdie
Highlights
Thyroid patients often experience dissatisfaction with care due to a focus on numerical markers rather than patient symptoms and feelings.
The thyroid pathway is complex, and issues at any step can lead to symptoms, emphasizing the importance of T4 to T3 conversion.
Understanding the thyroid pathway involves recognizing the brain's role in monitoring and adjusting thyroid hormone levels via TSH.
TSH is not a thyroid hormone; it's produced by the pituitary gland and acts as a signal to the thyroid gland to produce hormones.
The brain adjusts TSH levels based on the thyroid hormone output, creating an inverse relationship.
Thyroid hormone primarily comes in the form of T4, which needs to be converted into the more active T3 for greater impact.
Deiodinases, selenium-based enzymes, facilitate the conversion of T4 into T3 or the inactive reverse T3.
Type 2 deiodinase is crucial for converting T4 into active T3, but its efficiency can degrade over time with higher T4 levels.
There's a difference in the degradation speed of type 2 deiodinase in the brain versus the periphery, affecting hormone levels.
Higher T4 medication dosages can help some patients feel better due to differences in enzyme processing power.
Lab tests can indicate the need for additional T3 support, especially if free T3 levels are low despite normal TSH.
Research shows no difference in outcomes or increased risk between T4 therapy and T4 and T3 combo therapy.
Supporting conversion pathways can involve assessing T4 and T3 levels and potentially adding T3 medication.
Selenium supplementation can help with conversion, but it's essential to find the right dosage to avoid problems.
Inflammation can affect conversion enzymes, and addressing its sources can help improve thyroid function.
Dr. Brad Bodle offers one-on-one consultations for those seeking to address the root cause of thyroid issues.
Transcripts
- Thyroid patients typically have their condition managed
by their doctor looking at a select few markers
and making decisions about their health
based on the numbers alone.
This often ignores how you the patient feels and functions
and has led to widespread dissatisfaction
with thyroid care in general.
The problem with this approach
is that our thyroid pathway is complex and nuanced
and a breakdown at any step along the way
has the potential to lead to symptoms.
That's why in today's video,
we're gonna talk about thyroid hormone conversion
or the conversion of T4 into T3.
We'll discuss where it fits
in the thyroid pathway as a whole,
how conversion works
and also strategies that we can use
to help support this critical step of our thyroid pathway.
Hey guys, Dr. Brad Bodle here
and as always, thank you for joining me.
If you've been enjoying the content,
don't forget to subscribe to the channel
and also click on the bell icon.
That way you can continue to learn
about the best natural strategies that you can use
to help support your Hashimoto's and hypothyroid symptoms.
But let's jump right into things today
and start off by reviewing our thyroid pathway
and understanding where T4 to T3 conversion fits in
with the larger picture.
Now, as many of you already know,
our thyroid physiology doesn't necessarily start
with the thyroid gland itself.
It starts with our brain.
Our brain is constantly monitoring our bloodstream
and determining whether we have enough thyroid hormone
available for all of our cells.
If the levels of our thyroid hormone, T4 and T3
are either too high or too low,
the brain is going to make adjustments
in the amount of TSH that it sends out to the thyroid gland.
Again, I know this is something
that many of you are aware of,
but although TSH is part of our thyroid pathway,
it's not actually a thyroid hormone,
or it's not being produced by the thyroid gland.
It's produced by the pituitary gland in our brain.
And the way that I like to think about it
is the brain is kinda like the boss of a company.
And the thyroid gland is like a worker.
TSH is an order form for how much product that worker
or the thyroid gland needs to produce.
So, to simplify things down a little bit,
let's say it's the first day of the week,
and based on all of the internal and external factors
that are affecting the body,
the brain has determined that we need five units
of thyroid hormone.
To make sure that that amount is produced,
it writes up an order form in the form of TSH
and sends it down to the thyroid gland.
And if everything is working properly,
the thyroid gland receives that TSH and says,
oh, order is for five units today,
so I'm going to make five units.
What then happens is just like any boss,
the brain is going to monitor the thyroid's output.
And if it produces the proper amount of thyroid hormone
that is requested by TSH,
then the brain is going to say,
great, I don't need to make any changes
to the order form for tomorrow.
However, let's say for whatever reason,
the thyroid gland doesn't produce five.
Instead it only produces four.
Well on the following day, the brain is going to see that
and it's going to say, I asked for five yesterday,
and now we're behind our order for today.
So instead of requesting five today,
I'm going to need to request six.
And it does that by increasing the amount on the order form
or increasing TSH.
My point here is that in general,
there's going to be an inverse relationship
between the amount of thyroid hormone that's produced
and the release of TSH.
If we have low quantities of thyroid hormone
that's being released from the thyroid gland,
then TSH is going to go up
to try to stimulate more thyroid hormone release.
But as I alluded to in the intro of this video,
the interaction and relationship
between the brain and the thyroid gland
and the management of our TSH levels,
aren't the only important part of our thyroid pathway.
And there's other steps that we need to consider.
Once our thyroid gland is stimulated by TSH,
it produces thyroid hormone,
primarily in the form of T4
and a little bit of T3
and releases that into the bloodstream.
T4 is a much less metabolically active
and must be converted into T3
to have the greatest impact on our physiology.
As T3 is three to four times more potent than T4.
This conversion step is mediated by a group of enzymes
found in our peripheral cells called deiodinases.
But here's the thing,
even though our thyroid gland
might be making the right amount of thyroid hormone
and therefore our brain is observing that
and producing normal amounts of TSH,
if we're not converting T4 into the more active T3,
then we can still have hypothyroid symptoms.
And I wanna say that one more time,
just so we're clear.
So, even though the thyroid gland
is producing the proper amount of thyroid hormone,
so the total quantity of T4 and T3 together
is exactly what the brain requested,
therefore, TSH is still normal
and no changes are required there,
we can still have low thyroid symptoms
because there's an imbalance
or the ratio between T4 and T3 is off.
We're not doing a good job of converting that T4 into T3,
and therefore we have less metabolic activity
and low thyroid symptoms.
So just because the amount is right
and the TSH is normal,
doesn't mean that we're properly utilizing
the thyroid hormone that's available.
And I think I've used this example before,
but if we are gonna drive somewhere in our car,
we have to take all the necessary steps
from start to finish,
to be able to drive somewhere.
We have to get in the car,
buckle in, adjust our mirrors,
turn the ignition,
and then we have to step on the gas.
But none of those steps matter
unless we do that final step of stepping on the gas pedal.
And that's kind of where thyroid conversion
fits into our puzzle.
Yeah, we can do all the other steps correctly,
release TSH,
stimulate the thyroid gland,
produce thyroid hormone,
but if we don't convert T4 into the more active T3,
then we're really not stepping on the gas pedal.
And therefore, when we don't do that,
we can see slowing of the metabolic function
of every cell in the body.
So now that we know where the T4 to T3 conversion
fits in the larger picture,
let's look at the conversion step itself
and how it actually works.
As we already said,
it's very possible for someone to have a normal TSH value,
but still be experiencing hypothyroid symptoms.
And although it isn't always clear why this occurs,
problems with conversion is one definite possibility.
Again, as we said before,
conversion is mediated by a group of enzymes
called deiodinases.
These enzymes are selenium based
and there's three main kinds
that help to convert T4 into the active version of T3
or the inactive version of T3 called reverse T3.
This ability to modulate the amount
of active thyroid hormone at the level of the cell
acts as an additional check and protective measure
to make sure we don't get too hyper or hypo.
But when it comes to converting T4
into the active version of T3,
for most of our cells,
the type 2 deiodinase is the one that facilitates this.
Interestingly enough,
something that we need to keep
in the back of our mind for clinical purposes
is that the type 2 deiodinases in our periphery
is subject to degradation just like any other enzyme.
And the more that you use it,
the faster it degrades.
This means that if you're already on a T4 medication,
but continuing to have hypothyroid symptoms,
you might think that it's a good idea
to increase the amount of medication you're taking.
However, research has shown that higher levels of T4
does not always equate to improvements
in thyroid function and symptoms.
And this is likely due to the fact
that the T4 conversion into T3
that is mediated by this type 2 deiodinase
decreases over time with increasing levels of T4.
And to make things even more complicated,
there seems to be a difference in the speed of degradation
when it comes to the type 2 deiodinase in our brain
and the type 2 deiodinases in the periphery.
And the one in the periphery tends to degrade faster.
Why is this important?
Well, if the enzymes in our brain aren't degrading as fast,
that means they can handle higher levels of T4.
This means that clinically speaking,
less T4 is needed to normalize
the amount of hormone in our brain
and therefore normalize TSH
and more hormone is needed in our periphery
to normalize the conversion of T4 into T3.
And this is why people can feel better
with a higher dosage of T4 medication,
and a slightly suppressed TSH.
It's because there's a difference
in the processing power of our conversion enzymes
between our brain and all of our other cells.
So to summarize our conversion step real quickly,
our thyroid primarily produces T4,
which has to be converted
into the more metabolically active T3.
This is mediated by selenoproteins called deiodinases
and we have three different kinds.
The primary kind that is most active for most of our cells
is the type 2 deiodinase.
This enzyme turns T4 into the active version of T3
rather than the inactive version of reverse T3.
And although our type 2 deiodinase
is essential to our thyroid physiology,
it can only do so much.
And increased levels of T4,
whether natural production or from medication
eventually has a limit
in terms of how much can be converted into T3.
But we need to keep in mind that there's a difference
between the conversion rate in our periphery
and the conversion in our brain,
and therefore less T4 is needed to normalize the levels
and therefore normalized TSH in our brain
than is needed to produce adequate amounts of T3
for all the cells in our body.
This is one of the big reasons
why people can have such a different experience
in terms of how they feel
compared to what we're seeing on the lab panel.
But now that we know that conversion
is such an important part of our thyroid physiology,
and without it, we can notice big increases in symptoms,
how can we support this area of our health,
even if our numbers are normal,
or if we haven't responded to T4 medication?
Well, the first thing that we wanna do
is take a look at our labs
and see if there's any indication
that we could benefit from some additional T3 support.
The research shows us that in people
who are undergoing thyroid treatment
with T4 medication alone,
that about 15% of those people also have low free T3 levels.
Even if your T3 levels are normal,
you could still be having an issue with conversion
if your T4 levels are at the upper end of the lab range
and the T3 levels are trending towards the lower end.
So, if any of these scenarios sound familiar to you,
then it may be worth it to talk to your doctor
about adding T3 to your regimen
or choosing a medication that includes both T4 and T3.
Now, there is research out there
that says there's no difference in outcomes
when we compare T4 therapy to T4 and T3 combo therapy.
So don't be surprised if your doctor is skeptical.
However, that same research shows that there's no difference
in risk factors or negative outcomes.
So I think if someone is struggling
with one type of therapy,
then it's reasonable to explore other options,
especially if there's no increased risk.
In fact, recently there was a 17 year longitudinal study
that compared people undergoing T4 therapy
and combo T3, T4 therapy,
and in the end, there was no difference
or increased risk for cardiovascular disease,
atrial fibrillation,
or fractures between the two groups.
And the reason why I wanted to point this out
is just like I said,
if we're undergoing a particular treatment plan
or care plan, and we're not seeing results,
then I think it makes sense to adjust and change.
And if there doesn't seem to be any associated risk,
then I think it's at least worthwhile to experiment
and see how we respond.
Typically, if someone is having a problem with conversion,
then once they're provided with the T3 medication,
which bypasses that conversion step,
they'll usually feel much better,
but it's important to not stop here
and only focus on medication.
Our conversion enzymes are influenced by genetics,
nutrient deficiencies,
and very heavily by levels of inflammation
and its important to address each one of these factors
if possible.
Although it's obviously more difficult
to modify our genetics,
things like nutrient status and inflammation
are much more under our control.
While not immediately beneficial for everyone,
our deiodinases are selenium based
and low levels of selenium
can cause problems with conversion.
While we certainly don't wanna take too much selenium
as that can also cause problems,
taking about 200 micrograms of selenium,
preferably selenomethionine
rather than an inorganic form
has been shown to be beneficial
for a period of six to nine months.
When it comes to inflammation,
we always wanna ask ourselves,
where is the inflammation coming from?
If we can answer that question,
then we can do some things to support that area of the body,
as well as potentially take some anti-inflammatory compounds
to help reduce the inflammatory load in the short term.
So if you've been having hypothyroid-like symptoms
with normal labs,
or if you've been recommended T4 medications,
and haven't seen improvements,
then you may wanna consider
supporting your conversion pathways.
This can be done by first assessing
both your T4 and T3 levels on your labs,
then talking to your doctor
about potentially getting some T3 medication
or by doing things to directly support
our conversion pathways and enzymes.
Hopefully by addressing both of these key factors,
you'll be able to optimize your function overall
and finally see improvements.
But that is it for today you guys.
I hope you enjoyed the video
and if you have any questions,
leave them for me in the comments below.
Of course, if you are interested
in working with me one-on-one,
you can send me an email
and my staff will reach out to you with an application
so you can apply
and see if you're a good fit
to work with me and my program.
We don't work with everyone,
but for those of you who are looking to get
to the root cause of your problem
and make big changes
when it comes to nutrition and lifestyle,
we know that we can help you to identify those key factors
that you need to work on to feel your best.
But as always you guys,
thank you so much for watching
and hanging with me until the end of the video.
If you have any questions,
you can always reach out on social media
and don't forget to like, subscribe and share.
My name is Dr. Brad Bodle.
I hope you guys have a great week
and I'll see you next Thursday.
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