Experience with T2 ?

[Type-IIx]

Well I had read through the study posted earlier and it didn't relegate it's effectiveness to only hypothyroid rats

For example

Nonthyrotoxic prevention of diet-induced insulin resistance by 3,5-diiodo-L-thyronine in rats - PubMed

T2, by activating SIRT1, triggers a cascade of events resulting in improvement of the serum lipid profile, prevention of fat accumulation, and, finally, prevention of diet-induced insulin resistance.

pubmed.ncbi.nlm.nih.gov

"Male Wistar rats" Wistar rats are bred as a model of geriatric illness, they die very young and have all sorts of health problems. They cannot be used to extrapolate to bodybuilding. To be clear, rodent research can be extrapolated from if there is a mechanism that demonstrates an increase in RMR that could translate to a healthy human. So far I have not seen that.

I'm somewhat interested in micro2000's Abstract, want to read FT, particularly the methods and findings.

 

[Matsuo Munefusa]

Nobody just gonna buy the tabs and run like 4-5 of them a day?

 

[Type-IIx]

Nobody just gonna buy the tabs and run like 4-5 of them a day?

Someone can run it and report back with bloods so we can see thyroid function 4 weeks post. Though I certainly wouldn't advise it for a possible 4% increase in RMR. Sounds like a pretty bad idea to me. But YOLO!

 

[Type-IIx]

@Biggerp73 these guys are on https://www.professionalmuscle.com/forums/index.php?threads/t3-synergy-with-hgh-slin.165055/ dialing in T3+T4 with precision. Precision. And you're thinking of taking this experimental hormone that probably fucks up your TSH, T4 definitely, without any significant gains at unknown but very high dosages relative to T3/T4. Why exactly? So you're not plugged into the black market for thyroid hormones (but no big deal for the other shit, right?) It just makes no sense man. I appreciate what you have done with self-experimentation on the bodysculpting thread, but this is lunacy. Just throw that shit in the trash.

 

[Stewie]

That’s doesn’t negate the fact that some of the major medical institutions in the U.S. say T2 hormone is inert. There is no clinical value according to what I posted. Till you find more data the medical community sees the hormone as inert. I’m sure @Stewie would love to prove me wrong.

The simplicities to enlighten you on the active genomic and non-genomic modulations would fall upon deaf ears, ergo, provoke further entanglements with you. I'll pass on the -keyboard warrior pissing match-.

Apparently, you haven't sourced the proper information.

If curiosity piques your interest, plug this SMILES: N[C@@H
(Cc1cc(I)c(Oc2ccc(O)cc2)c(I)c1)C(O)=O into this projected physiochemical reaction ~ http://www.swissadme.ch/index.php

If by chance you'd like some tutoring on PK- ADME, don't hesitate to ask

To finalize this ridiculous dick measuring contest you're phishing to draw me into.

Here's your original "copy and paste" you posted.

Now, I'll ask you to contextualize
what's missing in your post (hint- citation). As well, how one (reader of your post) can certainly be persuaded -without- citations, or quotation marks to believe those are your words.

Take a step back and breathe and see how this can be contextualized.

Your copy and paste:

T2 has an affinity for the thyroid receptor that is roughly 2 orders of magnitude lower than that of the most active TH, T3. However, the results about T2's relative affinity may vary depending on the biochemical or physiological assay used and be influenced by the purity of the T2 preparation. Given its lower affinity for the TH receptors, most of the beneficial effects of T2 on metabolism reported to date have resulted from doses that were significantly higher than the dose of T3 that would be required for the same effect.

This is pulled from the citation you purportedly stated you copied and pasted it from. Now, take a peek at the second sentence in with the citation in place (8). Your inserted citation is missing.

T2 has an affinity for the thyroid receptor that is roughly 2 orders of magnitude lower than that of the most active TH, T3. However, the results about T2's relative affinity may vary depending on the biochemical or physiological assay used (8) and be influenced by the purity of the T2 preparation. Given its lower affinity for the TH receptors, most of the beneficial effects of T2 on metabolism reported to date have resulted from doses that were significantly higher than the dose of T3 that would be required for the same effect.

I wouldn't ask you to explain, as you'll continue to get emotionally disarranged. No need for that.

I was asked by the OP last week in a PM to generate my thoughts on the supplemental use of T2.

It's a mitochondrial uncoupler very similar to that of T3. If one browsers the above link I posted, you'll see the targets it's projected to hit.

Personally, I wouldn't use it.

 

[Stewie]

The simplicities to enlighten you on the active genomic and non-genomic modulations would fall upon deaf ears, ergo, provoke further entanglements with you. I'll pass on the -keyboard warrior pissing match-.

Apparently, you haven't sourced the proper information.

If curiosity piques your interest, plug this SMILES: N[C@@H
(Cc1cc(I)c(Oc2ccc(O)cc2)c(I)c1)C(O)=O into this projected physiochemical reaction ~ http://www.swissadme.ch/index.php

If by chance you'd like some tutoring on PK- ADME, don't hesitate to ask

To finalize this ridiculous dick measuring contest you're phishing to draw me into.

Here's your original "copy and paste" you posted.

Now, I'll ask you to contextualize
what's missing in your post (hint- citation). As well, how one (reader of your post) can certainly be persuaded -without- citations, or quotation marks to believe those are your words.

Take a step back and breathe and see how this can be contextualized.

Your copy and paste:





This is pulled from the citation you purportedly stated you copied and pasted it from. Now, take a peek at the second sentence in with the citation in place (8). Your inserted citation is missing.



I wouldn't ask you to explain, as you'll continue to get emotionally disarranged. No need for that.

I was asked by the OP last week in a PM to generate my thoughts on the supplemental use of T2.

It's a mitochondrial uncoupler very similar to that of T3. If one browsers the above link I posted, you'll see the targets it's projected to hit.

Personally, I wouldn't use it.

Late edit: Typographical error and lacking appropriate citation in question.

Talk to text erroneously used "phishing" rather than "fishing."

3,5-Diiodo-L-Thyronine (T2) in Dietary Supplements: What Are the Physiological Effects?

www.ncbi.nlm.nih.gov

 

[micro2000]

@Biggerp73 these guys are on https://www.professionalmuscle.com/forums/index.php?threads/t3-synergy-with-hgh-slin.165055/ dialing in T3+T4 with precision. Precision. And you're thinking of taking this experimental hormone that probably fucks up your TSH, T4 definitely, without any significant gains at unknown but very high dosages relative to T3/T4. Why exactly? So you're not plugged into the black market for thyroid hormones (but no big deal for the other shit, right?) It just makes no sense man. I appreciate what you have done with self-experimentation on the bodysculpting thread, but this is lunacy. Just throw that shit in the trash.

@Biggerp73 these guys are on https://www.professionalmuscle.com/forums/index.php?threads/t3-synergy-with-hgh-slin.165055/ dialing in T3+T4 with precision. Precision. And you're thinking of taking this experimental hormone that probably fucks up your TSH, T4 definitely, without any significant gains at unknown but very high dosages relative to T3/T4. Why exactly? So you're not plugged into the black market for thyroid hormones (but no big deal for the other shit, right?) It just makes no sense man. I appreciate what you have done with self-experimentation on the bodysculpting thread, but this is lunacy. Just throw that shit in the trash.

Not sure why the alterations in TSH and T4 would be a negative considering these same alterations would occur with T3 use. And the higher dose is related to it's lower potency to T3. No one claims that using test in gram quantities is bad when you can use methyltrienolone at single mg doses.

This whole board is filled with threads of people testing out Chinese produced peptides that have no more research than T2.

 

[Type-IIx]

Not sure why the alterations in TSH and T4 would be a negative considering these same alterations would occur with T3 use. And the higher dose is related to it's lower potency to T3. No one claims that using test in gram quantities is bad when you can use methyltrienolone at single mg doses.

This whole board is filled with threads of people testing out Chinese produced peptides that have no more research than T2.

Correlation-causation: an alteration in TSH and T4 does not imply a mechanism to effect an increase in RMR (in humans).

Risk-uncertainty: Whereas we do know T3's efficacy and mechanism of action to increase RMR in humans; we do not with T2's.

We don't know what's happening downstream with T2.

With T3, the user can run bloods and titrate accordingly because its dose-response (in humans) is reasonably well understood and the compound provably effective (risk-reward balance is possible); whereas T2 _may_ yield a 4% (!?!) RMR increase with 300mcg in euthyroid adults, dependent strongly on methods used in that paper.

If I could read the FT of your referenced abstract I'd feel better about even saying whether its alterations in TSH and T4 may even imply that T2 increases RMR in humans.

 

[Type-IIx]

Your final point (Chinese peptide experimentation) is inarguable. If the justification is that YOLO, I concede on that point. Just realize that the inability to balance risk and reward here is very real. Personally, I like to be able to at least balance risk-reward.

 

[Matsuo Munefusa]

Late edit: Typographical error and lacking appropriate citation in question.

Talk to text erroneously used "phishing" rather than "fishing."

3,5-Diiodo-L-Thyronine (T2) in Dietary Supplements: What Are the Physiological Effects?

www.ncbi.nlm.nih.gov

That’s kind of hilarious that phones opt for phishing over fishing

 

[Type-IIx]

The simplicities to enlighten you on the active genomic and non-genomic modulations would fall upon deaf ears, ergo, provoke further entanglements with you. I'll pass on the -keyboard warrior pissing match-.

Apparently, you haven't sourced the proper information.

If curiosity piques your interest, plug this SMILES: N[C@@H
(Cc1cc(I)c(Oc2ccc(O)cc2)c(I)c1)C(O)=O into this projected physiochemical reaction ~ http://www.swissadme.ch/index.php

If by chance you'd like some tutoring on PK- ADME, don't hesitate to ask

To finalize this ridiculous dick measuring contest you're phishing to draw me into.

Here's your original "copy and paste" you posted.

Now, I'll ask you to contextualize
what's missing in your post (hint- citation). As well, how one (reader of your post) can certainly be persuaded -without- citations, or quotation marks to believe those are your words.

Take a step back and breathe and see how this can be contextualized.

Your copy and paste:





This is pulled from the citation you purportedly stated you copied and pasted it from. Now, take a peek at the second sentence in with the citation in place (8). Your inserted citation is missing.



I wouldn't ask you to explain, as you'll continue to get emotionally disarranged. No need for that.

I was asked by the OP last week in a PM to generate my thoughts on the supplemental use of T2.

It's a mitochondrial uncoupler very similar to that of T3. If one browsers the above link I posted, you'll see the targets it's projected to hit.

Personally, I wouldn't use it.

It's clear to you that T2 is a mitochondrial uncoupler from SwissADME? You're a beast if that's clear to you.

I've read a good bit about T2, and from what I gather, I'd describe its potential for increasing RMR via the mitochondria like this:

T2 promotes activation including the respiratory chain involved in substrate oxidation while not primarily influencing reactions involved in the synthesis and export of ATP [1]. T2 promotes fatty acid-induced proton-leak, the components of which remain unknown [4]. Its effect is totally dependent on fatty acid presence [1].

Unlike T2, T3 is a potent mitochondrial uncoupler: it "regulates mitochondrial uncoupling by different mechanisms: (1) by sympathetic stimulation, (2) by increasing acylcarnitine production, thereby activating mitochondrial respiration/uncoupling, and (3) by directly stimulating the transcription of Ucp1 gene." [2]

T2 likely affects the kinetics of substrate oxidation by acting at complex IV (ETC) and the reaction block oxidizing Cyt-C [3]. T2 stimulates activity of the COX complex (subunit Va). T2 decreases COX efficiency (under conditions of low-energy utilization [ATP/ADP high]). Observed in vitro and only in hypothyroid rats, not in normal euthyroid ones [3].
_____
References:
[1] Lombardi A, Moreno M, de Lange P, Iossa S, Busiello RA and Goglia F (2015) Regulation of skeletal muscle mitochondrial activity by thyroid hormones: focus on the “old” triiodothyronine and the “emerging” 3,5-diiodothyronine. Front. Physiol. 6:237. doi: 10.3389/fphys.2015.00237
[2] Yau W.W., Singh B.K., Lesmana R., Zhou J., Sinha R.A., Wong K.A., Wu Y., Bay B.H., Sugii S., Sun L., et al. Thyroid hormone (T3) stimulates brown adipose tissue activation via mitochondrial biogenesis and MTOR-mediated mitophagy. Autophagy. 2019;15:131–150. doi: 10.1080/15548627.2018.1511263.
[3] Goglia, F., Silvestri, E., & Lanni, A. (2002). Thyroid hormones and mitochondria, 22(1), 17–32. doi:10.1023/a:1016056905347

 

[micro2000]

Correlation-causation: an alteration in TSH and T4 does not imply a mechanism to effect an increase in RMR (in humans).

Risk-uncertainty: Whereas we do know T3's efficacy and mechanism of action to increase RMR in humans; we do not with T2's.

We don't know what's happening downstream with T2.

With T3, the user can run bloods and titrate accordingly because its dose-response (in humans) is reasonably well understood and the compound provably effective (risk-reward balance is possible); whereas T2 _may_ yield a 4% (!?!) RMR increase with 300mcg in euthyroid adults, dependent strongly on methods used in that paper.

If I could read the FT of your referenced abstract I'd feel better about even saying whether its alterations in TSH and T4 may even imply that T2 increases RMR in humans.

Solid reasoning. I tried running the paper through sci hub but no luck.

Also from the abstract it says 4% decrease in body weight not 4% increase in RMR.

 

[Type-IIx]

Solid reasoning. I tried running the paper through sci hub but no luck.

Also from the abstract it says 4% decrease in body weight not 4% increase in RMR.

Exactly! I am optimistically assuming TDEE that resulted in body weight reduction is due entirely to RMR for the sake of argument, which is extremely unlikely, and that they used sensitive methods in measurement and statistical analysis. Like I've been saying, there is no evidence of any mechanism to effect an increase in RMR in healthy humans. I am being very open to it, but given the logic of taking a hormone that probably does nothing good and lots of things bad, I just think it's crazy to take this one. I won't bother trying to get this one since it's such a longshot for bodybuilding purposes unless someone just sends over the FT, and I will read it.

 

[Stewie]

It's clear to you that T2 is a mitochondrial uncoupler from SwissADME? You're a beast if that's clear to you.

I've read a good bit about T2, and from what I gather, I'd describe its potential for increasing RMR via the mitochondria like this:

T2 promotes activation including the respiratory chain involved in substrate oxidation while not primarily influencing reactions involved in the synthesis and export of ATP [1]. T2 promotes fatty acid-induced proton-leak, the components of which remain unknown [4]. Its effect is totally dependent on fatty acid presence [1].

Unlike T2, T3 is a potent mitochondrial uncoupler: it "regulates mitochondrial uncoupling by different mechanisms: (1) by sympathetic stimulation, (2) by increasing acylcarnitine production, thereby activating mitochondrial respiration/uncoupling, and (3) by directly stimulating the transcription of Ucp1 gene." [2]

T2 likely affects the kinetics of substrate oxidation by acting at complex IV (ETC) and the reaction block oxidizing Cyt-C [3]. T2 stimulates activity of the COX complex (subunit Va). T2 decreases COX efficiency (under conditions of low-energy utilization [ATP/ADP high]). Observed in vitro and only in hypothyroid rats, not in normal euthyroid ones [3].
_____
References:
[1] Lombardi A, Moreno M, de Lange P, Iossa S, Busiello RA and Goglia F (2015) Regulation of skeletal muscle mitochondrial activity by thyroid hormones: focus on the “old” triiodothyronine and the “emerging” 3,5-diiodothyronine. Front. Physiol. 6:237. doi: 10.3389/fphys.2015.00237
[2] Yau W.W., Singh B.K., Lesmana R., Zhou J., Sinha R.A., Wong K.A., Wu Y., Bay B.H., Sugii S., Sun L., et al. Thyroid hormone (T3) stimulates brown adipose tissue activation via mitochondrial biogenesis and MTOR-mediated mitophagy. Autophagy. 2019;15:131–150. doi: 10.1080/15548627.2018.1511263.
[3] Goglia, F., Silvestri, E., & Lanni, A. (2002). Thyroid hormones and mitochondria, 22(1), 17–32. doi:10.1023/a:1016056905347

The commentaries I brought forth of plugging in the SMILEs was due to the challenge, set forth by a particular member. In which you gracefully answered, T2 is not an inert hormone. The predicted pathways tell us it's an active hormone and not inert. Either be genomic or non-genomic, physiological responses have been described in several literatures. As you're aware.

However that may be, that's primarily why I shared the Canonical SMILEs along with SwissADME site.

Nevertheless.

That would be worthy of a noble prize if I had the capabilities to determine the pharmacodynamics via PK physicochemistry.

Although, one could, I suspect determine PD given the predicted distribution (a-D-me). Then determine if there's agonistic or antagonistic properties (partial or full of either) then plug-in the KEGG pathways to hypothesize a PD. Such as this particular KEGG mapping database- https://www.genome.jp/kegg/pathway.html


Fortunately, Lombardi A. et al, has done the legwork letting the world know T2 has the capacity to generate uncoupling of the mitochondrion. Yes, to a lesser degree than T3 and DNP


As it may be, I don't like airing too much of my personal life. Given so, this will be my last comment on here for awhile. My oldest daughter was Dx'd with oxyphilic cell carcinoma a few weeks ago. My focal points are going to be given towards her.

 

[Type-IIx]

The commentaries I brought forth of plugging in the SMILEs was due to the challenge, set forth by a particular member. In which you gracefully answered, T2 is not an inert hormone. The predicted pathways tell us it's an active hormone and not inert. Either be genomic or non-genomic, physiological responses have been described in several literatures. As you're aware.

However that may be, that's primarily why I shared the Canonical SMILEs along with SwissADME site.

Nevertheless.

That would be worthy of a noble prize if I had the capabilities to determine the pharmacodynamics via PK physicochemistry.

Although, one could, I suspect determine PD given the predicted distribution (a-D-me). Then determine if there's agonistic or antagonistic properties (partial or full of either) then plug-in the KEGG pathways to hypothesize a PD. Such as this particular KEGG mapping database- https://www.genome.jp/kegg/pathway.html


Fortunately, Lombardi A. et al, has done the legwork letting the world know T2 has the capacity to generate uncoupling of the mitochondrion. Yes, to a lesser degree than T3 and DNP


As it may be, I don't like airing too much of my personal life. Given so, this will be my last comment on here for awhile. My oldest daughter was Dx'd with oxyphilic cell carcinoma a few weeks ago. My focal points are going to be given towards her.

Oh my...... I am sorry to hear that man.

I was actually gonna run a quick (I think!!) PK ? by you. When you're back hit me up on PM here if you're in the right mind state.

Best wishes for you and your daughter.

 

[ripriot]

The simplicities to enlighten you on the active genomic and non-genomic modulations would fall upon deaf ears, ergo, provoke further entanglements with you. I'll pass on the -keyboard warrior pissing match-.

Apparently, you haven't sourced the proper information.

If curiosity piques your interest, plug this SMILES: N[C@@H
(Cc1cc(I)c(Oc2ccc(O)cc2)c(I)c1)C(O)=O into this projected physiochemical reaction ~ http://www.swissadme.ch/index.php

If by chance you'd like some tutoring on PK- ADME, don't hesitate to ask

To finalize this ridiculous dick measuring contest you're phishing to draw me into.

Here's your original "copy and paste" you posted.

Now, I'll ask you to contextualize
what's missing in your post (hint- citation). As well, how one (reader of your post) can certainly be persuaded -without- citations, or quotation marks to believe those are your words.

Take a step back and breathe and see how this can be contextualized.

Your copy and paste:





This is pulled from the citation you purportedly stated you copied and pasted it from. Now, take a peek at the second sentence in with the citation in place (8). Your inserted citation is missing.



I wouldn't ask you to explain, as you'll continue to get emotionally disarranged. No need for that.

I was asked by the OP last week in a PM to generate my thoughts on the supplemental use of T2.

It's a mitochondrial uncoupler very similar to that of T3. If one browsers the above link I posted, you'll see the targets it's projected to hit.

Personally, I wouldn't use it.

Not starting a dick measuring contest. Provoking you to get in the conversation. The best part of the thread is after you entered! Now I see why you were on the sidelines. My apologies. Thanks for the links.

I wish your family the best.

 

[Biggerp73]

The commentaries I brought forth of plugging in the SMILEs was due to the challenge, set forth by a particular member. In which you gracefully answered, T2 is not an inert hormone. The predicted pathways tell us it's an active hormone and not inert. Either be genomic or non-genomic, physiological responses have been described in several literatures. As you're aware.

However that may be, that's primarily why I shared the Canonical SMILEs along with SwissADME site.

Nevertheless.

That would be worthy of a noble prize if I had the capabilities to determine the pharmacodynamics via PK physicochemistry.

Although, one could, I suspect determine PD given the predicted distribution (a-D-me). Then determine if there's agonistic or antagonistic properties (partial or full of either) then plug-in the KEGG pathways to hypothesize a PD. Such as this particular KEGG mapping database- https://www.genome.jp/kegg/pathway.html


Fortunately, Lombardi A. et al, has done the legwork letting the world know T2 has the capacity to generate uncoupling of the mitochondrion. Yes, to a lesser degree than T3 and DNP


As it may be, I don't like airing too much of my personal life. Given so, this will be my last comment on here for awhile. My oldest daughter was Dx'd with oxyphilic cell carcinoma a few weeks ago. My focal points are going to be given towards her.

Stewie I am sorry to hear that.