Know a good T3 source in Argentina, or that can be ordered? Idealabs Tyronene is out of the question, didn't work (could have been a bunk product) so need an alternative.
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@HansAmato I get my Cynomel online from a Mexican pharmacy. Never had any issues. Idealabs has always been hit and miss for me, plus their droppers are crap
you can easily go from left to right in just 3 months
• 12mg reta
• 50mcg t3
• 10mg iranian anavar
that's it
retatrutide agonizes glp-1, gip, and glucagon receptors (gcgr) simultaneously. glp-1 and gip completely silence hypothalamic neuropeptide y (npy) hunger signaling and maximize insulin sensitivity, while hepatic gcgr activation forces continuous mitochondrial beta-oxidation and lipolysis melting visceral and subcutaneous fat on a brutal deficit with zero hunger pangs.
steep caloric deficits normally trigger adaptive thermogenesis by upregulating deiodinase type 3 (dio3), converting active thyroid hormone into inactive reverse t3 (rt3) to stall fat loss. 50mcg exogenous liothyronine (t3) bypasses hepatic deiodination entirely, saturating nuclear trα1/trβ1 receptors to upregulate uncoupling proteins (ucp1–3) and Na+/K+-atpase activity keeping basal metabolic rate redlined through the entire 12-week cut.
high-dose t3 and deep deficits are violently catabolic to skeletal muscle without androgenic shielding. 10mg oxandrolone (anavar) saturates muscle androgen receptors (ar), competitively antagonizes the glucocorticoid receptor (gr), and inhibits 11β-hsd1 to crush cortisol-driven proteolysis preserving 100% of myofibrillar tissue while stripping extracellular water and slashing shbg/tbg to amplify free t3 and androgen signaling.
IdeaLabs Tyronene liquid T3 only made my temperature go up from 37.1 celsius to 37.5 celsius
It didn't shed the last few kg of post-olanzapine abdominal fat I still have (lost most of it in late 2025 in 2 months by fasting and no new fat has grown since quitting olanzapine a year and half+ ago)
Even took high doses of like 60-240mcg
I assumed it'd directly boost calorie burning rate putting me in a constant deficit thus burning away the last post-olanzapine fat
PFS is fixable.
5ar requires nadph and 99% of you only have enough nadph to barely stay alive, not enough to kickstart stalled 5ar enzymes that downregulated over time from finasteride or dutasteride, and on top of that your mitochondrial complexes are inhibited too
most guys trapped in post-finasteride syndrome (pfs) think their androgen receptors or 5α-reductase (5ar) genes are permanently broken. they blast testosterone or dht derivatives and feel nothing because they are ignoring the rate-limiting bioenergetic cofactor that actually powers the enzyme: nicotinamide adenine dinucleotide phosphate (nadph).
finasteride and dutasteride are not simple competitive blockers. they are mechanism-based "suicide substrates" that require nadph to form an irreversible covalent nadp-dihydrofinasteride adduct locked inside the 5ar active site. when that adduct sits there for months, the cell tags the stalled enzyme complex for ubiquitin-proteasomal degradation and epigenetically hypermethylates the srd5a1, srd5a2, and srd5a3 gene promoters via dna methyltransferase (dnmt1), silencing new 5ar transcription.
once the drug clears, synthesizing and firing fresh 5α-reductase enzymes to reduce testosterone into dht and progesterone into 5α-dihydroprogesterone (the mandatory precursor to allopregnanolone) is strictly dependent on high intracellular nadph concentration.
5ar is an endoplasmic reticulum membrane-bound oxidoreductase that follows an ordered bi-bi kinetic reaction: it literally cannot bind testosterone or progesterone until nadph binds to the enzyme first. furthermore, as demonstrated in human genital skin fibroblast studies, unbound 5ar is thermally unstable and rapidly degrades unless saturated with nadph, which conformational-locks and stabilizes the protein structure.
if you are metabolically stressed, inflamed, or hypothyroid, 90% of your cellular nadph pool is hijacked just to keep you alive. your cell prioritizes nadph for glutathione reductase (to regenerate reduced glutathione and stop ferroptosis) and thioredoxin reductase. when oxidative stress is high, the cell starves "non-essential" steroidogenic enzymes like 5ar and 3α-hsd of nadph to save the cell from dying.
worse, finasteride and dutasteride directly sabotage mitochondrial electron transport chain complexes i, iii, and iv. stripping the brain and peripheral tissues of dht and allopregnanolone uncouples the mitochondria-associated er membrane (mam), causes cardiolipin peroxidation, and spikes mitochondrial reactive oxygen species (ros).
this creates a vicious trap:
1. inhibited mitochondrial complexes leak massive ros and stall the tricarboxylic acid (tca) cycle.
2. the cell drains its remaining nadph pool trying to neutralize that mitochondrial ros via glutathione peroxidase.
3. intracellular nad+ drops and nadph oxidase (nox) becomes hyperactive, burning through your remaining nadph to create even more superoxide radicals.
4. starved of its mandatory nadph cofactor, newly transcribed 5ar enzymes immediately misfold and degrade, leaving local tissue dht and brain allopregnanolone at zero even years after quitting the pill.
how to flood the cell with nadph, repair mitochondrial complexes, and force 5ar reactivation:
1. turbocharge the pentose phosphate pathway (ppp) via t3 and thiamine (b1)
over 60% of cytosolic nadph is generated by glucose-6-phosphate dehydrogenase (g6pd), the rate-limiting enzyme of the pentose phosphate pathway. g6pd expression is directly controlled by nuclear thyroid hormone receptors (trβ1). dosing exogenous t3 alongside high-dose lipophilic thiamine (benfotiamine or ttfd, which powers transketolase in the non-oxidative ppp branch) and riboflavin (b2) forces glucose through g6pd to flood the cytosol with fresh nadph.
2. restore mitochondrial complexes and nicotinamide nucleotide transhydrogenase (nnt)
inside the mitochondria, nadph is generated by isocitrate dehydrogenase 2 (idh2), malic enzyme, and nicotinamide nucleotide transhydrogenase (nnt), which uses the inner mitochondrial membrane proton gradient to convert nadh into nadph. deploying ss-31 (elamipretide) binds cardiolipin to seal electron transport chain complexes i-iv, restoring the proton motive force so nnt can pump out mitochondrial nadph while stopping the ros leak that was draining your cytosolic nadph pool.
3. unlock epigenetic 5ar silencing and mam calcium flux with fluvoxamine + butyrate
because chronic 5ar blockade hypermethylates srd5a promoters, adding a histone deacetylase (hdac) inhibitor like sodium butyrate loosens chromatin so the gene can be read again. simultaneously, low-dose fluvoxamine agonizes mam sigma-1 receptors (sig-1r) to restore er-to-mitochondria calcium flux (activating pyruvate dehydrogenase and idh2) while allosterically stimulating 3α-hsd, which also requires nadph to convert 5α-dhp into allopregnanolone and reboot gabaa receptor sensitivity.
4. bypass the glutathione sink with nacet or im glutathione
instead of forcing your depleted nadph stores to work overtime reducing oxidized glutathione (gssg back to gsh), supplying exogenous n-acetylcysteine ethyl ester (nacet) or intramuscular glutathione directly neutralizes lipid peroxides, freeing up 100% of your newly synthesized nadph to bind, stabilize, and fire 5α-reductase.
@Allextreme_PSSD@drnocopes He said that supposedly fixes PSSD?
I've used both of them from IdeaLabs and they did nothing, yeah
I have post-antipsychotic syndrome though which is like PSSD but by antipsychotics but mine isn't as bad as those who get it by SSRIs
@ChalkyyWhite Well if you're at 100mcg per day and free T3 hasn't budged...
I'm a fan of Idealabs and used their thyroid products before with good effect, but I've also heard mixed stories.
I see this sentiment often, but for some reason I've always had a much better experience with T3+T4
My only explanation is that my body both 1) converts T4->T3 quite well 2) increases DIO3 activity fast and I waste a lot of endogenous T4 on rT3
It's mainly guessing from my level of knowledge, and obviously assumes some extra complexity.
The point is, I don't think T3 solo is universally the best move. Especially few years ago I remember people used to be more in favor of T3 combined with T4
I tried a lot of different products, i.e. all idealabs products, cynomel, cynoplus, and some black market pharma grade ones (hopefully).
Always had the best experience with tyromix (1:2 T3 to T4)
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T3 is definitely over supplemented and mostly used as a band aid (as seems to be common these days). People know higher t3 is good so instead of improving their own thyroid they shut it down and just supplement.
One could argue this what people do with TRT so how is it any different. Imo it’s not the same thing.
Thyroid is actually easier to optimise with basic habits that people just like to skip these days.
If you’re genuinely hypogonadal then all the optimisation in the world won’t save you.
If you just want to get to 1200+ T then optimisation won’t help you there either.
If you just want to blast some t3 that’s fine.
Just be honest with yourself that you could optimise a lot easier with lifestyle and everything else would improve.
Simply adding in t3 when you sleep, diet (macros and micros), training and circadian habits are terrible is not doing you any favours for long term progress.
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metabolicManiac@alitz_joe28150
@DocAbirHealth Very true. I just dont like the new trend of everyone taking t3 when there is a high chance they may not need it. I put myself into hyper thyroid experimenting with it and that was not a good feeling at all! If your on stimulants for adhd the combo is not s good idea.
@DocAbirHealth Very true. I just dont like the new trend of everyone taking t3 when there is a high chance they may not need it. I put myself into hyper thyroid experimenting with it and that was not a good feeling at all! If your on stimulants for adhd the combo is not s good idea.
What do you think about the idealabs product line ie something like TyroMix (6T4/3T3) supplemental during times of stress along w food? Where do you see the potential for supression rising, at which threshold if you can generalize at all?
Dont mean to take your time for free, but I think this def. also something for the substack, like an article about thyroid and supplementation.
Good morning
You have a job? Sorry to hear that. I’m still unemployed
Used the free time to whip up a little something pro metabolic
Greek yoghurt
Date syrup
Raw honey
Coconut condensed milk
Dark chocolate
Mixed frozen berries
And a few fat solubles too
Urolithin A & CoQ10
Astaxanthin
Lutein & Zeaxanthin
K2 MK4
Vitamin E
Now I have lots of energy, where will my day take me? Who knows?!
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