I am interested In supplementing with t3 In the future with my next cycle, I have read different articles online regarding dosages, and side effects, however I can’t find a clear cut answer if it will likely permanently shut down your thyroid after use or not, lots of contradicting info. I plan on only using 25mcg if I do go ahead with it, and only for 4 weeks. Has anyone here used it without a prescription? If there is a high risk of permanent shutdown I am not going to add it in the mix.
Highly unlikely that you’d be permanently shut down from using it in the way most people do. The real question is why will you be doing this? Because unless the answer is “I’m competing” it’s not going to be a good enough reason to mess with your thyroid. Looooots of shit can go wrong when you go down that road.
No real risk of permanent shutdown. Also no guarantee of results. I assume that you want to take T3 for weight loss, but I have never found it to be very effective for that. I’ve used doses up to 75mg and not really seen any difference. And before anyone is a smartass, it was pharma grade, lol.
Thyroid hormone stacks with your natural production. There is no shutdown at all.
It’s also incredibly catabolic. Take too much and it will break down your muscle. It’s powerful enough to catabolize muscle when in a heavy steroid cycle. Consider taking clen instead if you’re doing it for fat loss.
I tried Clen for a couple weeks before and could not handle the sides, I was getting mad anxiety, jitters and kept dropping things even at a low dose. I’m already down to ~11% body fat, just wanted something to help get down to single digits. The more I look into it the less interested I am though now.
You pretty much have to start at 5mcg and taper up. But yeah. I’ve heard it’s pretty shitty for sides. I have some, but am afraid to take it, Lol.
Best bet is probably test + anavar or winsterol + masteron / proviron with a small calorie defecit if you want to be on cycle. Otherwise, just calorie defecit with caffeine and synephrine.
Eat less, combined with some low dose test and medium dose mast or anavar. Way easier than messing with your thyroid. Unless you’re competing it makes no sense to take those kind of risks.
PS I’m pretty fat right now (stress really is the ultimate killer) so me saying “eat less” wasn’t meant to be snarky. It’s just really the only way. I’m doing it right now and it sucks, but at least I’m not feeling like I lost my mind because I loaded up on crazy drugs to try to do what I know can be done with a plan and willpower. If you’re at 11% you have discipline. Use that to get to 9%. You have the power within you. Don’t doubt your vibe.
Thanks for the replies guys, I’m going to go with the advice and keep the thyroid meds out of my cycle. Recovery after is hard enough sometimes without throwing my thyroid out of whack lol
just for the reader, this is mcg or micrograms, not mg.
Way 2 go. Always nice when there is a positive outcome from these threads. If you can get to 11% then you can get to 8% without using thyroid hormones or other accessories. Question is how much muscle you want to carry at 8% or x% BF. Taking T3 will not help you carry more muscle at a lower BF% (I don’t agree with Dan Duchaine here). I’ve had an RT3 of 26 and an RT3 of 7 at the same BF and FFMI. But that’s my body.
Sorry yes micrograms. Bulking=fat fingers=typos.
IMO, having blood work showing you need it, is justification, but I’m this context that is very unlikely. I have the blood work showing I likely need it, but am tapering off of it because I just don’t want to run it forever. I think with the body recomp, that my thyroid will improve.
Totally agree. If it’s medically justified then carry on. But when it’s just about our own vanity—and that’s what 99% of steroid users are in it for, myself included—it’s simply not worth the risk.
Horrifying read and who really knows what he was on and for how long. T3/Clen/Tren.
At this point, the patient was back to his baseline physical health. Upon interviewing the patient after his recovery, he specifically reported taking: clenbuterol 1.5 mg daily, triiodothyronine 75 mcg/day, testosterone enanthate 500 mg weekly, and trenbolone (an anabolic steroid) 400 mg weekly for the past six months.
Holy balls that is a lot of clen. A lot for most people is 100-150 mcg. This dude was taking 1,500 mcg.
That’s why I try to correct people’s units on here. Someone writes T3 in mg and who knows will read that and try it out.
With that stack of drugs I doubt I would be able to sleep. It sounds absolutely horrible. It would feel like what I imagine being on meth would be like, while stuck in a sweat lodge.
It is a lot for sure but I think it’s more of a testament to how fast beta adrenergic receptors desensitize. Going from 20 mcg to 1.2 mg in 6 months is a 60 fold increase. If you’re looking at the average clen user they always start at 20 and go to 120 mcg in about 6-10 weeks. So in 6 months I would expect him to be at like 300-500 mcg if the increase is linear but it isn’t. Receptors desensitize exponentially ( B = S - (S-B0)e^-kt ) which means that you need to increase the dose more and more. That’s how you end up with 1.2 mg a day and you have the same side effects as you had all along. They desensitize too.
I gotta point out 2 things here.
Taking Clen is retarded. Taking Clen for more than a few weeks is beyond retarded. Beta-sympatomimetics have a direkt cardiotoxicity and decrease the oxygen supply (here: ratio) to the heart during exercise. They induce irreversible changes in the myocard. That this guy didn’t drop dead is a wonder.
The desensitization effect is linked to point 1. It’s a survival mechanism that prevents the heart from being under constant adrenergic stimulation which is exactly what you do with Clen (half life!).
IMO desensitization/tolerance is a remarkable process.
I read two case studies with Z-Substances and there is a guy who went from 10 mg/day to grams per day in a few weeks (more than a hundred pills a day). (In this case it’s not a simple desensitization but it is still a tolerance build up that is extremely fast.)
Desensitization is a process that is worth getting to know too. For example receptors can send signals into the nucleus after they are encapsulated in endocytosis. And that’s just one of the spooky things going on during this complex process. Good work has been done on the desensitization of beta-adrenergic receptors and u-opioid-receptors for people who want to look it up.
Thanks for sharing these points and good to read your points and the discussion of the paper above multiple times. Running clen (by itself for vanity reasons) and combining it with T3 (and then adding in AAS, tren no less) is really bad news. It’s amazing how much punishment the body can take. I used T3 (up to 50 mcg daily broken up 2x per day for a couple of years) as part of combination therapy (T4+T3).
One observation I made near the end of my usage was my pulse pressure started to widen 130/80 became 140/65. I also started having more involuntary jerks (increased myoclonic jerk) near/during bedtime. So even though RHR was low (60 bpm) and blood work showed peak serum T3 in range, I was still experiencing systemic effects that were subtle. Combine that with CNS effects of supraphysiogic dosage of Testosterone and you are asking for trouble. All without additional effect of something like clen.
The problem with T3 use is you never see tissue level impact of T3 use, only blood level. Although I understood this before I started use it, I didn’t fully appreciate the negative consequence it could have. You won’t get this disclaimer on all the internet sites pushing T3 or combo therapy for hypothyroidism. Running T3 by itself or in combination with T4 is bypassing the body’s safety valve in the peripheral tissue (the heart being of those tissues!).
I wish people would read more and develop an appreciation for impacts down the road before using these substances. But sometimes you aren’t really read to appreciate the impacts until something bad happens to you.
The use of PED is not only limited to professional athletes but has also expanded to non-athlete weightlifters and young adults in an attempt to achieve the portrayed socially accepted body image . A combination of PED is usually used with no oversight or recommendations from a health-care professional. In this case, our patient was found to have used a combination of anabolic steroids (trenbolone), triiodothyronine, testosterone, and clenbuterol. Given the patient’s rapid clinical improvement in parallel with a decrease in T3 serum levels, normal coronaries, absence of valvular pathology, no history of alcohol use or intravenous drug use, and a negative respiratory viral panel, other etiologies of acute decompensated HF were deemed less likely and no further cardiac evaluation and imaging was pursued.
The thyroid gland is a major regulator of the body’s basal metabolic rate and cardiovascular hemodynamics. Thyroxine (T4) and to a lesser extent T3 are produced in the thyroid and then released into the peripheral circulation. T4 is then converted by 5’ deiodinase enzyme in the peripheral tissue into the active T3 form which mediates most of the thyroid gland functions. T3 binds to the thyroid hormone receptor (THR) found on the cardiac myocytes and initiates a cascade of intracellular events and leads to direct modulation of membrane ion channels . These include an increased transcription of the alpha myosin gene and sarcoplasmic Ca-ATPase and increased expression of the membrane Na/K exchange pump, β adrenergic receptors, and voltage-gated potassium channels, all of which lead to increased cardiac contractility and heart rate. T3 also has a direct effect on peripheral vasculature. It decreases the arteriolar resistance and thus decreases the systemic vascular resistance. This is sensed by the kidneys which in turn activates the renin-angiotensin system that leads to an increase in the total blood volume and preload . The combined effects of the above-mentioned events lead to an increase in contractility and cardiac output. However, if such hemodynamic state is sustained chronically over a period of several months or years it can paradoxically lead to HF. This has been described by some experts in the literature as high output HF leading to dilated cardiomyopathy or tachycardia-induced HF in patients in which the heart function returned to normal after reversing the thyrotoxic state [6-7]. A proposed mechanism of cardiomyopathy in our patient’s case is increased cytosolic calcium due to decreased duration of the action potential and thus less calcium available for myocytic contraction leading to a decrease in EF .
Thyroid hormones are regulated by a negative feedback mechanism across the hypothalamic/pituitary/thyroid axis. Therefore, in patients taking exogenous T3, the body will sense a hyperthyroidism state and shut down the secretion of thyrotropin-releasing hormone, TSH, and T4 as seen in our case .
In the aforementioned case, the patient’s hypermetabolic state and cardiogenic shock can be attributed to exogenous triiodothyronine intake. It is evident that as the serum level of T3 decreased, the hemodynamic support requirements decreased, and the cardiac function improved simultaneously (Table (Table1).1). Given the short half-life of T3 and its high protein binding capacity in circulation; dialysis, plasmapheresis, and binding agents had no therapeutic role .
It is worth mentioning that clenbuterol is an agonist to β-1, β-2 and β-3 receptors . It is not FDA approved for medical use in the United States but has been reportedly used abroad as a bronchodilator in the setting of acute pulmonary exacerbations. β-3 agonism is responsible for enhancing the bodybuilder’s physique by increasing lipolysis and thus decreasing adipose tissue. Clenbuterol’s β-2 agonism has a double-edged effect. It induces the increase in muscle mass but also mediates most of the drug side effects including tachycardia, increased metabolic state, and hypotension. Therefore, toxicity with clenbuterol can mimic and portray septic-like picture leading physicians to treat empirically with intravenous fluids and vasopressors to achieve hemodynamic stability. However, treatment is dramatically different and such early interventions can be detrimental as vasopressors will further promote tachycardia and worsen the current cardiac state. Physicians should be very diligent when faced with such cases and have a wide differential in mind as the treatment of such toxicity is β-adrenergic antagonism. Esmolol, a short-acting easily titratable β-antagonist, is usually preferred . Consequently, clenbuterol and T3 likely potentiated each other’s effect leading to the patient’s near-fatal presentation.
Very nice review article covering finer points of HPTA/thyroid control theory. I am not dismissing use of T3 therapy in people who may really need it, just be very careful when you start adding in TRT, hCG, etc. Good luck discussing the details of Fig. 1 with your health care provider:
Theoretical and observed relationships between thyroid-stimulating hormone (TSH) and thyroid hormones. The central system provides an integrated solution to the location of the setpoint (settling point) of thyroid homeostasis, as determined by the various genetic, epigenetic, and allostatic parameters (27, 36). This includes monogenic factors such as polymorphic variants of receptors and transporters, changes in deiodinase activity or variations in T4 production efficiency, and environmental impacts, e.g., nutritional factors, body weight, body composition, age, and extends to diseases of the thyroid and other organs where severe disequilibria may arise and a “euthyroid” solution is not achieved (27, 36). (A) Schematic overview of main regulatory pathways and control loops in the hypothalamic–pituitary–thyroid regulation. External factors of influence include (1) obesity (hyperthyrotropinemia), (2) pregnancy (hCG-mediated suppression of TSH release and stimulation of T4 secretion), (3) non-thyroidal illness (NTI) (both pituitary and thyroid function down-regulated), and (4) certain psychiatric diseases (both pituitary and thyroid function stimulated). (B) The response of the thyroid to TSH by hormone release and corresponding feedback on pituitary TSH secretion produces a finite equilibrium solution, thereby defining interlocking TSH–FT4 pairs (setpoints). These are characteristic for each person and show only little variation unless disturbed by internal or external strain. In the event of progressive thyroid capacity stress, irrespective and independent of other influences, setpoints for FT4 and TSH translocate along a homeostatic pituitary response curve (isocline) unique for the individual. Hence, in the case of a diminished or exaggerated pituitary response the translocation moves along the thyroid isocline. The open circles indicate the expected variation (10% for FT4 and 30% for TSH) surrounding the individual setpoint. The percentiles for the isoclines of the response curves were derived from previous data in a healthy sample and the included area between the 2.5 and 97.5 percentiles represents the population’s reference range (37). © Influences additional to direct thyroid activity change (e.g., allostatic changes such as obesity, age, pregnancy, and NTI) may have dislocating effects on isoclines and setpoints. (D) Observed TSH–FT4 pairs (setpoints) in two individual patients (blue and green symbols) and the averaged group of 250 patients (black ellipse) followed long term on stable treatment conditions. Data ellipses indicate the 50 and 95% confidence limits for the setpoint. Levothyroxine dose was 100 μg/day, 1.5 µg/kg body weight for each of the individual patients, and 1.5 (SD 0.27) μg/kg for the whole group. Data are from a published longitudinal study (38). (E) Observed TSH–FT3 pairs depicted in the same patients as in (D) . FT3 concentrations vary with conversion efficiency and impact on the location of the TSH–FT4 setpoint (38).