• All new members please introduce your self here and welcome to the board:
    http://www.professionalmuscle.com/forums/showthread.php?t=259
Buy Needles And Syringes With No Prescription
M4B Store Banner
ddd
Riptropin Store banner
Generation X Bodybuilding Forum
Buy Needles And Syringes With No Prescription
Buy Needles And Syringes With No Prescription
Mysupps Store Banner
IP Gear Store Banner
Anabolic Hormones Store Banner
Ganabol Store Banner
Spend $100 and get bonus needles free at sterile syringes
Professional Muscle Store open now
LandmarkChem Email Banner
Medtech Store Banner
Bruce Labs Store banner
qtropin
Professional Muscle Store open now
over 5000 supplements on sale at professional muscle store
Buy Needles And Syringes With No Prescription
ESPECIL-2
Buy Needles And Syringes With No Prescription
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store

T3 synergy with HGH/Slin

thedorkyd1

Member
Registered
Newbies
Joined
Sep 5, 2018
Messages
56
There is a synergy that is spoken about quite regularly of the forums and that is the combo of HGH + Insulin + T3 and/or T4.

Im struggling to understand how t3 has any sort of synergy with these compounds. From my understanding, t3 reduces IGF-1 levels which is the whole reason we take GH in the first place, it makes us more insulin insensitive which requires higher doses of slin to accomplish the same job without the t3. Im currently taking 50mcg of T3 per day and initially hunger levels were through the roof. Around 4 days later they are lower than they were without it. My theory is that T3 has actually lowered IGF1.

The good things ive noticed is it does seem to counter a lot of the water retention issues on a big blast. I dropped 2kg almost immediately on 50mcg T3 per day and vascularity has definitely improved. And obviously fat loss comes on a lot quicker

Evaluating this situation I dont see where the synergy lies between T3 and Gh/slin. If anything it seems to hinder the combo of the 2. Would love to hear information from anyone on experiences or knowledge about this topic!
 

IronLion2

Well-known member
Registered
Joined
Nov 10, 2017
Messages
1,825
Thyroid hormones become essential for proper metabolism in some AAS users due the negative feedback loop of AR stimulation. There is no synergy they're just dependent on each other when abused in large quantities.
 

prodaf

Featured Member
Featured Member
Registered
Joined
Apr 23, 2011
Messages
869
More you use HGH, more you need T3/T4
 

thedorkyd1

Member
Registered
Newbies
Joined
Sep 5, 2018
Messages
56
More you use HGH, more you need T3/T4
Is that both? one or the other? I've tried T4 (100mcg) and now on T3 (50mcg) and I feel like the T4 was working better? More hunger, lower insulin dosages than the t3 for the same response etc.
 

IronLion2

Well-known member
Registered
Joined
Nov 10, 2017
Messages
1,825
@tren_plz is right the confirmation bias is getting unreal now of days.
 

Dtropin

Active member
Registered
Newbies
Joined
Oct 22, 2019
Messages
106
HGH increases T4 to T3 conversion.


Chronic supraphysiological levels of HGH in turn deplete both T4 and T3.
 

Gunsmith

Featured Member / Kilo Klub
Featured Member
Kilo Klub Member
Registered
Joined
Jul 30, 2006
Messages
7,550
HGH increases T4 to T3 conversion.


Chronic supraphysiological levels of HGH in turn deplete both T4 and T3.
Interesting , I wonder what the dose of HGH would be to "need" supplement T4.
 

Biggerp73

Well-known member
Registered
Joined
Jan 15, 2012
Messages
788
50mcg is way too much T3 for most people, in my opinion.

Try 12.5mcg instead. That's more like a replacement dose.

Going above that isn't smart, IMO, as T3 potentially negatively effects net protein synthesis when taken above replacement levels.
 

cmryan

Active member
Registered
Joined
Jul 23, 2018
Messages
557
50mcg is way too much T3 for most people, in my opinion.

Try 12.5mcg instead. That's more like a replacement dose.

Going above that isn't smart, IMO, as T3 potentially negatively effects net protein synthesis when taken above replacement levels.
I probably shouldn't speak for others but my replacement medication is 25mcg T3 and 50mcg T4. My endo has pondered raising my T4 a bit I'm good with both as is. Again, this is full replacement dosing. So, I think 50mcg is likely too much unless you intend to do that for very brief periods. 12.5mcg is a better starting point for sure. You don't notice it right away but i definitely is helpful and noticeable in less than 3 weeks and maybe less than 2.
 

Stewie

Featured Member / Verified Customer
Featured Member
Kilo Klub Member
Registered
Verified Customer
Joined
Feb 3, 2011
Messages
4,984
HGH increases T4 to T3 conversion.


Chronic supraphysiological levels of HGH in turn deplete both T4 and T3.
This is from the full literature. It's well established that GH increases peripheral conversion. We'll leave that aside.

What's your takeaway from the full literature?

The present study demonstrates that peripheral T4 metabolism is subject to distinct dose-dependent regulation by GH. Although the unblinded and non-randomized design demands a cautious interpretation, it extends and supports the conclusion from earlier studies that the most important impact of GH administration on thyroid function is a stimulation of extrathyroidal T4 to T3 conversion (Msller et al., 1992; Sat0 et al., 1977; Rezvani et al., 1981; Grunfeld ef al., 1988; Jsrgensen et al., 1989; 1992; Pirazzoli et al., 1992). Conversely, our findings challenge the speculation that GH administration induces hypothyroidism. Such speculation derives mainly from observations of a decline in circulating T4 levels during GH therapy in GH-deficient children. In situations in which such a decline in T4 resulted in subnormal levels it is reasonable to assume that GH substitution had unmasked a state of incipient central hypothyroidism (Municchi et al., 1992). Our patients were adults, who had been on stable T4 supplementation prior to the study due to clinical hypothyroidism, which implies that the observed effects of GH on T4 metabolism occur at extrathyroidal sites and at the same time excludes a potentially confounding factor, which may be present, when studying patients with untreated subclinical central hypothyroidism. Nevertheless, our patients exhibited biochemical evidence of hypothroidism in terms of subnormal total and free T3 levels when not receiving GH therapy. This occurred in spite of total and free T4 levels well within the normal range. Similar observations have been made in a study of GH-deficient adults who did not receive T4 supplementation (Jsrgensen et al., 1989). Since T3 levels normalized following GH therapy in both studies it seems plausible that endogenous GH is a physiological regulator of peripheral iodothyronine metabolism and action. As an index of thyroid hormone action we included measurements of resting EE in our patients. A weak but significant positive correlation was recorded between FT3 and EE. Furthermore, resting EE was lower than predicted when the patients were studied without GH and this parameter was nor- malized by GH administration (Msller et al., 1993). These data may suggest that the GH induced increase (nor- malization) in T3 concentrations is associated with increased T3 action. On the other hand, it is possible that the calorigenic actions of GH may involve additional mechanisms, since an increase in EE has been observed following co-administration of GH in T3 treated obese patients (Bray et al., 1971). It is likely that the stimulation of peripheral T4 to T3 conversion contributes to the composite effects of GH treatment in both normal and GH-deficient patients. Apart from the increase in EE, the changes in iodothyronine metabolism could also be causally linked to other clinical effects such as the increase in heart rate and improvements in lipoprotein patterns and psychological well-being. On the other hand, the well known GH induced effects on bone and muscle mass, exercise capacity and muscle strength indicate that GH actions are mediated by several additional mechanisms. How GH treatment induces its effects on peripheral T4 metabolism remains unknown. During catabolic states a decreased peripheral T4 to T3 deiodination is an unequivo- cal finding (Cavalieri & Rapoport, 1977). The fact that such conditions (e.g. fasting, chronic illness, convalescence after surgery) are accompanied by elevated GH levels seems to suggest that the effects observed during GH therapy are not directly GH mediated but may involve additional factors such as metabolic factors and IGF-I generation. The introduction of biosynthetic IGF-I for in-vivo use in humans may provide a feasible means of further elucida- tion of these issues. We were surprised by the pronounced GH-induced suppression of circadian TSH levels. Notably, this effect was recorded in patients with substituted central hypo- thyroidism. The physiological significance is difficult to assess and complicated by reports from other studies suggesting that circulating TSH in such patients may possess reduced biological activity (Faglia et al., 1979). We also observed a pronounced suppression of TSH in the two patients without clinical evidence of hypothyroidism. Suppression of TSH in single measurements or a blunted TSH response to TRH during GH administration have also previously been reported (Root et ul., 1970; 1973; Lippe et ul., 1975; Grunfeld et al., 1988; Jsrgensen et al., 1989). It is tempting to suggest that the decline in TSH during GH administration is secondary to increased T3 generation within the pituitary. Interestingly, we were able to detect a significant nocturnal increase in serum TSH levels in the patients with central hypothyroidism when they did not receive GH. This pattern is comparable to that reported in normal subjects (Weeke, 1973; Rose h Nisula, 1989). It has been suggested that a deficient nocturnal surge of TSH is a sensitive marker of central hypothyroidism in both children and adults (Caron et al., 1986; Rose et ul., 1990). Our findings indicate that such a screening test should be interpreted with caution, in patients on concomitant GH therapy.


In summary, GH administration in GH-deficient adults is associated with pronounced dose dependent actions on thyroid function in terms of a stimulation of peripheral T4 to T3 conversion. Since the circulating T3 levels were subnormal in these patients when not receiving GH replacement, despite T4 substitution in conventional doses and normal T4 levels, we speculate that the effects of GH on peripheral iodothyronine metabolism may be physiologically important.
 

IronLion2

Well-known member
Registered
Joined
Nov 10, 2017
Messages
1,825
Interesting , I wonder what the dose of HGH would be to "need" supplement T4.
It has much more to do with total metabolism. IMO thyroid function is going to closely mimic energy metabolism, one of our best mechanisms to check that is measuring for insulin resistance. I'm sure there's been plenty of SHW that have benefited greatly from adding thyroid to their stacks but that's because of their diets and PED use downgrading their metabolic function.
 

Stewie

Featured Member / Verified Customer
Featured Member
Kilo Klub Member
Registered
Verified Customer
Joined
Feb 3, 2011
Messages
4,984

Stewie

Featured Member / Verified Customer
Featured Member
Kilo Klub Member
Registered
Verified Customer
Joined
Feb 3, 2011
Messages
4,984
Interesting , I wonder what the dose of HGH would be to "need" supplement T4.

This citation by David T. Wyatt et al specifically mentions the citation you posted by J O Jørgensen et al.

 

Stewie

Featured Member / Verified Customer
Featured Member
Kilo Klub Member
Registered
Verified Customer
Joined
Feb 3, 2011
Messages
4,984
Sorry Gunsmith, I quoted the wrong person. Unfortunately, time lapsed before I could edit it.

Mods or admin, can we go back to the wee-bit longer time frame we used to have to edit? Wasn't it cut to 15 minutes in the past?

Thanks.
 

whacked

Member
Registered
Joined
Nov 27, 2009
Messages
150
Thanks Stewie

In summary, a transient decrease in T4, rT3, and FT4I and a transient increase in T3 occur almost universally in previously euthyroid children during the first year of GH therapy. These children remain clinically euthyroid and do not require T4 supplementation. All thyroid values return to pretreatment levels by 3–6 months of continued GH therapy. T4 supplementation should be considered only if there is a persistent decline in both T3 and T4 levels.”

The study was done on pediatric patients though. I imagine this is not an apples to apples comparison? Thoughts?
 

Dtropin

Active member
Registered
Newbies
Joined
Oct 22, 2019
Messages
106
This is from the full literature. It's well established that GH increases peripheral conversion. We'll leave that aside.

What's your takeaway from the full literature?
This is all with a replacement dose of HGH though right? It's my understanding that issues only arise at supraphysiological doses, but I'm far from an expert.

Considering only some people need to supplement T4/T3 while using large doses of GH, maybe they were borderline hypothyroid to begin with, or their thyroid can't produce enough T4 to keep up with increased T3 conversion.
 

Forum statistics

Total page views
503,026,865
Threads
123,576
Messages
2,358,156
Members
155,184
Latest member
JetBlack
Top