GH with or without T3, T4, or T3/T4?

[SAD]

If you frequent other boards you may have run across a thread debating the use of thyroid meds, and which thyroid meds, while running GH.

After sifting through the thread earlier and then doing my own research, I'm still about as clear as mud on whether or not to use T3, T4, or a combo of the two while running my GH.

The basics that I am getting are that if you want pure growth, then you shouldn't take any thyroid meds because they interfere with IGF-1 production. If you want to lose significant bodyfat and decrease some of the sides associated with GH use, such as water retention, carpal tunnel, and lethargy, then one should take T3 or T4 (depending on which study you read and whose theory you buy into).

On the particular thread I'm speaking of, there were a few different studies that showed conflicting conclusions based on contradictory results. I am far from a medical professional, so I'm going to post up a few of these studies so that ATW, Shine, GS, Mayo, and all the other guys/gals who have an affinity for medical studies can help me.

Thanks in advance.

 

[SAD]

Here's the original piece that started the thread, written by the infamous Anthony Roberts.

"We’re effectively shutting down the conversion pathway that is responsible for some of GH’s effects! And what would we be doing if we added in T4 instead of T3? You got it- we’d be enhancing the pathway by allowing the GH we’re using to have more T4 to convert to T3, thus giving us more of an effect from the GH we’re taking. Adding T4 into our GH cycles will actually allow more of the GH to be used effectively!

Remember, the thing that catalyzes the conversion process is the deiodinase enzyme. This is also why using low amounts of T3 would seem (again, anecdotally in bodybuilders) to be able to slightly increase protein synthesis and have an anabolic effect – they aren’t using enough to tell the body to stop or slow down production of the deiodinase enzyme, and hence .Although this analogy isn’t perfect, think of GH as a supercharger you have attached to your car…if you don’t provide enough fuel for it to burn at it’s increased output level, you aren’t going to derive the full effects. Thyroid status also may influence IGF-I expression in tissues other than the liver.So what we have here is a problem. When we take GH, it lowers T3 levels…but we need T3 to keep our GH receptor levels optimally upregulated. In addition, it’s suspected that many of GH’s anabolic effects are engendered as a result of production of IGF-1, so keeping our IGF receptors upregulated by maintaining adequate levels of T3 seems prudent. But as we’ve just seen, supplementing T3 with our GH will abolish Growth Hormone’s functional hepatic nitrogen clearance, possibly through the effect of reducing the bioavailability of insulin-like growth factor-I (12.)
So we want elevated T3 levels when we take GH, or we won’t be getting ANYWHERE NEAR the full anabolic effect of our injectable GH without enough T3. And now we know that not only do we need the additional T3, but we actually want the CONVERSION process of T4 into T3 to take place, because it’s the presence of those mediator enzymes that will allow the T3 to be synergistic with GH, instead of being inhibitory as is seen when T3 is simply added to a GH cycle. And remember, we don’t only want T3 levels high, but we want types 1 and 2 deiodinase to get us there- and when we take supplemental T3, that just doesn’t happen…all that happens is the type 3 deiodinase enzyme shows up and negates the beneficial effects of the T3 when we combine it with GH.

And that’s where myself and Dr. Daemon ended up, after a week of e-mails, researching studies, and gathering clues.

If you’ve been using GH without T4, you’ve been wasting half your money – and if you’ve been using it with T3, you’ve been wasting your time. Start using T4 with your GH, and you’ll finally be getting the full results from your investment."

 

[SAD]

First study. The interaction between growth hormone and the thyroid axis in hypopituitary patients - Behan - 2010 - Clinical Endocrinology - Wiley Online Library

Here's an excerpt.

Increased T4 to T3 conversion
The hypothesis that GH alters the peripheral deiodination of T4 to T3 is supported by the findings from most but not all studies. Several studies showed an increase in T3 and/or a reduction in rT3 after GH therapy2,4-14,24 which parallel the reduction in serum T4 concentration. Jorgensen postulated that this effect may not be mediated directly by GH but by IGF-I, based on the observation that conditions often accompanied by impaired T4 to T3 conversion such as malnutrition and critical illness are associated with high GH and low IGF-I.5 However, Klinger et al.66 noted that individuals with Laron-type GH resistance given exogenous IGF-I demonstrate only transient decreases within the normal range of T4 and TSH and no effect on T3 and Hussain et al.67 demonstrated a much higher increase in serum T3 levels after GH alone than after IGF-I administration in GHD patients suggesting that while both IGF-I and GH stimulate extrathyroidal conversion of T4 to T3, GH has a more direct potent effect on thyroid hormone metabolism.

As the finding of increased T3 is not a consistent effect throughout the literature,1,3,15 altered T4 to T3 conversion may not be the only mechanism involved in thyroid hormone alterations with GH therapy. No ex vivo studies examining the effect of GHD and GH replacement on the 5′deiodinases activities or m-RNA expression are available.

Altered TSH dynamics
It has been postulated that there is an inhibition of TSH secretion through pulse doses of GH1,24 possibly through increased somatostatinergic tone.1,68 While absolute basal TSH levels measured in many studies did not appear to change, others have shown altered TSH dynamics following GH therapy. Jorgensen et al.24 demonstrated a 10-fold decrease in mean 24-hour serum TSH profiles with GH therapy along with a blunted nocturnal surge of TSH. (Fig. 3) In another study, GH replacement was associated with a greater reduction in serum free T4 than the observed small increase in serum T3 concentrations and the reduction in serum free T4 concentration was also more marked in the apparently euthyroid group at baseline who had measurable serum TSH concentration compared to the already treated hypothyroid group which had undetectable TSH at baseline.14 Together these findings suggest a dual role for GH in modulating thyroid hormone concentration through both stimulation of peripheral conversion of T4 to T3 and also a central inhibitory effect on TSH release.

Conclusions and recommendations
GH replacement is a well-established component of the clinical care for hypopituitary patients and, despite its clear benefits,71 it is associated with a reduction in serum free T4, unmasking clinical and biochemical hypothyroidism in a significant number of patients. The high risk group is those who have serum free T4 near the lower end of the normal reference range in the setting of organic pituitary disease and multiple pituitary hormone deficiencies

The target level of free T4 in patients with hypopituitarism will depend on the assay used, the local reference range and importantly on the correlation with clinical status. It has been suggested that physicians should aim for free T4 in the upper half of the normal range; however, recent evidence suggests the mid-normal range may be adequate in GH replaced GHD subjects.46

It is our recommendation that patients starting GH should have their thyroid function monitored closely particularly in the first 6 months to identify those who will develop hypothyroidism. In those who develop hypothyroidism following GH therapy or in patients with preexisting CH, it would be reasonable to target thyroxine therapy to achieve serum free T4 concentration in the middle of the normal reference range.46 In the event of GH withdrawal patients should have thyroid function assessed at 6–12 weeks post withdrawal and treatment adjusted accordingly.

 

[SAD]

Don't have the link for this one, but here's the excerpt.

T3 negates hgh anabolism
1: J Hepatol. 1996 Mar;24(3):313-9. Related Articles, Links


Effects of long-term growth hormone (GH) and triiodothyronine (T3) administration on functional hepatic nitrogen clearance in normal man.

Wolthers T, Grofte T, Moller N, Vilstrup H, Jorgensen JO.

Department of Medicine M (Endocrinology and Diabetes), Aarhus University Hospital, Denmark.

BACKGROUND/AIMS: A decline in urea excretion is seen following long-term growth hormone administration, reflecting overall protein anabolism. Conversely, hyperthyroidism is characterized by increased urea synthesis and negative nitrogen metabolism. These seemingly opposite effects are presumed to reflect different actions on peripheral protein metabolism. The extent to which these hormonal systems have different direct effects on hepatic urea genesis has not been fully characterized. METHODS: We measured urea nitrogen synthesis rates and blood alanine levels concomitantly before, during, and after a 4-h constant intravenous infusion of alanine (2 mmol.kg bw-1.h-1). Urea nitrogen synthesis rate was estimated hourly as urinary excretion corrected for gut hydrolysis and accumulation in body water. The slope of the linear relationship between urea nitrogen synthesis rate and alanine concentration represents the liver function as to conversion of amino-N, and is denoted the functional hepatic nitrogen clearance. Eight normal male subjects (age 21-27 years; body mass index 22.4-27.0 kg/m2) were randomly studied four times: 1) after 10 days of subcutaneous saline injections, 2) after 10 days of subcutaneous growth hormone injections (0.1 IU/kg per day), 3) after 10 days of triiodothyronine administration (40 micrograms on even dates, 20 micrograms on uneven dates) and 4) after 10 days given 2)+3). All injections were given at 20 00 h. RESULTS: Growth hormone decreased functional hepatic nitrogen clearance (l/h) by 30% (from 33.8 +/- 3.2 l/h (control) to 23.8 +/- 1.5 l/h (10 days growth hormone) (mean +/- SE) (ANOVA; p < 0.01)). Triiodothyronine did not change functional hepatic nitrogen clearance (36.7 +/- 3.2 l/h), but triiodothyronine given together with growth hormone abolished the effect of growth hormone functional hepatic nitrogen clearance (38.8 +/- 4.8 l/h). CONCLUSIONS: The results show that long-term growth hormone administration acts on liver by decreasing functional hepatic nitrogen clearance, thereby retaining amino-N in the body. Triiodothyronine has no effect on functional hepatic nitrogen clearance, but given together with growth hormone, it abolishes the effect of growth hormone on functional hepatic nitrogen clearance. A possible mechanism is the known effect of thyroid hormones in reducing the bioavailability of insulin-like growth factor-I. Thus, the effects of growth hormone and triiodothyronine on amino-N homeostasis are interdependent and to some extent exerted via interplay in their regulation of liver function as to amino-N conversion.

Publication Types:
Clinical Trial
Randomized Controlled Trial

PMID: 8778198 [PubMed - indexed for MEDLINE]

 

[SAD]

And another.....

Growth hormone administration stimulates energy expenditure and extrathyroidal conversion of thyroxine to triiodothyronine in a dose-dependent manner and suppresses circadian thyrotrophin levels: studies in GH-deficient adults.

Jørgensen JO, Møller J, Laursen T, Orskov H, Christiansen JS, Weeke J.

Medical Department M (Endocrinology and Diabetes), Aarhus Kommunehospital, Denmark.
Abstract

OBJECTIVE: The impact of exogenous GH on thyroid function remains controversial although most data add support to a stimulation of peripheral T4 to T3 conversion. For further elucidation we evaluated iodothyronine and circadian TSH levels in GH-deficient patients as part of a GH dose-response study.

PATIENTS: Eight GH-deficient adults, who received stable T4 substitution due to central hypothyroidism; two patients, who were euthyroid without T4 supplementation were studied separately.

DESIGN: All patients were initially studied after at least 4 weeks without GH followed by 3 consecutive 4-week periods in fixed order during which they received daily doses of 1, 2 and 4 IU of GH/m2 body surface area. The patients were hospitalized for 24 hours at the end of each period.

MEASUREMENTS: Circulating total and free concentrations of T4 and T3, total rT3 and TSH were measured once at the end of each study period. Circadian TSH levels were recorded during the period without GH and during GH treatment with 2 IU GH.

RESULTS: Highly significant GH dose-dependent increases in total and free T3 and a reduction in rT3 were observed. The T3/T4 ratio also increased with increasing GH dosages (P < 0.001). In seven patients subnormal T3 levels were recorded in the period off GH, despite T4 levels well within the normal range. Resting energy expenditure also increased and correlated with free T3 levels (r = 0.47, P < 0.05). The circadian TSH levels exhibited a significant nocturnal increase during the period without GH, whereas GH therapy significantly suppressed the TSH levels and blunted the circadian rhythm (mean TSH levels (mU/l) 0.546 +/- 0.246 (no GH) vs 0.066 +/- 0.031 (2 IU GH) (P < 0.05)). The two euthyroid non-T4 substituted patients exhibited qualitatively similar changes in all parameters.

CONCLUSIONS: GH administration stimulated peripheral T4 to T3 conversion in a dose-dependent manner. Serum T3 levels were subnormal despite T4 substitution when the patients were off GH but normalized with GH therapy. Energy expenditure increased with GH and correlated with free T3 levels. GH caused a significant blunting of serum TSH. These findings suggest that GH plays a distinct role in the physiological regulation of thyroid function in general, and of peripheral T4 metabolism in particular.

PMID: 7828350 [PubMed - indexed for MEDLINE]

 

[tommyguns2]

I've run GH with and without T3. In my experience, running T3 daily at a dose of 0.25mcg provided me better results. Unfortunately, I can't completely discount other factors like better diet, etc. Will be interested to see the comments on this.

 

[AllTheWay]

i didnt read it all, sorry SAD, my head hurts. my only contribution right now would be why one would even consider using T4. i think T3 would/should be the only thing considered taking unless of course expense is part of the equation as T4 is dirt cheap and freaking T3is pretty spendy.

 

[SAD]

i didnt read it all, sorry SAD, my head hurts. my only contribution right now would be why one would even consider using T4. i think T3 would/should be the only thing considered taking unless of course expense is part of the equation as T4 is dirt cheap and freaking T3is pretty spendy.

It has to do with the by-products of conversion from T4 to T3 and the lack of said by-products when T3 is taken exogenously. When you get a chance to read through it all, it will make much more sense than I just did.

 

[Get Some]

Of all the reading I've done it appears that T3 levels are inhibited with the use of GH. However, I wouldn't be surprised if concurrent GHRH and GHRP usage would help normalize those levels. If you are older and stay on GH year round, you may want to consider running T3. If you are younger and only run gh without peptides, then it's probably nothing to worry about because you are cycling gh off and on and your T3 and TSH levels will likely return to normal without any exogenous stimulation.

That being said, I'm seeing more and more reason to use peptides in conjunction with gh as a healthier way of maintaining LBM. Yes, it's more of a hassle, but it may be worth it

 

[sparten]

Just read and now I have a headache, I'm 50 and pinning both ghrh and ghrp with very good results for body recomp, I have the T3 and was contemplating using so if I read the correctly my age and using long term GH and peps the t3 would benefit in fat loss?

 

[SAD]

Just read and now I have a headache, I'm 50 and pinning both ghrh and ghrp with very good results for body recomp, I have the T3 and was contemplating using so if I read the correctly my age and using long term GH and peps the t3 would benefit in fat loss?

Are you running exogenous GH as well? If you are only running peps, the T3 wouldn't be necessary. You say you're pinning the peptides but don't mention GH. Then you kinda mention "long term GH" use. If you are using GH it's possible that the peptides are helping to curtail some of the negative sides from the GH, but a thyroid med would certainly help with fatloss. That being said, it all comes back to the golden question again. WHICH thyroid med? That's why I started this thread in the first place, to see if anyone had anymore studies or any concrete data on which thyroid meds and in what doses are most effective at minimizing the inhibition of GH benefits while maximizing fatloss and anti-catabolism.

 

[sparten]

Sorry was away but not using exogenous just peps. I want to rid my self of the visceral fat around my midsection and recomp. but over at datbetrue he had some great insight and explanation between the exo.gh and why using using t4is almost a must but with the peps. if using just for fat loss a good thermo. and t3 will burn nicely, have you looked into helios?