T3 synergy with HGH/Slin

[DarrenG29]

Also look at Roman Fritz 2 week diet he’s ready no cardio but does use t3 year round I believe from what said on here always dry glutes striated

also eating 8000 calories 500 protein 1200 carbs 90 fats.

 

[DarrenG29]

Link https://www.professionalmuscle.com/forums/index.php?threads/roman-fritz-8000kcal.166310/

 

[luki7788]

Also look at Roman Fritz 2 week diet he’s ready no cardio but does use t3 year round I believe from what said on here always dry glutes striated

also eating 8000 calories 500 protein 1200 carbs 90 fats.

Roman does cardio all year round, he has two daily gym workouts and one cardio workout. And what and how much he actually uses, he only knows himself

 

[beastmode121]

the excess is when the t3 values are above the normal range, for 100mcg you had to have at least 2x the upper normal range, that's way too much

And still nothing happened and came in on stage bigger and fuller than the year before..

So idk bud

 

[Stewie]

Single injections of T3 (7 ng·g−1 i.p.) rapidly and markedly attenuated hyperglycemia. Treatment with T3 (14 ng·g−1·day−1, 18 days) dose-dependently attenuated blood glucose and increased insulin sensitivity in db/db mice. Higher doses of T3 (28 ng·g−1·day−1) reversed insulin resistance in db/db mice. T3 also increased insulin levels in plasma and the neurogenic differentiation factor (an insulin synthesis transcription factor) and insulin storage in pancreatic islets in db/db mice. These anti-diabetic effects of T3 were abolished by the PI3-kinase inhibitor (LY294002). In 3T3-L1 preadipocytes, T3 enhanced insulin-induced tyrosine phosphorylation of insulin receptor substrate (IRS)-1 and activation of PI3-kinase, effects blocked by siRNA for TRα1.

CONCLUSIONS AND IMPLICATIONS​

T3 potentiated insulin signaling, improved insulin sensitivity, and increased insulin synthesis, which may contribute to its anti-diabetic effects. These findings may provide new approaches to the treatment of type 2 diabetes.

Link https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3041250/

For the sake of conversation, we'll set to the side the previous denotations of interspecies modeling, Incretin hormones differences between murine and humans, ect. For the time being, we'll act like these things aren't important.

If you was to determine the HED (human equivalent dose) administered as given in this citation. Would this translate theses dosages in mcgs from ng/g to the net effects as euthyroid (physiological levels) or factitious hyperthyroidism (supraphysiological levels)?

I've already done the math. Given so, I know what the dosages of the varying amounts equate to. As well, what this may reflect on thyroid parameters immunoassays.

 

[Stewie]

Hopefully this gives clarification on the differentiation between euthyroid and factitious hyperthyroidism (exogenous induced hyperthyroidism).The citation you shared is demonstrating normalization of thyroid perimeters.

To put things in perspective of human equivalent dose from the given literature are as follows:

First we need to convert end equations from ng•g to mcg. Which as you're aware, mcg are the metrics used for human thyroid hormone dosages. Then use allometric interspecies scaling. This configuration is used to determine the equivalency of each dose. For simplicity, I used 90.718 (200lbs) as the adjusted weight between mouse and human. The dosages will vary if a higher or lower body weight of human is used as adjusted weight.

You can use this allometric scaling calculator if so desired.

Allometric Scaling Calculator

However, these are the varying dosages of T3 used from the citation you shared.

•7ng•g= 4mcgs

•14ng•g= 8mcgs

•28ng•g= 15mcgs

As you can see, these are fairly low dosages of liothyronine (T3).


Given the information below, supraphysiological doses inducing factitious hyperthyroidism in humans doesn't enhance insulin sensitivity. In contrast, quite the opposite.


Here's a few snippets from the citation you shared.

Point of reference: two different subject models were used.

1)db/db mice are genetically modified models, in turn lacking proper leptin receptor signalling, therefore inducing type two diabetes (T2D).

2)Lean mouse models with intact leptin receptors.

As we can see from this segment of their endpoints, T3 did not affect insulin sensitivity in lean mice. Only the murine models with T2D.

T3 increased insulin sensitivity in db/db mice.


Insulin sensitivity was decreased in db/db mice (Figure 2A–C). T3 enhanced insulin sensitivity in db/db mice during weeks 1, 2 and 3 of treatment (Figure 2A–C). It is noted that T3 at 28 ng·g−1·day−1 restored insulin sensitivity (Figure 2C). LY294002 completely blocked this effect in db/db mice (Figure 2A–C). These results suggested that T3 can enhance insulin sensitivity in db/db mice and this effect is PI3-kinase dependent. -->T3 did not affect insulin sensitivity in lean mice<-- (Figure 2A–C), suggesting that the acute blood glucose-lowering effect of T3 (Figure 1A) may be due to rapid insulin release.


The present study suggest that there may be an increase in T3 metabolism associated with the db/db mice because the same dose of exogenous T3 increased plasma T3 levels to a lesser degree in db/db mice, --->compared to the lean mice.<---

T3 did not affect insulin sensitivity in lean mice.

Hyperglycemia has been found in patients with hyperthyroidism due to an increase in hepatic glucose production (Crunkhorn and Patti, 2008). Treatments with a large dose of T3 have been shown to increase plasma glucose levels in humans (Dimitriadis et al., 1985).

Given the different physiological and biological metrics with each given dose, drug induced thyrotoxicosis (factitious hyperthyroidism) wasn't observed. As noted below.

In addition, T3 did not alter body weights in lean or db/db mice. Thus, T3 at the doses used was safe and restored physiological function in db/db mice.

To summarize, there's vast differences between euthyroid and factitious hyperthyroidism on glucoregulatory functions. The citation you shared has clearly demonstrated these net outcomes are within physiological levels of T3. Or normalization of thyroid parameters.

These citation discusses different parameters of thyroid hormones on insulin regulations, in humans.

3. Insulin Resistance as a Consequence of Hyperthyroidism
Thyrotoxic subjects frequently show impaired glucose tolerance. This is a result of increased glucose turnover with increased glucose absorption through the gastrointestinal tract, postabsorptive hyperglycemia, elevated hepatic glucose output, with elevated fasting and/or postprandial insulin and proinsulin levels, elevated free fatty acid concentrations and elevated peripheral glucose transport and utilization. The literature about this topic is vast and has been previously comprehensively reviewed by Dimitriadis and Raptis [34]. Thyrotoxic diabetic patients are more prone to ketosis [35]. Although ketoacidosis may result per se from the insulin resistance present in thyrotoxicosis, the stimulatory action of thyroid hormones in excess on lipolysis and free fatty acids availability can also contribute to increased ketogenesis [36].

3.1. Increased Hepatic Glucose Output in Hyperthyroidism
Thyrotoxicosis has been reported to increase endogenous glucose production in the liver in the basal state and to decrease hepatic insulin sensitivity in humans [37]. The different mechanisms to explain this phenomenon include increased rates of gluconeogenesis and glycogenolysis [38] mainly explained by the above-mentioned effects on the liver by thyroid hormones. To summarize, these effects include thyroid receptor-mediated effects on liver gene transcription [5], increased sympathetic action in the liver mediated by hypothalamus [33], and increased concentrations of the GLUT2 glucose transporters in the liver plasma membrane that allows for glucose efflux [8, 39] together with increased concentration of free fatty acids in plasma [40].

3.2. Peripheral Tissues Glucose Metabolism in Hyperthyroidism
The interpretation of the effects of hyperthyroidism on glucose utilization by peripheral tissues is by far the most complex issue on this topic. On one hand, the rates of glucose uptake in peripheral tissues have been found increased by thyroid hormones, suggesting that glucose utilization is highly increased, specially in skeletal muscle [34, 37, 41–44]. This increased utilization, as shown by indirect calorimetry during euglycemic hyperinsulinemic clamps, is mainly due to an increase in insulin-stimulated glucose oxidation rates [43, 45–48]. However, a decrease in insulin-stimulated nonoxidative glucose disposal, through reduced glycogenogenesis [43, 44, 49], takes place, with intracellular glucose being redirected towards glycolysis and lactate formation. The release of lactate from peripheral tissues back to the liver is a major contributor to the Cori cycle where more hepatic glucose is being produced [43, 49–51].

Although glucose intolerance in hyperthyroidism can be easily explained by hepatic insulin resistance without involvement of peripheral tissues, impaired insulin-stimulated peripheral glucose uptake has also been proven in some studies. By means of the arteriovenous difference technique in the forearm muscles of hyperthyroid subjects after the consumption of a mixed meal, it has been clearly demonstrated that muscle blood flow is increased, masking a defect in insulin-stimulated glucose uptake [52]. Moreover, in disagreement with previous reports [41, 45], Shen et al. [53] also described decreased peripheral insulin sensitivity in hyperthyroidism.

Alternative explanations for peripheral insulin resistance in hyperthyroidism include an increased secretion of bioactive mediators (adipokines) such as interleukin 6 (IL6) and tumour necrosis factor a (TNFα) from adipose tissue in hyperthyroidism [54]. These adipokines, that exert both proinflammatory and insulin resistant effects, have been found elevated in hyperthyroid women [54].

3.3. Insulin and Glucagon Secretion and Degradation in Hyperthyroidism
In hyperthyroidism, decreased, normal, or even increased levels of plasma insulin have been reported [34]. However, a rather consistent finding has been the increased degradation of insulin in hyperthyroid subjects [43, 55]. It has been postulated that, in the long run, severe thyrotoxicosis can lead to irreversible pancreatic damage [56, 57].

With regards to glucagon, its secretion and metabolic clearance rates have been reported increased, explaining the normal fasting plasma levels described in hyperthyroidism [58].

3.4. Subclinical Hyperthyroidism and Insulin Resistance
Subclinical hyperthyroidism has also been associated with insulin resistance [59–61] in some but not all studies [62]. The heterogenous nature of this condition can partly explain this controversy. Endogenous subclinical hyperthyroidism may have a larger impact on glucose metabolism due to its chronicity and higher T3 levels when compared to exogenous administration of T4 [61].

Why Can Insulin Resistance Be a Natural Consequence of Thyroid Dysfunction?

Evidence for a relationship between T4 and T3 and glucose metabolism appeared over 100 years ago when the influence of thyroid hormone excess in the deterioration of glucose metabolism was first noticed. Since then, it has been known that hyperthyroidism is associated with insulin resistance...

www.hindawi.com

And

Association between altered thyroid state and insulin resistance

To determine the association between altered thyroid hormones and insulin resistance (IR).Eight euthyroid (EU), eight hypothyroid (HO), and eight hyperthyroid (HR) patients with no past medical history were studied in this cross-sectional study at the ...

www.ncbi.nlm.nih.gov

Be mindful that continuously induced factitious hyperthyroidism can potentially set the stage for thromboembolism, pulmonary hypertension, Afib and left ventricular hypertrophy to name a few.

Given your dosages of T3 and T4. It's highly doubtful you're within physiological levels of your thyroid parameters. Unless you have some serious antibodies present.

 

[madg]

Stewie in the house !

 

[Freak Monster]

Roman does cardio all year round, he has two daily gym workouts and one cardio workout. And what and how much he actually uses, he only knows himself

Of course we all know this top level athletes cant go to youtube and tell all the truth what they use .
Do you think we need use t4 or t3 when using high dosages hgh offseason?

 

[luki7788]

Of course we all know this top level athletes cant go to youtube and tell all the truth what they use .
Do you think we need use t4 or t3 when using high dosages hgh offseason?

in my opinion, 100% yes, otherwise we lose a lot of hgh benefits and risk side effects

 

[Wolf79]

I asked a friend who is trained by Tuor. Patrick believes that the t3 + t4 should be optimally taken so that the thyroid results are normal. By not using t3 for hgh, in his opinion, we lose a lot of benefits.

 

[madg]

in my opinion, 100% yes, otherwise we lose a lot of hgh benefits and risk side effects

Would love hear your opinion in this in more detail

What benefits ? What side effects?

 

[luki7788]

Would love hear your opinion in this in more detail

What benefits ? What side effects?

There is really nothing complicated here. GH increases the conversion of t4 to t3. Hence, high t3 and low t4 values are often observed in people using gh and not supplementing t4. The conversion is so large that it does not keep up with the production of t4 and gh drives the conversion process, so in the long run it will lead to hypothyroidism. So we need to supplement t4. Usually 50-100mcg per day is enough, but with higher doses of gh 10-15iu and more we need a lot more because the conversion is so strong.

 

[Wolf79]

Luki I know I asked but I didn't get an answer. would then using low dose t3 + t4 be less beneficial than using t4 alone during hgh?

 

[luki7788]

Luki I know I asked but I didn't get an answer. would then using low dose t3 + t4 be less beneficial than using t4 alone during hgh?

Friend, I do not have this knowledge, I am not a scientist and I do not want to mislead anyone. Everything I write here is my personal experience and thoughts and I can be wrong.

But as for your question, I think a small dose of t3 like 12.5mcg (along with t4) if we're using gh and it's not completely blocking the thyroid gland. I can conclude this from my and my clients' blood tests

 

[Wolf79]

Friend, I do not have this knowledge, I am not a scientist and I do not want to mislead anyone. Everything I write here is my personal experience and thoughts and I can be wrong.

But as for your question, I think a small dose of t3 like 12.5mcg (along with t4) if we're using gh and it's not completely blocking the thyroid gland. I can conclude this from my and my clients' blood tests

thank you! i think to use 15mcg t3 + 100mcg t4. I don't think 15 mcg t3 won't block my thyroid either. I have poor conversion and I'm afraid that the t4 itself will not work.

 

[whacked]

Let’s say we take 100mcg of T4 while on GH but the body only needed 75mcg

....what happens to the 25mcg of T4? Is this a problem?

Does the extra adversely affect the Thyroid axis?

Or does it just get pissed out?

 

[warlock]

in my opinion, 100% yes, otherwise we lose a lot of hgh benefits and risk side effects

Do you think the use of T4 is necessary if GH is only used at 2-3iu daily?

 

[Stewie]

Let’s say we take 100mcg of T4 while on GH but the body only needed 75mcg

....what happens to the 25mcg of T4? Is this a problem?

Does the extra adversely affect the Thyroid axis?

Or does it just get pissed out?

Your body won't differentiate what's usable then dumping the rest out as waste on a as needed basis. If this was the case, the definition and known side effects of too much levothyroxine (T4) causing factitious hyperthyroidism (thyrotoxicosis) would be omitted from medical literature.

Same can be said with liothyronine (T3).

 

[whacked]

Ugggg
Thanks Stewie

 

[Bobik]

Do you think the use of T4 is necessary if GH is only used at 2-3iu daily?

you have to do blood work .... Only now after two years of taking GH 3-4iu / day I see lower thyroid function. TSH is higher, FT4 lower, FT3 higher.