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T- 3 info...........

OMEGA

New member
Posted by BigAndy69 on elite;
Disclaimer

T3 is not a drug that should be taken lightly. It's a very potent thyroid hormone. Messing with your natural hormone levels is very dangerous and unpredictable. The potential for complications is very high, and abuse can lead to thyroid disease and low thyroid output not only immediately upon discontinuation, but also later in life.

There is no such thing as safe use of T3 outside of a medical setting. There is only "safer" use. Use at your own risk.

Introduction: What is T3 and what are the side effects?

This article is pushing 2000 words, so here's a link for anyone who's interested: http://arbl.cvmbs.colostate.edu/hbo...roid/index.html

What about T4?

Bodybuilders should not use T4. It's a much weaker drug designed for long term use in patients with chronic thyroid disease. 100mcg of T4 corresponds to 25mcg of T3 and offers equivalent thyroid support; however, this does not translate to equal weight loss benefits. It has made itself on sources' lists simply because it is widely available and extremely cheap.

Is T3 catabolic?

It may shock many people to know that T3 is NOT catabolic per se. Corticosteroids are catabolic drugs that attack muscle tissue directly; T3 does not. It is a very potent calorie burner and it does not discriminate between carbohydrates, protein and fat. Unlike DNP, it has no protein sparing properties. T3 is also more likely to burn muscle than fat in lean users (10-12% BF), but this can be said for any extreme drop in caloric intake and uptake such as starvation diets (Caloric intake <10 X BW).

Muscle loss can be avoided with the use of anabolic agents. T3's alleged catabolic properties have become legendary. Excessive amounts of T3 (more than 75mcg), will have a very strong calorie burning effect, and since some bodybuilder use 150 mcg, it's easy to see why such misinformation has been so prevalent. The average bodybuilder will not need several grams of steroids to counter a reasonable dose of T3. There is no need to use more than 75mcg-100mcg. Going beyond this dose will cause more harm than good, as massive doses of steroids need to be used to counter the muscle loss, further stressing the body for minimal, if any additional benefits.

I think I've lost 20 lbs of muscle!

T3 can also give your muscles an extremely flat look and very soft feel. This side effect of extreme glycogen depletion can have a very profound psychological impact in bodybuilders. It often feels and looks like muscle loss when it's simply a lack of muscle "pump" because of restricted blood flow to that area and depletion of glycogen stores in muscles. Generally, carbohydrate loading does not solve this problem. "Pumping up" (or training for that matter) brings more blood into the muscles and is a temporary albeit effective solution. Clenbuterol and certain steroids can offset the lack of muscle pump because these drugs tend to "harden up" users by bringing more blood into to the muscles.


Are steroids absolutely necessary on T3?

This is very dependent on the user. Diet must be flawless, only reasonable doses should be considered (50mcg) and the user must know his body to a tee. Those who don't know what that last statement entails should not even consider T3. This is a veteran drug and should not be used by bodybuilders who are new to the game or do not have a deep understanding of how there bodies react to certain foods and training philosophies.

T3 can be used alone or better yet with Clenbuterol without fear of muscle loss in overly fat people (20-25% BF). This is not recommended, however, since these people will generally return to overeating upon discontinuation of their cycle and may likely end up with more weight than they started with.


How should I eat on T3?

Protein should be kept at 1.5-2g per lb of bodyweight. The majority of protein should come from lean meats. Shakes can be used, but should not be heavily relied on as they are more likely to be turned into glucose and used immediately for energy. Caloric reduction should come from carbs and fat only.


What is T3 used for?

Fat-loss: The main use for T3.

Increase Nutrient Uptake: Not very well known, but this is a great use for T3. Doses between 6.25-12.5mcg do not shutdown endogenous thyroid output. T3 at this dose can be used to add LBM and help in keeping the fat off. When doses are kept at 6.25-12.5mcg, muscles are full and rock hard, and energy is through the roof. At these light doses, it's common for people to go to the bathroom 5-6 times a day because there bodies are making more efficient use of the food they eat.

Can I permanently shutdown my Thyroid?


Simply put, NO, it can't happen. Natural thyroid production will be completely shutdown for a good period of time after using T3, but it will eventually recover. Bruce Kneller posted this study on the Testosterone website:

N Engl J Med 1975 Oct 2;293(14):681-4
Recovery of pituitary thyrotropic function after withdrawal of prolonged thyroid-suppression therapy.
Vagenakis AG, Braverman LE, Azizi F, Portinay GI, Ingbar SH.

The pattern of thyrotropin secretion was analyzed in seven euthyroid women, before and after withdrawal of long-term thyroid hormone, by serial measurements of thyroid 131l uptake, serum thyroxine, tri-iodothyronine, and thyrotropin concentrations, and the response to thyrotropin-releasing hormone. During exogenous hormone administration, 131l uptake was suppressed, and serum thyrotropin concentrations before and after administration of thyrotropin-releasing hormone were undetectable.
After withdrawal of exogenous hormone, thyrotropin secretory function was transiently impaired, as indicated by undetectable basal thyrotropin concentrations together with absence of response to thyrotropin-releasing hormone, and subsequently by normal values of basal thyrotropin concentration and normal responses to releasing hormone while serum thyroxine and tri-iodothyronine concentrations were subnormal.
Decreased thyrotropin reserve persisted for two to five weeks. Detectable values of serum thyrotropin (less than 1.2 muU per milliliter) and a normal 131l uptake usually occurred concurrently in two to three weeks. Serum thyroxine concentration returned to normal at least four weeks after hormone withdrawal.

Basically, it is extremely important to eat cleanly and keep up with cardio for at least 4 weeks and up to 6 weeks following a T3 cycle. It's also very important to ramp down properly and not use any drug that have an effect on metabolism and thyroid function, i.e. Clen, Ephedrine, Steroids, DNP, T2…

Calories should be kept in check, even lowered in some cases, and High Intensity Cardio is a must; at least 20mins, 3times a week. L-Tyrosine can be used at 1-3g a day to help thyroid function, but its effectiveness is debatable.

Switching to a higher carb, lower fat and lower protein diet is crucial in helping your thyroid bounce back after a cycle. A three-day carb up would be a good idea following a T3 cycle. This study demonstrates how important carbohydrates are for normal thyroid function. (Note: Some people seem to think of carbs as Lucky Charms and toast when there are far better carb choices that won't make you look like the Michelin Man.)

Dietary-induced alterations in thyroid hormone metabolism during overnutrition.
Danforth E Jr, Horton ES, O'Connell M, Sims EA, Burger AG, Ingbar SH, Braverman L, Vagenakis AG.

Diet-induced alterations in thyroid hormone concentrations have been found in studies of long-term (7 mo) overfeeding in man (the Vermont Study). In these studies of weight gain in normal weight volunteers, increased calories were required to maintain weight after gain over and above that predicted from their increased size. This was associated with increased concentrations of triiodothyronine (T3). No change in the caloric requirement to maintain weight or concentrations of T3 was found after long-term (3 mo) fat overfeeding. In studies of short-term overfeeding (3 wk) the serum concentrations of T3 and its metabolic clearance were increased, resulting in a marked increase in the production rate of T3 irrespective of the composition of the diet overfed (carbohydrate 29.6 +/- 2.1 to 54.0 +/- 3.3, fat 28.2 +/- 3.7 to 49.1 +/- 3.4, and protein 31.2 +/- 2.1 to 53.2 +/- 3.7 microgram/d per 70 kg). Thyroxine production was unaltered by overfeeding (93.7 +/- 6.5 vs. 89.2 +/- 4.9 microgram/d per 70 kg). It is still speculative whether these dietary-induced alterations in thyroid hormone metabolism are responsible for the simultaneously increased expenditure of energy in these subjects and therefore might represent an important physiological adaptation in times of caloric affluence. During the weight-maintenance phases of the long-term overfeeding studies, concentrations of T3 were increased when carbohydrate was isocalorically substituted for fat in the diet. In short-term studies the peripheral concentrations of T3 and reverse T3 found during fasting were mimicked in direction, if not in degree, with equal or hypocaloric diets restricted in carbohydrate were fed. It is apparent from these studies that the caloric content as well as the composition of the diet, specifically, the carbohydrate content, can be important factors in regulating the peripheral metabolism of thyroid hormones.

A post cycle crash is inevitable; this is the time when your diet really matters.

So how do I cycle this stuff?

T3/Clen/Anavar Cycle

Anavar is the single best steroid to stack with T3. Its anti catabolic properties are unmatched and it will not shut you down. There's nothing like simultaneous sex hormone and thyroid hormone shutdown; I bet it feels great. Primobolan at 200mg a week would be a good substitute since it doesn't shut you down. Dbol at 10-15mg taken in the morning can also be used but Arimidex must be included with the Dbol. T3 increases the amount of beta-3-adregenic receptors (by 500%!) in white adipose tissue, i.e. the fat that covers muscle. Since clen exerts most of its effect on the same receptors; the combination with T3 would yield quite a strong synergistic effect. T3/Clen may be too much for the heart in some people.

T3:

12.5mcg for 5-7 days (optional but recommended)

37.5mcg for 5 days
75mcg for 15 days
50mcg for 5 days
37.5mcg for 5 days
25mcg for 5 days
12.5 mcg for 5 days
6.25mcg for 5-7 days

Clen:

30 days: 60-120mcg ED. Use clen from the first 37.5mcg dose to the last 25mcg dose. Ketotifen will make you more sensitive to clenbuterol so doses should be adjust accordingly.

Ketotifen:

Stacked with Clenbuterol, 2mg ED. This drug may not be an option for some people since it can make them extremely hungry. If this is the case, Clen should be used 2 weeks on 2 weeks off.

Anavar:

Oxandrin;

15mg ED with 37.5mcg of T3,
25mg ED with 75mcg of T3,
20mg ED with 50mcg of T3.


Here's a more sensitive approach that can be used between cycles since it doesn't include AS:

BigAndy69's T3 Cycle:

The cycle can actually be used to add muscle mass or drop body fat depending on caloric intake. For gaining muscle mass, the Yohimbine and Anastrozole are not necessary.

W1-W4:

T3: 12.5mg ED
Clen: 60-100mcg ED
Ketotifen: 2mg ED
Anastrozole: 0.5mg ED
Yohimbine: 10-15mg ED (maybe too much to handle in some)

Carb/Pro/Fat:

20-30/50-60/20

ALA: 1500mg ED
Taurine: 3g ED

W5:

T3: 6.25mg ED

L-Tyrosine: 1-2g ED
ALA: 2500mg ED
Taurine: 3g ED

Carb/Pro/Fat:

50-60/20-30/20

(High Intensity Cardio)

W6:

ALA: 1500mg ED

Carb/Pro/Fat:

40/40/20

(High Intensity Cardio)


BigAndy69's T3 Post Cycle Therapy (4-6 weeks):

Initial 3 day carb up:

Carbs: 1.75g X BW
Protein: 0.75g X BW
Fat: 0.25g X BW

Supplements:

L-Tyrosine: 1-3g ED
ALA: 1500mg ED
Flaxseed oil + Fish oil: 20g total ED

Diet: >50% Carbs/ 30% Protein/ <20% Fat, calories at maintenance (+ or - 12 X BW)

High intensity cardio: 75-80% of Max Heart Rate; 15-20 min 3-4 times a week.

No Steroids, Ephedrine, Clen, T2, DNP, or anything that has an effect on metabolism. Moderate doses of caffeine can be used before cardio.


Anything Else I should know?

T3 should be taken on an empty stomach, in the morning. If more than 50mcg is being taken, then it should be split through the day.

BigAndy69


References:


N Engl J Med 1975 Oct 2;293(14):681-4
Recovery of pituitary thyrotropic function after withdrawal of prolonged thyroid-suppression therapy.
Vagenakis AG, Braverman LE, Azizi F, Portinay GI, Ingbar SH.

Dietary-induced alterations in thyroid hormone metabolism during overnutrition.
Danforth E Jr, Horton ES, O'Connell M, Sims EA, Burger AG, Ingbar SH, Braverman L, Vagenakis AG.

A paradigm of experimentally induced mild hyperthyroidism: effects on nitrogen balance, body composition, and energy expenditure in healthy young men.

J Clin Endocrinol Metab 1997 Mar;82(3):765-70 (ISSN: 0021-972X)
Lovejoy JC; Smith SR; Bray GA; De Lany JP; Rood JC; Gouvier D; Windhauser M; Ryan DH; Macchiavelli R; Tulley R
Pennington Biomedical Research Center, Louisiana State University, Baton Rouge 70808, USA. [email protected].

Metabolism 1981 Aug;30(8):783-91
Whole body leucine and lysine metabolism studied with [1-13C]leucine and [alpha-15N]lysine: response in healthy young men given excess energy intake.
Motil KJ, Bier DM, Matthews DE, Burke JF, Young VR.

Rubio A, et al. "Thyroid hormone and norepinephrine signaling in brown adipose tissue. II: Differential effects of thyroid hormone on beta 3-adrenergic receptors in brown and white adipose tissue." Endocrinology 1995 Aug
 
My comments are not flames (I am just a little excited at the moment), BigAndy69 is a good bro, but we all make mistakes.

FYI: Comments are listed between this *** and this ***.



Posted by BigAndy69 on elite;
Disclaimer

T3 is not a drug that should be taken lightly. It's a very potent thyroid hormone. Messing with your natural hormone levels is very dangerous and unpredictable. The potential for complications is very high, and abuse can lead to thyroid disease ***where on gods earth did he pull that out of his ass*** and low thyroid output not only immediately upon discontinuation, but also later in life. ***his wording here is seriously flawed***

There is no such thing as safe use of T3 outside of a medical setting. There is only "safer" use. Use at your own risk.

Introduction: What is T3 and what are the side effects?

This article is pushing 2000 words, so here's a link for anyone who's interested: http://arbl.cvmbs.colostate.edu/hbo...roid/index.html

What about T4?

Bodybuilders should not use T4. It's a much weaker drug designed for long term use in patients with chronic thyroid disease. 100mcg of T4 corresponds to 25mcg of T3 and offers equivalent thyroid support; however, this does not translate to equal weight loss benefits. ***Correct some people have trouble converting t4 to t3*** It has made itself on sources' lists simply because it is widely available and extremely cheap.

Is T3 catabolic?

It may shock many people to know that T3 is NOT catabolic per se. Corticosteroids are catabolic drugs that attack muscle tissue directly; T3 does not. It is a very potent calorie burner and it does not discriminate between carbohydrates, protein and fat. Unlike DNP, it has no protein sparing properties. T3 is also more likely to burn muscle than fat in lean users (10-12% BF), but this can be said for any extreme drop in caloric intake and uptake such as starvation diets (Caloric intake <10 X BW).

Muscle loss can be avoided with the use of anabolic agents. T3's alleged catabolic properties have become legendary. Excessive amounts of T3 (more than 75mcg), will have a very strong calorie burning effect, and since some bodybuilder use 150 mcg, it's easy to see why such misinformation has been so prevalent. The average bodybuilder will not need several grams of steroids to counter a reasonable dose of T3. There is no need to use more than 75mcg-100mcg. Going beyond this dose will cause more harm than good, as massive doses of steroids need to be used to counter the muscle loss, further stressing the body for minimal, if any additional benefits.

I think I've lost 20 lbs of muscle!

T3 can also give your muscles an extremely flat look and very soft feel. This side effect of extreme glycogen depletion can have a very profound psychological impact in bodybuilders. It often feels and looks like muscle loss when it's simply a lack of muscle "pump" because of restricted blood flow to that area and depletion of glycogen stores in muscles. Generally, carbohydrate loading does not solve this problem. "Pumping up" (or training for that matter) brings more blood into the muscles and is a temporary albeit effective solution. Clenbuterol and certain steroids can offset the lack of muscle pump because these drugs tend to "harden up" users by bringing more blood into to the muscles.


Are steroids absolutely necessary on T3?

This is very dependent on the user. Diet must be flawless, only reasonable doses should be considered (50mcg) ***I beg to differ, US pharmacy bought T3 has eaten mine and many people’s muscle at that dosage while experiencing fat accumulation*** and the user must know his body to a tee. Those who don't know what that last statement entails should not even consider T3. This is a veteran drug and should not be used by bodybuilders who are new to the game or do not have a deep understanding of how there bodies react to certain foods and training philosophies.

T3 can be used alone or better yet with Clenbuterol without fear of muscle loss in overly fat people (20-25% BF) ***I respectfully disagree; T3 was my first drug of choice in the world of BB, and I got fat on it while losing LBM at 290lbs, 30% BF, although carbohydrate consumption was relatively high at the time, I’ve been up to 400mcg of SBC T3***. This is not recommended, however, since these people will generally return to overeating upon discontinuation of their cycle and may likely end up with more weight than they started with.


How should I eat on T3?

Protein should be kept at 1.5-2g per lb of bodyweight. The majority of protein should come from lean meats. Shakes can be used, but should not be heavily relied on as they are more likely to be turned into glucose and used immediately for energy. Caloric reduction should come from carbs and fat only.


What is T3 used for?

Fat-loss: The main use for T3.

Increase Nutrient Uptake: Not very well known, but this is a great use for T3. Doses between 6.25-12.5mcg do not shutdown endogenous thyroid output. T3 at this dose can be used to add LBM and help in keeping the fat off. When doses are kept at 6.25-12.5mcg, muscles are full and rock hard, and energy is through the roof. At these light doses, it's common for people to go to the bathroom 5-6 times a day because there bodies are making more efficient use of the food they eat. ***This never happened to me***

Can I permanently shutdown my Thyroid?


Simply put, NO, it can't happen. Natural thyroid production will be completely shutdown for a good period of time after using T3, but it will eventually recover. Bruce Kneller posted this study on the Testosterone website: ***Well it happened to me***

N Engl J Med 1975 Oct 2;293(14):681-4
Recovery of pituitary thyrotropic function after withdrawal of prolonged thyroid-suppression therapy.
Vagenakis AG, Braverman LE, Azizi F, Portinay GI, Ingbar SH.

The pattern of thyrotropin secretion was analyzed in seven euthyroid women, before and after withdrawal of long-term thyroid hormone, by serial measurements of thyroid 131l uptake, serum thyroxine, tri-iodothyronine, and thyrotropin concentrations, and the response to thyrotropin-releasing hormone. During exogenous hormone administration, 131l uptake was suppressed, and serum thyrotropin concentrations before and after administration of thyrotropin-releasing hormone were undetectable.
After withdrawal of exogenous hormone, thyrotropin secretory function was transiently impaired, as indicated by undetectable basal thyrotropin concentrations together with absence of response to thyrotropin-releasing hormone, and subsequently by normal values of basal thyrotropin concentration and normal responses to releasing hormone while serum thyroxine and tri-iodothyronine concentrations were subnormal.
Decreased thyrotropin reserve persisted for two to five weeks. Detectable values of serum thyrotropin (less than 1.2 muU per milliliter) and a normal 131l uptake usually occurred concurrently in two to three weeks. Serum thyroxine concentration returned to normal at least four weeks after hormone withdrawal.

Basically, it is extremely important to eat cleanly and keep up with cardio for at least 4 weeks and up to 6 weeks following a T3 cycle. It's also very important to ramp down properly and not use any drug that have an effect on metabolism and thyroid function, i.e. Clen, Ephedrine, Steroids, DNP, T2… ***WTF no ephedrine, steroids, DNP, Clenbuterol, he must have been smoking crack while writing this***

Calories should be kept in check, even lowered in some cases, and High Intensity Cardio is a must; at least 20mins, 3times a week. L-Tyrosine can be used at 1-3g a day to help thyroid function, but its effectiveness is debatable.

Switching to a higher carb, lower fat and lower protein diet is crucial in helping your thyroid bounce back after a cycle. *** WTF lower protein, higher carb*** A three-day carb up would be a good idea following a T3 cycle. This study demonstrates how important carbohydrates are for normal thyroid function. (Note: Some people seem to think of carbs as Lucky Charms and toast when there are far better carb choices that won't make you look like the Michelin Man.) ****some carbs are needed but high carb, low fat, low protein is just plain wrong***

Dietary-induced alterations in thyroid hormone metabolism during overnutrition.
Danforth E Jr, Horton ES, O'Connell M, Sims EA, Burger AG, Ingbar SH, Braverman L, Vagenakis AG.

Diet-induced alterations in thyroid hormone concentrations have been found in studies of long-term (7 mo) overfeeding in man (the Vermont Study). In these studies of weight gain in normal weight volunteers, increased calories were required to maintain weight after gain over and above that predicted from their increased size. This was associated with increased concentrations of triiodothyronine (T3). No change in the caloric requirement to maintain weight or concentrations of T3 was found after long-term (3 mo) fat overfeeding. In studies of short-term overfeeding (3 wk) the serum concentrations of T3 and its metabolic clearance were increased, resulting in a marked increase in the production rate of T3 irrespective of the composition of the diet overfed (carbohydrate 29.6 +/- 2.1 to 54.0 +/- 3.3, fat 28.2 +/- 3.7 to 49.1 +/- 3.4, and protein 31.2 +/- 2.1 to 53.2 +/- 3.7 microgram/d per 70 kg). ***THIS DOES NOT MAKE ANY F-ING SENSE, EVEN IF THEY MEANT GRAMS/D PER 70 KG*** Thyroxine production was unaltered by overfeeding (93.7 +/- 6.5 vs. 89.2 +/- 4.9 microgram/d per 70 kg). It is still speculative whether these dietary-induced alterations in thyroid hormone metabolism are responsible for the simultaneously increased expenditure of energy in these subjects and therefore might represent an important physiological adaptation in times of caloric affluence. During the weight-maintenance phases of the long-term overfeeding studies, concentrations of T3 were increased when carbohydrate was isocalorically substituted for fat in the diet. In short-term studies the peripheral concentrations of T3 and reverse T3 found during fasting were mimicked in direction, if not in degree, with equal or hypocaloric diets restricted in carbohydrate were fed. It is apparent from these studies that the caloric content as well as the composition of the diet, specifically, the carbohydrate content, can be important factors in regulating the peripheral metabolism of thyroid hormones.

A post cycle crash is inevitable; this is the time when your diet really matters.

So how do I cycle this stuff?

T3/Clen/Anavar Cycle ***contradiction***

Anavar is the single best steroid to stack with T3. Its anti catabolic properties are unmatched and it will not shut you down ***I disagree***. There's nothing like simultaneous sex hormone and thyroid hormone shutdown; I bet it feels great. Primobolan at 200mg a week would be a good substitute since it doesn't shut you down. Dbol at 10-15mg taken in the morning can also be used but Arimidex must be included with the Dbol. T3 increases the amount of beta-3-adregenic receptors (by 500%!) in white adipose tissue, i.e. the fat that covers muscle. Since clen exerts most of its effect on the same receptors; the combination with T3 would yield quite a strong synergistic effect. T3/Clen may be too much for the heart in some people.

T3:

12.5mcg for 5-7 days (optional but recommended)

37.5mcg for 5 days
75mcg for 15 days
50mcg for 5 days
37.5mcg for 5 days
25mcg for 5 days
12.5 mcg for 5 days
6.25mcg for 5-7 days

Clen:

30 days: 60-120mcg ED. Use clen from the first 37.5mcg dose to the last 25mcg dose. Ketotifen will make you more sensitive to clenbuterol so doses should be adjust accordingly.

Ketotifen:

Stacked with Clenbuterol, 2mg ED. This drug may not be an option for some people since it can make them extremely hungry. If this is the case, Clen should be used 2 weeks on 2 weeks off.

Anavar:

Oxandrin;

15mg ED with 37.5mcg of T3,
25mg ED with 75mcg of T3,
20mg ED with 50mcg of T3.


Here's a more sensitive approach that can be used between cycles since it doesn't include AS:

BigAndy69's T3 Cycle:

The cycle can actually be used to add muscle mass or drop body fat depending on caloric intake. For gaining muscle mass, the Yohimbine and Anastrozole are not necessary.

W1-W4:

T3: 12.5mg ED
Clen: 60-100mcg ED
Ketotifen: 2mg ED
Anastrozole: 0.5mg ED
Yohimbine: 10-15mg ED (maybe too much to handle in some)

Carb/Pro/Fat: ***good ratios***

20-30/50-60/20

ALA: 1500mg ED
Taurine: 3g ED ***props***

W5:

T3: 6.25mg ED

L-Tyrosine: 1-2g ED
ALA: 2500mg ED ***I am assuming this is an old post, since he must mean s and r isomers***
Taurine: 3g ED

Carb/Pro/Fat:

50-60/20-30/20 ***BAD, BAD, BAD***

(High Intensity Cardio)

W6:

ALA: 1500mg ED

Carb/Pro/Fat:

40/40/20

(High Intensity Cardio)


BigAndy69's T3 Post Cycle Therapy (4-6 weeks):

Initial 3 day carb up:

Carbs: 1.75g X BW
Protein: 0.75g X BW
Fat: 0.25g X BW

Supplements:

L-Tyrosine: 1-3g ED
ALA: 1500mg ED
Flaxseed oil + Fish oil: 20g total ED

Diet: >50% Carbs/ 30% Protein/ <20% Fat, calories at maintenance [+ or - 12 X BW)

High intensity cardio: 75-80% of Max Heart Rate; 15-20 min 3-4 times a week.

No Steroids, Ephedrine, Clen, T2, DNP, or anything that has an effect on metabolism. (WTF???) Moderate doses of caffeine can be used before cardio.


Anything Else I should know?

T3 should be taken on an empty stomach, in the morning. If more than 50mcg is being taken, then it should be split through the day. ***good boy***

BigAndy69


References:


N Engl J Med 1975 Oct 2;293(14):681-4
Recovery of pituitary thyrotropic function after withdrawal of prolonged thyroid-suppression therapy.
Vagenakis AG, Braverman LE, Azizi F, Portinay GI, Ingbar SH.

Dietary-induced alterations in thyroid hormone metabolism during overnutrition.
Danforth E Jr, Horton ES, O'Connell M, Sims EA, Burger AG, Ingbar SH, Braverman L, Vagenakis AG.

A paradigm of experimentally induced mild hyperthyroidism: effects on nitrogen balance, body composition, and energy expenditure in healthy young men.

J Clin Endocrinol Metab 1997 Mar;82(3):765-70 (ISSN: 0021-972X)
Lovejoy JC; Smith SR; Bray GA; De Lany JP; Rood JC; Gouvier D; Windhauser M; Ryan DH; Macchiavelli R; Tulley R
Pennington Biomedical Research Center, Louisiana State University, Baton Rouge 70808, USA. [email protected].

Metabolism 1981 Aug;30(8):783-91
Whole body leucine and lysine metabolism studied with [1-13C]leucine and [alpha-15N]lysine: response in healthy young men given excess energy intake.
Motil KJ, Bier DM, Matthews DE, Burke JF, Young VR.

Rubio A, et al. "Thyroid hormone and norepinephrine signaling in brown adipose tissue. II: Differential effects of thyroid hormone on beta 3-adrenergic receptors in brown and white adipose tissue." Endocrinology 1995 Aug

SWIMMING IN GPLENISH

_____________________________________________________________________________________

If I post anything foolish, incorrect or stupid please correct me.

Thank you for your cooperation

International Intellectual Masturbation Proponent Society (IIMPS) Member
 
iteresting note

I have never reclieved as much karma in my days than from this thread alone

its good to know people know a good thing when they see it

thanks for this thread to the original author
 
MY RESPONSES ARE IN ALL-CAPS AND BOLDED.. YOU SEEMED TO MISUNDERSTAND ALOT OF WHAT HE WAS SAYING. BTW: ONLY REASON THAT ONCE COMMENT IS IN SIZE 6 IS B/C YOU USED CAPS TOO SO IT WAS HARD TO DISTINGUISH. DIDNT WANT YOU TO THINK I WAS BEING AN ASS BY MAKING IT LARGE, IT'S SIMPLY TO DISTINGUISH OUR COMMENTS.

BTW, BEFORE SAYING LOW-PROTEIN MAKES NO SENSE PLEASE SEE THIS STUDY:

Proc Soc Exp Biol Med 2000 Sep;224(4):256-63


Low-protein diet changes thyroid function in lactating rats.

Ramos CF, Teixeira CV, Passos MC, Pazos-Moura CC, Lisboa PC, Curty FH, de Moura EG.

LOW-PROTEIN FED RATS HAD HIGHER FREE-T-3 LEVELS THAN DID THE OTHERS. THEREFORE HE IS COMPLETELY CORRECT IN HIS RECCOMENDATION. BESIDES PROTEIN TURNOVER WILL BE LOW (SINCE THYROID FUNCTION IS IMPAIRED)

E23 said:
My comments are not flames (I am just a little excited at the moment), BigAndy69 is a good bro, but we all make mistakes.

FYI: Comments are listed between this *** and this ***.



Posted by BigAndy69 on elite;
Disclaimer

T3 is not a drug that should be taken lightly. It's a very potent thyroid hormone. Messing with your natural hormone levels is very dangerous and unpredictable. The potential for complications is very high, and abuse can lead to thyroid disease ***where on gods earth did he pull that out of his ass*** (YOU ARE WELL AWARE THAT MEDICALLY, HYPOTHYROIDISM IS THYROID DISEASE CORRECT?) and low thyroid output not only immediately upon discontinuation, but also later in life. ***his wording here is seriously flawed*** (HOW DO YOU FIGURE, SEE ABOVE?)

There is no such thing as safe use of T3 outside of a medical setting. There is only "safer" use. Use at your own risk.

Introduction: What is T3 and what are the side effects?

This article is pushing 2000 words, so here's a link for anyone who's interested: http://arbl.cvmbs.colostate.edu/hbo...roid/index.html

What about T4?

Bodybuilders should not use T4. It's a much weaker drug designed for long term use in patients with chronic thyroid disease. 100mcg of T4 corresponds to 25mcg of T3 and offers equivalent thyroid support; however, this does not translate to equal weight loss benefits. ***Correct some people have trouble converting t4 to t3*** It has made itself on sources' lists simply because it is widely available and extremely cheap.

Is T3 catabolic?

It may shock many people to know that T3 is NOT catabolic per se. Corticosteroids are catabolic drugs that attack muscle tissue directly; T3 does not. It is a very potent calorie burner and it does not discriminate between carbohydrates, protein and fat. Unlike DNP, it has no protein sparing properties. T3 is also more likely to burn muscle than fat in lean users (10-12% BF), but this can be said for any extreme drop in caloric intake and uptake such as starvation diets (Caloric intake <10 X BW).

Muscle loss can be avoided with the use of anabolic agents. T3's alleged catabolic properties have become legendary. Excessive amounts of T3 (more than 75mcg), will have a very strong calorie burning effect, and since some bodybuilder use 150 mcg, it's easy to see why such misinformation has been so prevalent. The average bodybuilder will not need several grams of steroids to counter a reasonable dose of T3. There is no need to use more than 75mcg-100mcg. Going beyond this dose will cause more harm than good, as massive doses of steroids need to be used to counter the muscle loss, further stressing the body for minimal, if any additional benefits.

I think I've lost 20 lbs of muscle!

T3 can also give your muscles an extremely flat look and very soft feel. This side effect of extreme glycogen depletion can have a very profound psychological impact in bodybuilders. It often feels and looks like muscle loss when it's simply a lack of muscle "pump" because of restricted blood flow to that area and depletion of glycogen stores in muscles. Generally, carbohydrate loading does not solve this problem. "Pumping up" (or training for that matter) brings more blood into the muscles and is a temporary albeit effective solution. Clenbuterol and certain steroids can offset the lack of muscle pump because these drugs tend to "harden up" users by bringing more blood into to the muscles.


Are steroids absolutely necessary on T3?

This is very dependent on the user. Diet must be flawless, only reasonable doses should be considered (50mcg) ***I beg to differ, US pharmacy bought T3 has eaten mine and many people’s muscle at that dosage while experiencing fat accumulation*** and the user must know his body to a tee. Those who don't know what that last statement entails should not even consider T3. This is a veteran drug and should not be used by bodybuilders who are new to the game or do not have a deep understanding of how there bodies react to certain foods and training philosophies.

T3 can be used alone or better yet with Clenbuterol without fear of muscle loss in overly fat people (20-25% BF) ***I respectfully disagree; T3 was my first drug of choice in the world of BB, and I got fat on it while losing LBM at 290lbs, 30% BF, although carbohydrate consumption was relatively high at the time, I’ve been up to 400mcg of SBC T3***. (400!!!?!?)This is not recommended, however, since these people will generally return to overeating upon discontinuation of their cycle and may likely end up with more weight than they started with.


How should I eat on T3?

Protein should be kept at 1.5-2g per lb of bodyweight. The majority of protein should come from lean meats. Shakes can be used, but should not be heavily relied on as they are more likely to be turned into glucose and used immediately for energy. Caloric reduction should come from carbs and fat only.


What is T3 used for?

Fat-loss: The main use for T3.

Increase Nutrient Uptake: Not very well known, but this is a great use for T3. Doses between 6.25-12.5mcg do not shutdown endogenous thyroid output. T3 at this dose can be used to add LBM and help in keeping the fat off. When doses are kept at 6.25-12.5mcg, muscles are full and rock hard, and energy is through the roof. At these light doses, it's common for people to go to the bathroom 5-6 times a day because there bodies are making more efficient use of the food they eat. ***This never happened to me***

Can I permanently shutdown my Thyroid?


Simply put, NO, it can't happen. Natural thyroid production will be completely shutdown for a good period of time after using T3, but it will eventually recover. Bruce Kneller posted this study on the Testosterone website: ***Well it happened to me***

N Engl J Med 1975 Oct 2;293(14):681-4
Recovery of pituitary thyrotropic function after withdrawal of prolonged thyroid-suppression therapy.
Vagenakis AG, Braverman LE, Azizi F, Portinay GI, Ingbar SH.

The pattern of thyrotropin secretion was analyzed in seven euthyroid women, before and after withdrawal of long-term thyroid hormone, by serial measurements of thyroid 131l uptake, serum thyroxine, tri-iodothyronine, and thyrotropin concentrations, and the response to thyrotropin-releasing hormone. During exogenous hormone administration, 131l uptake was suppressed, and serum thyrotropin concentrations before and after administration of thyrotropin-releasing hormone were undetectable.
After withdrawal of exogenous hormone, thyrotropin secretory function was transiently impaired, as indicated by undetectable basal thyrotropin concentrations together with absence of response to thyrotropin-releasing hormone, and subsequently by normal values of basal thyrotropin concentration and normal responses to releasing hormone while serum thyroxine and tri-iodothyronine concentrations were subnormal.
Decreased thyrotropin reserve persisted for two to five weeks. Detectable values of serum thyrotropin (less than 1.2 muU per milliliter) and a normal 131l uptake usually occurred concurrently in two to three weeks. Serum thyroxine concentration returned to normal at least four weeks after hormone withdrawal.

Basically, it is extremely important to eat cleanly and keep up with cardio for at least 4 weeks and up to 6 weeks following a T3 cycle. It's also very important to ramp down properly and not use any drug that have an effect on metabolism and thyroid function, i.e. Clen, Ephedrine, Steroids, DNP, T2… ***WTF no ephedrine, steroids, DNP, Clenbuterol, he must have been smoking crack while writing this*** (ALL WILL HAVE A NEGATIVE EFFECT ON THYROID RECOVERY..MAKES SENSE FOR HIM TO SAY THIS)

Calories should be kept in check, even lowered in some cases, and High Intensity Cardio is a must; at least 20mins, 3times a week. L-Tyrosine can be used at 1-3g a day to help thyroid function, but its effectiveness is debatable.

Switching to a higher carb, lower fat and lower protein diet is crucial in helping your thyroid bounce back after a cycle. *** WTF lower protein, higher carb*** (HE'S ASSUMING YOU RAISED PROTEIN EXTREMELY HIGH TO COMPENSATE FOR POSSIBLE CATABOLISM..AGAIN...MAKES SENSE)A three-day carb up would be a good idea following a T3 cycle. This study demonstrates how important carbohydrates are for normal thyroid function. (Note: Some people seem to think of carbs as Lucky Charms and toast when there are far better carb choices that won't make you look like the Michelin Man.) ****some carbs are needed but high carb, low fat, low protein is just plain wrong*** (SEE ABOVE)

Dietary-induced alterations in thyroid hormone metabolism during overnutrition.
Danforth E Jr, Horton ES, O'Connell M, Sims EA, Burger AG, Ingbar SH, Braverman L, Vagenakis AG.

Diet-induced alterations in thyroid hormone concentrations have been found in studies of long-term (7 mo) overfeeding in man (the Vermont Study). In these studies of weight gain in normal weight volunteers, increased calories were required to maintain weight after gain over and above that predicted from their increased size. This was associated with increased concentrations of triiodothyronine (T3). No change in the caloric requirement to maintain weight or concentrations of T3 was found after long-term (3 mo) fat overfeeding. In studies of short-term overfeeding (3 wk) the serum concentrations of T3 and its metabolic clearance were increased, resulting in a marked increase in the production rate of T3 irrespective of the composition of the diet overfed (carbohydrate 29.6 +/- 2.1 to 54.0 +/- 3.3, fat 28.2 +/- 3.7 to 49.1 +/- 3.4, and protein 31.2 +/- 2.1 to 53.2 +/- 3.7 microgram/d per 70 kg). ***THIS DOES NOT MAKE ANY F-ING SENSE, EVEN IF THEY MEANT GRAMS/D PER 70 KG*** JUDING FROM SENTANCE DIRECTLY BELOW THIS ONE, THEY ARE REFERRING TO PRODUCTION RATES OF T-3 BASED ON TYPE OF NUTRIENT OVER-FED, WHICH MAKES PERFECT SENSE) Thyroxine production was unaltered by overfeeding (93.7 +/- 6.5 vs. 89.2 +/- 4.9 microgram/d per 70 kg). It is still speculative whether these dietary-induced alterations in thyroid hormone metabolism are responsible for the simultaneously increased expenditure of energy in these subjects and therefore might represent an important physiological adaptation in times of caloric affluence. During the weight-maintenance phases of the long-term overfeeding studies, concentrations of T3 were increased when carbohydrate was isocalorically substituted for fat in the diet. In short-term studies the peripheral concentrations of T3 and reverse T3 found during fasting were mimicked in direction, if not in degree, with equal or hypocaloric diets restricted in carbohydrate were fed. It is apparent from these studies that the caloric content as well as the composition of the diet, specifically, the carbohydrate content, can be important factors in regulating the peripheral metabolism of thyroid hormones.

A post cycle crash is inevitable; this is the time when your diet really matters.

So how do I cycle this stuff?

T3/Clen/Anavar Cycle ***contradiction*** (HOW SO, HE SAID NOT TO USE THEM WHEN COMING OFF, NOT WHILE ON)

Anavar is the single best steroid to stack with T3. Its anti catabolic properties are unmatched and it will not shut you down ***I disagree***. There's nothing like simultaneous sex hormone and thyroid hormone shutdown; I bet it feels great. Primobolan at 200mg a week would be a good substitute since it doesn't shut you down. Dbol at 10-15mg taken in the morning can also be used but Arimidex must be included with the Dbol. T3 increases the amount of beta-3-adregenic receptors (by 500%!) in white adipose tissue, i.e. the fat that covers muscle. Since clen exerts most of its effect on the same receptors; the combination with T3 would yield quite a strong synergistic effect. T3/Clen may be too much for the heart in some people.

T3:

12.5mcg for 5-7 days (optional but recommended)

37.5mcg for 5 days
75mcg for 15 days
50mcg for 5 days
37.5mcg for 5 days
25mcg for 5 days
12.5 mcg for 5 days
6.25mcg for 5-7 days

Clen:

30 days: 60-120mcg ED. Use clen from the first 37.5mcg dose to the last 25mcg dose. Ketotifen will make you more sensitive to clenbuterol so doses should be adjust accordingly.

Ketotifen:

Stacked with Clenbuterol, 2mg ED. This drug may not be an option for some people since it can make them extremely hungry. If this is the case, Clen should be used 2 weeks on 2 weeks off.

Anavar:

Oxandrin;

15mg ED with 37.5mcg of T3,
25mg ED with 75mcg of T3,
20mg ED with 50mcg of T3.


Here's a more sensitive approach that can be used between cycles since it doesn't include AS:

BigAndy69's T3 Cycle:

The cycle can actually be used to add muscle mass or drop body fat depending on caloric intake. For gaining muscle mass, the Yohimbine and Anastrozole are not necessary.

W1-W4:

T3: 12.5mg ED
Clen: 60-100mcg ED
Ketotifen: 2mg ED
Anastrozole: 0.5mg ED
Yohimbine: 10-15mg ED (maybe too much to handle in some)

Carb/Pro/Fat: ***good ratios***

20-30/50-60/20

ALA: 1500mg ED
Taurine: 3g ED ***props***

W5:

T3: 6.25mg ED

L-Tyrosine: 1-2g ED
ALA: 2500mg ED ***I am assuming this is an old post, since he must mean s and r isomers***
Taurine: 3g ED

Carb/Pro/Fat:

50-60/20-30/20 ***BAD, BAD, BAD*** (SEE STUDY BELOW THIS POST)

(High Intensity Cardio)

W6:

ALA: 1500mg ED

Carb/Pro/Fat:

40/40/20

(High Intensity Cardio)


BigAndy69's T3 Post Cycle Therapy (4-6 weeks):

Initial 3 day carb up:

Carbs: 1.75g X BW
Protein: 0.75g X BW
Fat: 0.25g X BW

Supplements:

L-Tyrosine: 1-3g ED
ALA: 1500mg ED
Flaxseed oil + Fish oil: 20g total ED

Diet: >50% Carbs/ 30% Protein/ <20% Fat, calories at maintenance [+ or - 12 X BW)

High intensity cardio: 75-80% of Max Heart Rate; 15-20 min 3-4 times a week.

No Steroids, Ephedrine, Clen, T2, DNP, or anything that has an effect on metabolism. (WTF???) IT MAKES NO SENSE TO USE DRUGS THAT WILL ADVERSLY EFFECT RECOVERY Moderate doses of caffeine can be used before cardio.


Anything Else I should know?

T3 should be taken on an empty stomach, in the morning. If more than 50mcg is being taken, then it should be split through the day. ***good boy***

BigAndy69


References:


N Engl J Med 1975 Oct 2;293(14):681-4
Recovery of pituitary thyrotropic function after withdrawal of prolonged thyroid-suppression therapy.
Vagenakis AG, Braverman LE, Azizi F, Portinay GI, Ingbar SH.

Dietary-induced alterations in thyroid hormone metabolism during overnutrition.
Danforth E Jr, Horton ES, O'Connell M, Sims EA, Burger AG, Ingbar SH, Braverman L, Vagenakis AG.

A paradigm of experimentally induced mild hyperthyroidism: effects on nitrogen balance, body composition, and energy expenditure in healthy young men.

J Clin Endocrinol Metab 1997 Mar;82(3):765-70 (ISSN: 0021-972X)
Lovejoy JC; Smith SR; Bray GA; De Lany JP; Rood JC; Gouvier D; Windhauser M; Ryan DH; Macchiavelli R; Tulley R
Pennington Biomedical Research Center, Louisiana State University, Baton Rouge 70808, USA. [email protected].

Metabolism 1981 Aug;30(8):783-91
Whole body leucine and lysine metabolism studied with [1-13C]leucine and [alpha-15N]lysine: response in healthy young men given excess energy intake.
Motil KJ, Bier DM, Matthews DE, Burke JF, Young VR.

Rubio A, et al. "Thyroid hormone and norepinephrine signaling in brown adipose tissue. II: Differential effects of thyroid hormone on beta 3-adrenergic receptors in brown and white adipose tissue." Endocrinology 1995 Aug

SWIMMING IN GPLENISH

_____________________________________________________________________________________

If I post anything foolish, incorrect or stupid please correct me.

Thank you for your cooperation

International Intellectual Masturbation Proponent Society (IIMPS) Member
 
Last edited:
Proc Soc Exp Biol Med 2000 Sep;224(4):256-63


Low-protein diet changes thyroid function in lactating rats.

Ramos CF, Teixeira CV, Passos MC, Pazos-Moura CC, Lisboa PC, Curty FH, de Moura EG.

Departamento de Ciencias, Faculdade de Formacao de Professores de Sao Goncalo, Universidade do Estado do Rio de Janeiro, 20550-030 Rio de Janeiro, RJ, Brazil.

Lactating rats were fed with free access to an 8% protein-restricted diet (PR); the control group was fed a 23% protein diet (C). An energy-restricted (pair-fed) group was given the same food as the animals in the control group, but the amounts of food consumed by both PF and PR were about the same. The body weight and serum albumin concentration of PR and PF dams were significantly (P < 0. 05) lower than that of the controls. The PR group had a significant increase in serum-free triiodothyronine (FT3) concentration, 24-hr mammary gland and milk radioiodine (I131) uptake (67%, 278%, and 200%, respectively) as compared with the controls. On the other hand, those animals had a significantly lower serum-free thyroxine (FT4) concentration and 2- and 24-hr thyroid I131 uptake (67%, 64%, and 74%, respectively). Protein malnutrition during lactation did not alter thyroid or liver 5'-deiodinase activity significantly. However, PF dams had a significantly lower (25%) thyroid 5'-deiodinase activity. These data suggest that protein-restricted lactating dams had an adaptive change in the thyroid function, which could be important to increase the transference of iodine or triiodothyronine through the milk to their pups and prevent sequelae of neonatal hypothyroidism.
Proc Soc Exp Biol Med 1997 May;215(1):82-6
 
Dietary carbohydrate and fat do not alter the thyroid response to protein deficiency in chicks.

Carew LB, Alster FA

Department of Animal and Food Sciences, University of Vermont, Burlington 05405, USA.

Consumption of low-protein diets consistently causes elevations in circulating levels of triiodothyronine (T3) in several species of animals. In chicks this is often accompanied by lower levels of circulating thyroxine (T4). Since low-protein diets are usually formulated by replacing the detected protein with carbohydrate, the question arises as to whether the changes in thyroid hormones are a result of the lower protein or higher amounts of carbohydrate in such diets. Male broiler chicks, 13-26 days of age, were fed experimental diets that contained either an adequate level of protein (24%) or levels that were slightly (17%) or moderately (10%) deficient in protein. The deleted protein was replaced, isocalorically, with either glucose, soybean oil, or hydrogenated coconut fat. Though the level of protein and source of energy differed among diets, all diets contained identical amounts of all nutrients and energy, and were of similar weight densities. Circulating levels of thyroid hormones were measured from blood samples taken at the end of the study. Plasma T3 was elevated to a similar degree in all protein-deficient animals compared with control. Plasma T4 decreased in all protein-deficient chicks and was lowest with 10% dietary protein. Changes in circulating levels of thyroid hormones occurred independently of the source of dietary energy. Therefore, it is concluded that alterations in circulating levels of thyroid hormones that occur in chicks fed low-protein diets are a specific effect of the protein deficit and are not a related to the amounts of carbohydrate or fat present in the diet.
 
If anyone is interested in further research on the topic you canperuse this article, courtesy of nandi:

Thyroid Hormone for Weight Loss:
Physiologic and Metabolic Effects
by Nandi



Introduction


It has been over 100 years since the discovery by Magnus-Levy that thyroid hormones play a central role in energy homeostasis, and 75 years since the hormones were first used for weight loss. Despite this great length of time, the precise mechanisms by which thyroid hormones exert their calorigenic effect are not completely characterized, and still actively debated. Despite numerous clinical studies having shown that the administration of thyroid hormone induces weight loss, it is not currently indicated as a weight loss agent. This is probably due to the number of side effects observed during thyroid hormone use at the relatively high doses used in the majority of obesity treatment studies. These deleterious effects include cardiac problems such as tachycardia and atrial arrhythmias, loss of muscle mass as well as fat, increased bone resorption and muscle weakness. Nevertheless, thyroid hormones, particularly triiodothyronine (T3) are a mainstay in the arsenal of drugs used by bodybuilders for fat loss. The widespread underground use of T3 warrants an understanding of its mechanism of action, as well as a knowledge of how it is most effectively and safely used, with an eye to minimizing side effects.



Thyroid Function and Physiology


Before jumping right into a discussion of the use of thyroid hormone for fat loss, a little review of thyroid function and physiology might be in order. The thyroid gland secretes two hormones of interest to us, thyroxine (T4) and triiodothyronine (T3). T3 is considered the physiologically active hormone, and T4 is converted peripherally into T3 by the action of the enzyme deiodinase. The bulk of the body's T3 (about 80%) comes from this conversion. The secretion of T4 is under the control of Thyroid Stimulating Hormone (TSH) which is produced by the pituitary gland. TSH secretion is in turn controlled through release of Thyrotropin Releasing Hormone which is produced in the hypothalamus. This is analogous to testosterone production, where GnRH from the hypothalamus causes the pituitary to release LH, which in turn stimulates the testes to produce testosterone.

In addition to T3, it has recently been recognized that there exist two additional active metabolites of T3: 3,5 and 3,3' diiodothyronines, which we will collectively call T2. Studies have shown that 3,3'-T2 may be more effective in raising resting metabolic rate when hypothyroid subjects are treated with T3, than when normal (euthyroid) subjects are given T3. Therefore in normal subjects 3,5-T2 may be the principal active metabolite of T3 (1)

Like the hypothalamic-pituitary-gonadal axis, the thyroid gland is under negative feedback control. When T3 levels go up, TSH secretion is suppressed. This is the mechanism whereby exogenous thyroid hormone suppresses natural thyroid hormone production. There is a difference though between the way anabolic steroids suppress natural testosterone production and the way T3 suppresses the thyroid. With steroids, the longer and heavier the cycle is, the longer your natural testosterone is suppressed. This is not the case with exogenous thyroid hormone.

An early study that looked at thyroid function and recovery under the influence of exogenous thyroid hormone was undertaken by Greer (2). He looked at patients who were misdiagnosed as being hypothyroid and put on thyroid hormone replacement for as long as 30 years. When the medication was withdrawn, their thyroids quickly returned to normal.

Here is a remark about Greer's classic paper from a later author:


"In 1951, Greer reported the pattern of recovery of thyroid function after stopping suppressive treatment with thyroid hormone in euthyroid [normal] subjects based on sequential measurements of their thyroidal uptake of radioiodine. He observed that after withdrawal of exogenous thyroid therapy, thyroid function, in terms of radioiodine uptake, returned to normal in most subjects within two weeks. He further observed that thyroid function returned as rapidly in those subjects whose glands had been depressed by several years of thyroid medication as it did in those whose gland had been depressed for only a few days" (3)

These results have been subsequently verified in several studies.(3)(4) So contrary to what has been stated in the bodybuilding literature, there is no evidence that long term thyroid supplementation will somehow damage your thyroid gland. Nevertheless, most bodybuilders will choose to cycle their T3 (or T4 which in most cases works just as well) as part of a cutting strategy, since T3 is catabolic with respect to muscle just as it is with fat. As previously mentioned, long term T3 induced hyperthyroidism is also catabolic to bone as well as muscle.

The proviso about T4 vs T3 for weight loss alluded to above needs some elaboration. There have been a number of studies that have shown that during starvation, or when carbohydrate intake is reduced to approximately 25 to 50 grams per day, levels of deiodinase decline, hindering the conversion of T4 to the physiologically active T3.(5) From an evolutionary standpoint this makes sense: during periods of starvation the body, teleologically speaking, would like to reduce its basal metabolic rate to preserve fat and especially muscle stores. However, a recent study demonstrating the effectiveness and safety of the ketogenic diet for weight loss recorded no change in circulating T3 levels.(6) So this issue not completely settled. Nevertheless, persons contemplating thyroid supplementation during ketogenic dieting might prefer T3 over T4 since the bulk of the research does suggest a decline in the peripheral conversion of T4 to T3 during low carb dieting.

Now that we have reviewed a little about thyroid function, let's consider just how it is that thyroid hormone exerts its fat burning effects.



Increased Oxidative Energy Metabolism


Thyroid hormone has long been recognized as a major regulator of the oxidative metabolism of energy producing substrates (food or stored substrates like fat, muscle, and glycogen) by the mitochondria. The mitochondria are often called the "cell's powerhouses" because this is where foodstuffs are turned into useful energy in the form of ATP. T3 and T2 increase the flux of nutrients into the mitochondria as well as the rate at which they are oxidized, by increasing the activities of the enzymes involved in the oxidative metabolic pathway. The increased rate of oxidation is reflected by an increase in oxygen consumption by the body.

T3 and T2 appear to act by different mechanisms to produce different results. T2 is believed to act on the mitochondria directly, increasing the rate of mitochondrial respiration, with a consequent increase in ATP production. T3 on the other hand acts at the nuclear level, inducing the transcription of genes controlling energy metabolism, primarily the genes for so-called uncoupling proteins, or UCP (see below). The time course of these two actions is quite different. T2 begins to increase mitochondrial respiration and metabolic rate immediately. T3 on the other hand requires a day or longer to increase RMR since the synthesis of new proteins, the UCP, is required (1).

There are a number of putative mechanisms whereby T2 is believed to increase mitochondrial energy production rates, resulting in increased ATP levels. These include an increased influx of Ca++ into the mitochondria, with a resulting increase in mitochondrial dehydrogenases. This in turn would lead to an increase in reduced substrates available for oxidation. An increase in cytochrome oxidase activity has also been observed. This would hasten the reduction of O2, speeding up respiration. These and a number of other proposed mechanisms for the action of T2 are reviewed by Lannie et al.(7)

What is the fate of the extra ATP produced during hyperthyroidism? There are a number of ways by which the increased ATP promotes an increase in metabolic activity, including the following:

Increased Na+/K+ATPase. This is the enzyme responsible for controlling the Na/K pump, which regulates the relative intracellular and extracellular concentrations of these ions, maintaining the normal transmembrane ion gradient. Sestoft(7) has estimated this effect may account for up to to 10% of the increased ATP usage.


Increased Ca++-dependent ATPase. The intracellular concentration of calcium must be kept lower than the extracellular concentration to maintain normal cellular function. ATP is required to pump out excess calcium. It has been estimated that 10% of a cell's energy expenditure is used just to maintain Ca++ homeostasis. (1)


Substrate cycling. Hyperthyroidism induces a futile cycle of lipogenesis/lipolysis in fat cells. The stored triglycerides are broken down into free fatty acids and glycerol, then reformed back into triglycerides again. This is an energy dependent process that utilizes some of the excess ATP produced in the hyperthyroid state (8). Futile cycling has been estimated to use approximately 15% of the excess ATP created during hyperthyroidism (8)


Increased Heart Work. This puts perhaps the greatest single demand on ATP usage, with increased heart rate and force of contraction accounting for up to 30% to 40% of ATP usage in hyperthyroidism (9)



Mitochondrial Uncoupling


As mentioned, the mitochondria are often characterized as the cell's powerhouse. They convert foodstuffs into ATP, which is used to fuel all the body's metabolic processes. Much research suggests that T3, like another much more potent agent DNP, has the ability to uncouple oxidation of substrates from ATP production. T3 is believed to increase the production of so called uncoupling proteins. Uncoupling protein (UCP) is a transporter family that is present in the mitochondrial inner membrane, and as its name suggests, it uncouples respiration from ATP synthesis by dissipating the transmembrane proton gradient as heat. Instead of useful ATP being produced from energy substrates, heat is generated instead. There are conflicting studies about the importance of T3 induced uncoupling. Animal studies have demonstrated an actual increase in ATP production commensurate with increased oxygen consumption as we discussed above. Other studies in humans have shown that in fact uncoupling in skeletal muscle does occur. This would contribute to T3 induced thermogenesis, with a resulting increase in basal metabolic rate.(10)

To make up for the deficit in ATP production (as well as provide fuel for the extra ATP production discussed above) more substrates must be burned for fuel, resulting in fat loss. Unfortunately, along with the fat that is burned, some protein from muscle is also catabolized for energy. This is the downside of T3 use, and the reason many people choose to use an anabolic steroid or prohormone during a T3 cycle to help preserve muscle mass. Studies have shown this to be an effective strategy (11). (Muscle glycogen is also more rapidly depleted, and less efficiently stored during hyperthyroidism. This may account for some of the muscle weakness generally associated with T3 use.)

Countering T3 induced muscle loss with AAS or prohormones makes sense from a physiological viewpoint as well. Thyroid hormone muscle protein breakdown is mainly mediated via the so-called ubiquitin-proteasome pathway. (12). (There are several independent metabolic pathways of protein breakdown in the body. For instance, another pathway, the lysosomal pathway, is responsible for the accelerated rate of muscle protein breakdown during and after exercise.) Testosterone administration has been shown to decrease ubiquitin-proteasome activity. (13) So AAS specifically target the muscle protein breakdown process stimulated by T3.

What may not be an effective strategy to maintain muscle mass during a T3 cycle is the use of exogenous growth hormone (GH). Studies have shown that when GH and T3 are administered concurrently, the increased nitrogen retention normally associated with GH use is abolished. This has been attributed to the observation that T3 increases levels of insulin like growth factor binding protein, reducing the bioavailability of igf-1 (14). Nevertheless, GH has fat burning properties independent of igf-1, so using GH with T3 would act additively to speed fat burning, but with little if any preservation of lean body mass. So again, if GH is used in conjunction with T3, anabolic steroid/prohormone use would be indicated.



Andregenic Receptor Modulation


Administration of T3 has been shown to upregulate the so-called beta 2 adrenergic receptor in fat tissue. What is the significance of this effect for fat loss? Before fat can be used as fuel, it must be mobilized from the fat cells where it is stored. An enzyme called Hormone Sensitive Lipase (HSL) is the rate-controlling enzyme in lipolysis, or fat mobilization. The body produces two catecholamines, epinephrine and norepinephrine, which bind to the beta 2 receptor and activate HSL. The upregulation of the beta 2 receptor due to T3 results in an increased ability of catecholamines to activate HSL, leading to increased lipolysis.

Bodybuilders often use drugs like clenbuterol, which bind to the beta 2 receptors and activate them in the same way as the body's endogenous catecholamines. The use of clenbuterol along with T3 can produce an additive lipolytic effect: T3 increases the number of receptors, while clenbuterol binds to the receptors activating HSL and increasing lipolysis. Since clenbuterol itself downregulates the beta 2 receptor, most bodybuilders use clenbuterol in a two week on/ two week off cycle, the rationale being that this minimizes downregulation and allows receptor recovery. Another option is to use the antihistamine ketotifen concurrently with the clenbuterol. Studies have shown that ketotifen attenuates the beta 2 receptor downregulation caused by clenbuterol (15). Moreover, research in AIDS patients has shown that ketotifen blocks the production of the proinflammatory and catabolic cytokine TNF-alpha (16). This may be of relevance to bodybuilders since there is evidence showing TNF lowers both testosterone and IGF-1 levels quite significantly (17) (18), while strenuous exercise elevates TNF levels. (19)

Besides increasing beta 2 receptor density in adipose tissue, T3 upregulates this receptor in human skeletal muscle (12). This has some very intriguing if somewhat speculative implications for the combined use of clenbuterol and T3. Animal studies have shown that catecholamines, particularly clenbuterol, inhibit Ca++ dependent skeletal muscle proteolysis (20). Like the lysosomal and ubiquitin-proteasome pathways discussed above, Ca++ regulated proteolysis is yet another way for the body to degrade muscle protein. Again the implications are enticing: Increased beta 2 receptor density from T3 use, coupled with the beta 2 agonist clenbuterol, could slow this pathway of muscle catabolism.

Another adrenergic receptor important to lipolysis is the alpha 2 receptor, which impedes fat mobilization by counteracting the effects of the beta 2 receptor. There are some conflicting studies about the effects of T3 on the alpha 2 receptor, with studies showing either a downregulation (21) or no effect (22). If T3 does in fact downregulate alpha 2 receptors, this would further aid lipolysis.

Studies in rats have shown that inducing hyperthyroidism increases the lipolytic beta 3 receptor density in white adipose tissue by 70% (23). Beta 3 receptors are abundant in human white adipose tissue as well, and if T3 administration has the same effect in humans, this could could contribute significantly to T3 induced fat loss. This might also argue for taking a currently available beta 3 agonist such as octopamine along with T3 and perhaps clenbuterol.



Decreased Phosphodiesterase Expression


In hyperthyroid patients as well as in normal subjects given T3, levels of the enzyme phosphodiesterase are lowered in fat cells (20). When lipolytic hormones like epinephrine (adrenaline) bind to the beta 2 receptor described above, they initiate a signaling cascade mediated by the so called “second messenger” cyclic AMP (cAMP). cAMP in turn acts on other cellular enzymes to initiate and maintain lipolysis. The original signal is terminated when cAMP is degraded by the enzyme phosphodiesterase. Clearly, maintaining elevated cAMP levels, by lowering phosphodiesterase concentrations with T3, will prolong lipolysis.

As an aside, caffeine is thought to exert at least a portion of its lipolytic action by lowering phosphodiesterase in fat cells. Interestingly, Viagra and Cialis are also phosphodiesterase inhibitors but their action seems to be limited to relaxing vascular smooth muscles.



Increased Growth Hormone Secretion


In vitro, animal, and human studies have all demonstrated that T3 administration increases growth hormone production. (24)(25) Since GH is calorigenic aside from any increase in igf-1, elevated GH may contribute to some of the fat burning associated with T3 administration. This effect may obviate the need for the use of expensive recombinant HGH, as mentioned above.



Decreased Insulin Secretion


Insulin is well known as a lipogenic hormone. It promotes fat storage by facilitating the uptake of fatty acids by adipocytes, and reducing lipid oxidation in muscle tissue. Several studies have shown that thyroid hormone is associated with glucose intolerance resulting from decreased glucose stimulated insulin secretion (26).

This defect in insulin secretion is believed to result from an increase in the rate of apoptosis (programmed cell death) of pancreatic beta cells as a direct effect of thyroid hormone excess.(27) This process is reversible, since when thyroid hormone is withdrawn the rate of beta cell replication increases until homeostasis returns. However, there are conflicting studies regarding the effects of T3 on insulin. For example, Dimitriadis et al (28) showed a decrease in glucose stimulated insulin secretion, consistent with (25), but an increase in basal insulin. They also observed increased insulin clearance, with a compensatory increase in basal insulin secretion.

So if in fact the hyperthyroid state is associated with lower insulin levels, this could explain a portion of hyperthyroid stimulated lipolysis. The obvious downside here is that insulin is also an anabolic hormone. Basal insulin concentration is thought to limit the action of the ubiquitin-proteasome degradative pathway of muscle protein breakdown (29). Of course supplementing with insulin during T3 use would be counterproductive. However, as mentioned above, anabolic steroids inhibit ubiquitin-proteasome activity, so their use could counter any loss in muscle anabolism resulting from a drop insulin levels.



The Future


As mentioned at the beginning of this article, a major roadblock in the adoption of T3 by the medical community as an antiobesity agent is its deleterious effect on the heart. Recent research has identified two isoforms of the thyroid hormone receptor, TRalpha and TRbeta. The TRalpha-form may preferentially regulate the heart rate, and an experimental agent, GC-1, has been developed that selectively binds the TRbeta receptor, with minimal effects on the heart (30). The distribution and actions of TRalpha and TRbeta throughout the body are not yet well characterized. However should it turn out that TRalpha is specific to the heart, then drugs like GC-1 may turn out to be effective fat burning agents with a much safer profile that T3 or T4.

One alleged “futuristic” agent that is here now is T2, or 3,5-Di-iodo-L-thyronine, the T3 metabolite discussed above. Unfortunately, this product does not live up to its hype. It has been claimed to be as or more effective that T3 for fat burning with minimal suppression of endogenous thyroid production. Regarding the relative effectiveness of T2 as a lipolytic agent, and its effect on TSH, this topic was thoroughly covered in a recent article by Bryan Haycock in Muscle Monthly:




All of my research into this subject has led me to the same conclusion reached by Mr. Haycock. That is, T2 is only slightly less suppressive of TSH than is T3, and only packs a portion of the lipolytic punch of T3, with no ability to increase the expression of the UCPs, which is a major determinant of the action of thyroid hormone.



Summary


We have discussed a number of ways by which T3, and its active metabolite T2 act to increase resting energy expenditure. Also discussed were some drawbacks of T3 use, such as cardiac stress, as well as the potential loss of muscle mass. It is ironic that the latter may be of more concern to many bodybuilders that the other more serious potential impacts on health. Nevertheless, used moderately and for short periods (a couple of months or less) in people with no preexisting cardiovascular disease T3 has a relatively safe medical profile, compared to other lipolytic agents like DNP. Perhaps most importantly we have presented substantial evidence that even the long-term use of supraphysiological levels of T3 does not damage the thyroid gland.


References:

(1) Endocrinology 2002 Feb;143(2):504-10 Are the effects of T3 on resting metabolic rate in euthyroid rats entirely caused by T3 itself? Moreno M, Lombardi A, Beneduce L, Silvestri E, Pinna G, Goglia F, Lanni A.

(2)(Greer,M. N Engl J Med 244:385, 1951)

(3)N Engl J Med 1975 Oct 2;293(14):681-4 Recovery of pituitary thyrotropic function after withdrawal of prolonged thyroid-suppression therapy. Vagenakis AG, Braverman LE, Azizi F, Portinay GI, Ingbar SH.

(4) J Clin Endocrinol Metab 1975 Jul;41(1):70-80 Patterns off recovery of the hypothalamic-pituitary-thyroid axis in patients taken of chronic thyroid therapy. Krugman LG, Hershman JM, Chopra IJ, Levine GA, Pekary E, Geffner DL, Chua Teco GN

(5) Int J Obes 1983;7(2):123-31 The effect of a low-calorie diet alone and in combination with triiodothyronine therapy on weight loss and hypophyseal thyroid function in obesity. Koppeschaar HP, Meinders AE, Schwarz F.

(6) Am J Med 2002 Jul;113(1):30-6 Effect of 6-month adherence to a very low carbohydrate diet program. Westman EC, Yancy WS, Edman JS, Tomlin KF, Perkins CE.

(7) J Endocrinol Invest 2001 Dec;24(11):897-913 Control of energy metabolism by iodothyronines.
Lanni A, Moreno M, Lombardi A, de Lange P, Goglia F

(8) Clin Endocrinol (Oxf) 1980 Nov;13(5):489-506 Metabolic aspects of the calorigenic effect of thyroid hormone in mammals. Sestoft L.

(9)Annu Rev Nutr 1995;15:263-91 Thermogenesis and thyroid function. Freake HC, Oppenheimer JH.

(10) J Clin Invest 2001 Sep;108(5):733-7 Effect of triiodothyronine on mitochondrial energy coupling in human skeletal muscle. Lebon V, Dufour S, Petersen KF, Ren J, Jucker BM, Slezak LA, Cline GW, Rothman DL, Shulman GI.

(11)J Clin Endocrinol Metab 1999 Jan;84(1):207-12 Testosterone administration preserves protein balance but not muscle strength during 28 days of bed rest. Zachwieja JJ, Smith SR, Lovejoy JC, Rood JC, Windhauser MM, Bray GA.

(12) Genome Res 2002 Feb;12(2):281-91 In vivo regulation of human skeletal muscle gene expression by thyroid hormone. Clement K, Viguerie N, Diehn M, Alizadeh A, Barbe P, Thalamas C, Storey JD, Brown PO, Barsh GS, Langin D.

(13) J Clin Endocrinol Metab 2003 Jan;88(1):358-62 Related Articles, Links Differential anabolic effects of testosterone and amino Acid feeding in older men. Ferrando AA, Sheffield-Moore M, Paddon-Jones D, Wolfe RR, Urban RJ.

(14) J Hepatol 1996 Mar;24(3):313-9 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.

(15) Cardiovasc Res 1998 Oct;40(1):211-22 Terbutaline-induced desensitization of human cardiac beta 2-adrenoceptor-mediated positive inotropic effects: attenuation by ketotifen. Poller U, Fuchs B, Gorf A, Jakubetz J, Radke J, Ponicke K, Brodde OE.

(16) Eur J Clin Pharmacol 1996;50(3):167-70 Ketotifen in HIV-infected patients: effects on body weight and release of TNF-alpha. Ockenga J, Rohde F, Suttmann U, Herbarth L, Ballmaier M, Schedel I.

(17)Endocrinology 1998 Jun;139(6):2863-8 Tumor necrosis factor-alpha inhibits leydig cell steroidogenesis through a decrease in steroidogenic acute regulatory protein expression. Mauduit C, Gasnier F, Rey C, Chauvin MA, Stocco DM, Louisot P, Benahmed M.

(18) Growth Horm IGF Res 2001 Aug;11(4):250-60 Tissue-specific regulation of IGF-I and IGF-binding proteins in response to TNFalpha. Lang CH, Nystrom GJ, Frost RA.

(19) Exerc Immunol Rev 2001;7:18-31 Exercise and cytokines with particular focus on muscle-derived IL-6. Pedersen BK, Steensberg A, Fischer C, Keller C, Ostrowski K, Schjerling P.

(20) Am J Physiol Endocrinol Metab 2001 Sep;281(3):E449-54 Catecholamines inhibit Ca(2+)-dependent proteolysis in rat skeletal muscle through beta(2)-adrenoceptors and cAMP. Navegantes LC, Resano NM, Migliorini RH, Kettelhut IC

(21) J Clin Endocrinol Metab 2002 Feb;87(2):630-4 Regulation of human adipocyte gene expression by thyroid hormone Viguerie N, Millet L, Avizou S, Vidal H, Larrouy D, Langin D.

(22) Metabolism 1987 Nov;36(11):1031-9 Alpha 2- and beta-adrenergic receptor binding and action in gluteal adipocytes from patients with hypothyroidism and hyperthyroidism. Richelsen B, Sorensen NS

(23) Br J Pharmacol 2000 Feb;129(3):448-56 Regulation of beta 1- and beta 3-adrenergic agonist-stimulated lipolytic response in hyperthyroid and hypothyroid rat white adipocytes. Germack R, Starzec A, Perret GY

(24) Braz J Med Biol Res 1994 May;27(5):1269-72 Role of thyroid hormone in the control of growth hormone gene expression. Volpato CB, Nunes MT.

(25) Am J Physiol 1999 Aug;277(2 Pt 1):E370-9 Related Articles, Links Low-dose T(3) improves the bed rest model of simulated weightlessness in men and women. Lovejoy JC, Smith SR, Zachwieja JJ, Bray GA, Windhauser MM, Wickersham PJ, Veldhuis JD, Tulley R, de la Bretonne JA.

(26) Life Sci 2002 Jul 19;71(9):1059-70 Evidence for a deficient pancreatic beta-cell response in a rat model of hyperthyroidism. Fukuchi M, Shimabukuro M, Shimajiri Y, Oshiro Y, Higa M, Akamine H, Komiya I, Takasu N.

(27) Diabetologia 2002 Jun;45(6):851-5 Thyroxine induces pancreatic beta cell apoptosis in rats.
Jorns A, Tiedge M, Lenzen S.

(28) Am J Physiol 1985 May;248(5 Pt 1):E593-601 Effect of thyroid hormone excess on action, secretion, and metabolism of insulin in humans.= Dimitriadis G, Baker B, Marsh H, Mandarino L, Rizza R, Bergman R, Haymond M, Gerich J

(29) Curr Opin Clin Nutr Metab Care 2000 Jan;3(1):67-71 Effects of insulin on muscle tissue.
Wolfe RR.

(30) J Steroid Biochem Mol Biol 2001 Jan-Mar;76(1-5):31-42 Selective modulation of thyroid hormone receptor action. Baxter JD, Dillmann WH, West BL, Huber R, Furlow JD, Fletterick RJ, Webb P, Apriletti JW, Scanlan TS.
 
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