I am now in a lean mass phase with a small t3 dose.25-30 mcgs as a nutrient partitioner.Most my my training has been done in a low carb/deficit state because of my love hate relationship with my genetics.Father is a rather large man and has been for most of his life.Mom is the same.Needless to say I lose alot of muscle staying lean or atleast trying to.Carbs are my enemy so to speak and excess calories seem to store quickly. So far my first dose today and I feel better after eating carbs than I used to,not tired at all.
Over the next 3 weeks I'll be playing around with this serious drug.Here are some myths/misconceptions about t3 I have found in my research.
T3 causes damage to your thyroid myth
It dose indeed cause your natural t3 production to stop but you do recover as long as you don't go overboard.25mcgs ED even over 3 months won't damage your thyroid permanently .Of course this is for the general population mind you.If you go above 150mcgs thats getting a little much.Although rebound weight gain is almost writen in stone.
T3 burns muscle!
This is true at high doses (above 50 mcgs) coupled with low calories.At lower doses this shouldn't be a problem as long as your eating enough OVER maint level.
T3 is a cutting drug and nothing more!
Not true,nutrient partitioning aspect is great!Can be used in bulk/lean mass for better breakdown of/partitioning fats,carbs and protein.
Heres info on the effects
Effects of T3
T3 increases the basal metabolic rate and, thus, increases the body's oxygen and energy consumption. The basal metabolic rate is the minimal caloric requirement needed to sustain life in a resting individual. T3 acts on the majority of tissues within the body, with a few exceptions including the spleen and testis. It increases the production of the Na+/K+ -ATPase and, in general, increases the turnover of different endogenous macromolecules by increasing their synthesis and degradation.
Protein
T3 stimulates the production of RNA Polymerase I and II and, therefore, increases the rate of protein synthesis. It also increases the rate of protein degradation, and, in excess, the rate of protein degradation exceeds the rate of protein synthesis. In such situations, the body may go into negative ion balance.
Glucose
T3 potentiates the effects of the β-adrenergic receptors on the metabolism of glucose. Therefore, it increases the rate of glycogen breakdown and glucose synthesis in gluconeogenesis.
Lipids
T3 stimulates the breakdown of cholesterol and increases the number of LDL receptors, thereby increasing the rate of lipolysis.
Heart
T3 increases the heart rate and force of contraction, thus increasing cardiac output, by increasing β-adrenergic receptor levels in myocardium. This results in increased systolic blood pressure and decreased diastolic blood pressure. The latter two effects act to produce the typical bounding pulse seen in hyperthyroidism.
Development
T3 has profound effect upon the developing embryo and infants. It affects the lungs and influences the postnatal growth of the central nervous system. It stimulates the production of myelin, the production of neurotransmitters, and the growth of axons. It is also important in the linear growth of bones.
Neurotransmitters
T3 may increase serotonin in the brain, in particular in the cerebral cortex, and down-regulate 5HT-2 receptors, based on studies in which T3 reversed learned helplessness in rats and physiological studies of the rat brain.
T3 has a short half life!
This may be started by doctors,bro science or w/e but the half life of Liothyronine or cytomel is 2.5 days.Confirmed by a local pharmacy and a doctor and the internet.No need to split dosage unless you feel hypo symptoms caused by the bigger doses(50-75 mcgs or higher)
T3 must be used with an anabolic so you don't waste away!
Again not for the lower doses but for the higher doses you MUST to retain even alittle muscle.At50 to 100 plus mcgs you will be burning muscle even with anabolics.This is a fact.
You must taper up and down!
God I wish this would die.After hundreds of post and everyone posting the same reason(perm thyroid damage) I found one that lead me to the conclusion this is a myth.Confirmed it aswell.Just like with clen,no need to tapper up or down but the sides can be a bit much if you don't.Also it's easier for your thyroid to recover if you come down slowly but you still can recover if you don't.This is one of those drugs where you need to acess how it reacts with your body.Start at 25 mcgs cause nobody wants to faint/throw it up by jumping right to 100mcgs.
Interesting read about Regulation of Human Skeletal Muscle Gene Expression by Thyroid Hormone
http://genome.cshlp.org/content/12/2/281.full
Interesting read on Effects of hyperthyroidism on the sensitivity of glycolysis and
glycogen synthesis to insulin in the soleus muscle of the rat ( hyperthyroidism effects at doses of 60+mcgs I'll look for a human study later)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1149261/pdf/biochemj00228-0095.pdf
NEW USEFULL INFO!
While the primary athletic purpose of using thyroid drugs is to maintain an upgraded metabolism in the hope of burning bodyfat faster, such drugs are also used for other purposes. For example, injecting human growth hormone (GH) temporarily inhibits the release of a pituitary hormone called thyroid-stimulating hormone (TSH) that controls thyroid hormone release from the thyroid gland. Some athletes seek to overcome this GH side effect by taking thyroid drugs.
In addition, GH itself will not work without an adequate thyroid output. This illustrates the many interactions between the body's hormones and why taking an isolated hormone can lead to imbalances in other hormones. GH also fosters the conversion of inactive T4 thyroid to the active T3 version. However, the fat-mobilizing effects associated with GH are not the result of this upgraded thyroid activity.
Studies have concluded that bodybuilders who use anabolic steroids show impaired thyroid functions (Journal of Clinical Endocrinology and Metabolism 76:1069-7 1, 1993/American Journal of Sports Medicine, 15:357-61, 1987). The research confirmed that bodybuilders using large doses of steroids had increased TSH release, coupled with lower T3 levels. How the steroids do this isn't known.
One theory is that large doses of steroids decrease a protein that binds with thyroid hormone in the blood. This, in turn, leads to higher blood levels of free thyroid hormone. This increased free-thyroid blood level is monitored by the brain's hypothalamus, which reacts by releasing less thyroid-stimulating hormone, leading to less thyroid output from the thyroid gland. This scenario is called "negative feedback inhibition," and is characteristic of several other hormones, including testosterone.
For body composition purposes, the primary problem with using thyroid hormone at high doses is that it isn't specific to fat tissue. The upgraded metabolism that results from taking thyroid drugs also leads to increased muscle catabolism, or breakdown. This is particularly evident during the initial two weeks of using thyroid drugs. After that time, the body appears to compensate for the added thyroid intake, and muscle catabolism subsides to a limited degree.
A SEMI recent report, published in the Journal of Clinical Endocrinology and Metabolism (82:765-70, 1997), examined what happens when a group of healthy young men used high doses of T3 drugs for 63 days. The study focused on the drug's effects on nitrogen balance (a measure of muscle function), body composition and energy expenditure. The men in the experiment were also randomly assigned to either low-fat or high-fat diets to assess the effects of thyroid and diet composition.
By the six-week point in the study, the men using thyroid drugs showed losses in both muscle mass and bodyfat. As expected, nitrogen balance was negative during the first three weeks, pointing to increased muscle catabolism. But after three weeks, the nitrogen balance in the men on thyroid drugs returned to baseline values. At the nine-week mark, no significant changes in protein turnover occurred, but the men still showed increased usage of protein as energy.
Consuming a high-fat diet appeared to decrease the fat-oxidizing effects associated with thyroid intake. However, the doses ofT3 drugs in this study were less than those typically used by some athletes. Regardless, this finding does indicate that thyroid drugs work belier at reducing fat stores if a low-fat diet is used in conjunction with the drug. CALMING THE STORM Another study, published in Medicine and Science in Sports and Exercise (29:175- 80, 1997), looked at the effects of excess thyroid hormone on muscle function. It was discovered that having a surplus of active thyroid hormone, whether it results from a malady such as Graves' disease or from taking thyroid drugs, can lead to decreased muscular function through several mechanisms. People with Graves' disease, a clinical form of excess thyroid output, often display muscle weakness and impaired exercise tolerance.
Bodybuilders who use thyroid drugs while attempting to carb load during the final week of their contest preparations may be wasting their time. The purpose of carb loading is to provide a fuller, more dense appearance to muscles. But taking thyroid drugs will inhibit glycogen synthesis at high doses. If a bodybuilder reduced his carb intake before the loading phase - as is the common practice - he may wind up looking "flat" onstage because the carbs simply won't kick in as expected due to the concomitant thyroid usage.
Small amounts of thyroid, however, may be advantageous during low-carb dieting. If less than 40 grams of carbohydrate are consumed, the body turns on a survival mechanism to conserve lean body mass. One way it does this is by converting active thyroid hormone into an inactive version called "reverse T3." This mitigates muscle-tissue breakdown, but it also lowers the rate of fat- burning. To compensate, some athletes use small doses of Cytomel.
The danger with this "solution," besides all the other inherent problems related to higher thyroid activity discussed earlier, is that excess(high doses) thyroid may also interfere with testosterone activity. Excess(high dose) thyroid hormone also increases the rate of synthesis of another protein that binds to insulinlike growth factor-I (IGF-l). This is significant because IGF 1 is thought to be the active ingredient of GH's beneficial effect on muscle. And, because it affects specialized satellite cells in muscle, IGF-l is also needed for muscle repair after exercise.
I hope that cleared up some foggy info and thank you for reading.Sub for updates on my results.
Over the next 3 weeks I'll be playing around with this serious drug.Here are some myths/misconceptions about t3 I have found in my research.
T3 causes damage to your thyroid myth
It dose indeed cause your natural t3 production to stop but you do recover as long as you don't go overboard.25mcgs ED even over 3 months won't damage your thyroid permanently .Of course this is for the general population mind you.If you go above 150mcgs thats getting a little much.Although rebound weight gain is almost writen in stone.
T3 burns muscle!
This is true at high doses (above 50 mcgs) coupled with low calories.At lower doses this shouldn't be a problem as long as your eating enough OVER maint level.
T3 is a cutting drug and nothing more!
Not true,nutrient partitioning aspect is great!Can be used in bulk/lean mass for better breakdown of/partitioning fats,carbs and protein.
Heres info on the effects
Effects of T3
T3 increases the basal metabolic rate and, thus, increases the body's oxygen and energy consumption. The basal metabolic rate is the minimal caloric requirement needed to sustain life in a resting individual. T3 acts on the majority of tissues within the body, with a few exceptions including the spleen and testis. It increases the production of the Na+/K+ -ATPase and, in general, increases the turnover of different endogenous macromolecules by increasing their synthesis and degradation.
Protein
T3 stimulates the production of RNA Polymerase I and II and, therefore, increases the rate of protein synthesis. It also increases the rate of protein degradation, and, in excess, the rate of protein degradation exceeds the rate of protein synthesis. In such situations, the body may go into negative ion balance.
Glucose
T3 potentiates the effects of the β-adrenergic receptors on the metabolism of glucose. Therefore, it increases the rate of glycogen breakdown and glucose synthesis in gluconeogenesis.
Lipids
T3 stimulates the breakdown of cholesterol and increases the number of LDL receptors, thereby increasing the rate of lipolysis.
Heart
T3 increases the heart rate and force of contraction, thus increasing cardiac output, by increasing β-adrenergic receptor levels in myocardium. This results in increased systolic blood pressure and decreased diastolic blood pressure. The latter two effects act to produce the typical bounding pulse seen in hyperthyroidism.
Development
T3 has profound effect upon the developing embryo and infants. It affects the lungs and influences the postnatal growth of the central nervous system. It stimulates the production of myelin, the production of neurotransmitters, and the growth of axons. It is also important in the linear growth of bones.
Neurotransmitters
T3 may increase serotonin in the brain, in particular in the cerebral cortex, and down-regulate 5HT-2 receptors, based on studies in which T3 reversed learned helplessness in rats and physiological studies of the rat brain.
T3 has a short half life!
This may be started by doctors,bro science or w/e but the half life of Liothyronine or cytomel is 2.5 days.Confirmed by a local pharmacy and a doctor and the internet.No need to split dosage unless you feel hypo symptoms caused by the bigger doses(50-75 mcgs or higher)
T3 must be used with an anabolic so you don't waste away!
Again not for the lower doses but for the higher doses you MUST to retain even alittle muscle.At50 to 100 plus mcgs you will be burning muscle even with anabolics.This is a fact.
You must taper up and down!
God I wish this would die.After hundreds of post and everyone posting the same reason(perm thyroid damage) I found one that lead me to the conclusion this is a myth.Confirmed it aswell.Just like with clen,no need to tapper up or down but the sides can be a bit much if you don't.Also it's easier for your thyroid to recover if you come down slowly but you still can recover if you don't.This is one of those drugs where you need to acess how it reacts with your body.Start at 25 mcgs cause nobody wants to faint/throw it up by jumping right to 100mcgs.
Interesting read about Regulation of Human Skeletal Muscle Gene Expression by Thyroid Hormone
http://genome.cshlp.org/content/12/2/281.full
Interesting read on Effects of hyperthyroidism on the sensitivity of glycolysis and
glycogen synthesis to insulin in the soleus muscle of the rat ( hyperthyroidism effects at doses of 60+mcgs I'll look for a human study later)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1149261/pdf/biochemj00228-0095.pdf
NEW USEFULL INFO!
While the primary athletic purpose of using thyroid drugs is to maintain an upgraded metabolism in the hope of burning bodyfat faster, such drugs are also used for other purposes. For example, injecting human growth hormone (GH) temporarily inhibits the release of a pituitary hormone called thyroid-stimulating hormone (TSH) that controls thyroid hormone release from the thyroid gland. Some athletes seek to overcome this GH side effect by taking thyroid drugs.
In addition, GH itself will not work without an adequate thyroid output. This illustrates the many interactions between the body's hormones and why taking an isolated hormone can lead to imbalances in other hormones. GH also fosters the conversion of inactive T4 thyroid to the active T3 version. However, the fat-mobilizing effects associated with GH are not the result of this upgraded thyroid activity.
Studies have concluded that bodybuilders who use anabolic steroids show impaired thyroid functions (Journal of Clinical Endocrinology and Metabolism 76:1069-7 1, 1993/American Journal of Sports Medicine, 15:357-61, 1987). The research confirmed that bodybuilders using large doses of steroids had increased TSH release, coupled with lower T3 levels. How the steroids do this isn't known.
One theory is that large doses of steroids decrease a protein that binds with thyroid hormone in the blood. This, in turn, leads to higher blood levels of free thyroid hormone. This increased free-thyroid blood level is monitored by the brain's hypothalamus, which reacts by releasing less thyroid-stimulating hormone, leading to less thyroid output from the thyroid gland. This scenario is called "negative feedback inhibition," and is characteristic of several other hormones, including testosterone.
For body composition purposes, the primary problem with using thyroid hormone at high doses is that it isn't specific to fat tissue. The upgraded metabolism that results from taking thyroid drugs also leads to increased muscle catabolism, or breakdown. This is particularly evident during the initial two weeks of using thyroid drugs. After that time, the body appears to compensate for the added thyroid intake, and muscle catabolism subsides to a limited degree.
A SEMI recent report, published in the Journal of Clinical Endocrinology and Metabolism (82:765-70, 1997), examined what happens when a group of healthy young men used high doses of T3 drugs for 63 days. The study focused on the drug's effects on nitrogen balance (a measure of muscle function), body composition and energy expenditure. The men in the experiment were also randomly assigned to either low-fat or high-fat diets to assess the effects of thyroid and diet composition.
By the six-week point in the study, the men using thyroid drugs showed losses in both muscle mass and bodyfat. As expected, nitrogen balance was negative during the first three weeks, pointing to increased muscle catabolism. But after three weeks, the nitrogen balance in the men on thyroid drugs returned to baseline values. At the nine-week mark, no significant changes in protein turnover occurred, but the men still showed increased usage of protein as energy.
Consuming a high-fat diet appeared to decrease the fat-oxidizing effects associated with thyroid intake. However, the doses ofT3 drugs in this study were less than those typically used by some athletes. Regardless, this finding does indicate that thyroid drugs work belier at reducing fat stores if a low-fat diet is used in conjunction with the drug. CALMING THE STORM Another study, published in Medicine and Science in Sports and Exercise (29:175- 80, 1997), looked at the effects of excess thyroid hormone on muscle function. It was discovered that having a surplus of active thyroid hormone, whether it results from a malady such as Graves' disease or from taking thyroid drugs, can lead to decreased muscular function through several mechanisms. People with Graves' disease, a clinical form of excess thyroid output, often display muscle weakness and impaired exercise tolerance.
Bodybuilders who use thyroid drugs while attempting to carb load during the final week of their contest preparations may be wasting their time. The purpose of carb loading is to provide a fuller, more dense appearance to muscles. But taking thyroid drugs will inhibit glycogen synthesis at high doses. If a bodybuilder reduced his carb intake before the loading phase - as is the common practice - he may wind up looking "flat" onstage because the carbs simply won't kick in as expected due to the concomitant thyroid usage.
Small amounts of thyroid, however, may be advantageous during low-carb dieting. If less than 40 grams of carbohydrate are consumed, the body turns on a survival mechanism to conserve lean body mass. One way it does this is by converting active thyroid hormone into an inactive version called "reverse T3." This mitigates muscle-tissue breakdown, but it also lowers the rate of fat- burning. To compensate, some athletes use small doses of Cytomel.
The danger with this "solution," besides all the other inherent problems related to higher thyroid activity discussed earlier, is that excess(high doses) thyroid may also interfere with testosterone activity. Excess(high dose) thyroid hormone also increases the rate of synthesis of another protein that binds to insulinlike growth factor-I (IGF-l). This is significant because IGF 1 is thought to be the active ingredient of GH's beneficial effect on muscle. And, because it affects specialized satellite cells in muscle, IGF-l is also needed for muscle repair after exercise.
I hope that cleared up some foggy info and thank you for reading.Sub for updates on my results.