Cytomel is a thyroid hormone supplement that contains liothyronine. Liothyronine is a synthetic form of the hormone T3, which is naturally produced by the thyroid gland. This medication is given when the body does not produce enough of the hormone T3 on its own, a condition known as hypothyroidism.
Human growth hormone is naturally produced by the anterior lobe of the pituitary gland. There are HGH medications available by prescription for those with kidney failure, Turner's syndrome or other diseases. HGH medications, such as somatropin, humatrope, norditropin, are only not available in pill form, they come as injections. The DEA also states, " HGH is only bio available in the injectable form. The HGH molecule is too large for absorption across the lining of the oral mucosa and the hormone is digested by the stomach before absorption can occur."
Both Cytomel and HGH are hormones that are used for medical reasons to regulate growth in individuals whose bodies do not produce enough of these hormones naturally. When a person needs the medication Cytomel, she most likely has an underactive thyroid and she will gain weight, according to the Mayo Clinic. When a person needs an HGH medication, his body is not growing enough. Cytomel is liothyronine, a man-made medication designed to mimic the action of the T3 that is naturally produced by the thyroid gland. Somatropin is an injectable form of the HGH produced by the pituitary gland.
Cytomel up-regulates the beta-2 adrenergic receptors in fat tissues. In lipolysis, or the breakdown of fat in fat tissues, the enzyme HSL (hormone sensitive lipase) plays a significant part. HSL controls the rate of lipolysis. For HSL to be activated, epinephrine and nonepinephrine (catecholomines) are necessary. These catecholomines bind to the beta-2 receptors, and thus when Cytomel up-regulates the beta-receptors, there is a corresponding increase in the ability of catecholomines to activate HSL, resulting to increased lipolysis.
This drug is likewise known to increase the UCP-3 or uncoupling protein-3. This process significantly increases lipolysis. Further, Cytomel also stimulates growth hormone (GH) production, as substantiated by several studies. And since GH is a thermogenic, it contributes to this drug’s fat-burning action. This is why when athletes are using Cytomel they find no need to use HGH. With AAS use, the suppression occurs even after the therapy is stopped, sometimes in periods of weeks or months (especially in cases of long-term use). The same thing is observed during insulin intake, whereby the pancreas (the organ responsible for insulin production) ceases its production of insulin. Such is not the case with exogenous T3 hormone therapy. Several studies have concluded that thyroid therapy does not cause prolonged suppression of thyroid normal production. Thyroid function is normalized just days after medication is discontinued. In other words, there is no thyroid shutdown due to T3 supplementation; there is only a down-regulation of thyroid output during therapy.
Side effects of this class of drug include tachycardia and atrial arrhythmia, bone resorption, and loss of lean muscle tissue. Secondary side effects include insomnia, diarrhea, and nausea. These adverse reactions are highly possible if the user takes high dosages. Notice that some of its major side effects relate to the cardiovascular system. This is because thyroid hormones have significant effects on cardiac structures (including cardiac muscles) and systems that alter cardiovascular hemodynamics. Hyperthyroidism increases virtually all cardiac functions including heart rate and contractility, diastolic relaxation, and rate of ventricular pressure development. This results to an increased cardiac output by as much as 250 percent. These physiological changes are (most likely) the consequences of an increase in the expression of ATP and a decrease in the expression of ATP’s inhibitor, phospholamban.
Another drawback of Cytomel is its catabolic ability. When Cytomel exerts this ability on stored fats, this is an asset. However, this becomes a liability when it exerts this on bones and muscles. The negative result is bone resorption and muscle wasting (mentioned above). Moreover, this drug also diminishes GH’s nitrogen retention ability (although it stimulates GH’s production, as mentioned earlier). There is consensus among Cytomel users that the dosage protocol with this drug is to ramp it up, which means you start at the lowest dosage then gradually move upward. However, there are divergent opinions on how long the ‘gradually’ part should be. There are those who say it should be every three days, and then some pharmacological studies endorse it from 1 to 2 weeks. However, the user’s tolerance level ultimately determines the time frame; that is, if the user reacts really well with Cytomel, then the dosage can gradually increase every three days. Users are advised not to ramp up and down the dosage during therapy as this causes fluctuations in hormone levels, which further results to hormonal imbalance. The more prudent practice is to taper off the dosage. The minimum daily dosage of T3 is 5mcg and the maximum is 100mcg.
Cytomel intake is not dependent on body weight or gender, but rather on the individual’s blood level. This means that females can take the same dosage volume and schedule as males.
Both Cytomel and HGH are hormones that are used for medical reasons to regulate growth in individuals whose bodies do not produce enough of these hormones naturally. When a person needs the medication Cytomel, she most likely has an underactive thyroid and she will gain weight, according to the Mayo Clinic. When a person needs an HGH medication, his body is not growing enough. Cytomel is liothyronine, a man-made medication designed to mimic the action of the T3 that is naturally produced by the thyroid gland. Somatropin is an injectable form of the HGH produced by the pituitary gland.
Cytomel up-regulates the beta-2 adrenergic receptors in fat tissues. In lipolysis, or the breakdown of fat in fat tissues, the enzyme HSL (hormone sensitive lipase) plays a significant part. HSL controls the rate of lipolysis. For HSL to be activated, epinephrine and nonepinephrine (catecholomines) are necessary. These catecholomines bind to the beta-2 receptors, and thus when Cytomel up-regulates the beta-receptors, there is a corresponding increase in the ability of catecholomines to activate HSL, resulting to increased lipolysis.
This drug is likewise known to increase the UCP-3 or uncoupling protein-3. This process significantly increases lipolysis. Further, Cytomel also stimulates growth hormone (GH) production, as substantiated by several studies. And since GH is a thermogenic, it contributes to this drug’s fat-burning action. This is why when athletes are using Cytomel they find no need to use HGH. With AAS use, the suppression occurs even after the therapy is stopped, sometimes in periods of weeks or months (especially in cases of long-term use). The same thing is observed during insulin intake, whereby the pancreas (the organ responsible for insulin production) ceases its production of insulin. Such is not the case with exogenous T3 hormone therapy. Several studies have concluded that thyroid therapy does not cause prolonged suppression of thyroid normal production. Thyroid function is normalized just days after medication is discontinued. In other words, there is no thyroid shutdown due to T3 supplementation; there is only a down-regulation of thyroid output during therapy.
Side effects of this class of drug include tachycardia and atrial arrhythmia, bone resorption, and loss of lean muscle tissue. Secondary side effects include insomnia, diarrhea, and nausea. These adverse reactions are highly possible if the user takes high dosages. Notice that some of its major side effects relate to the cardiovascular system. This is because thyroid hormones have significant effects on cardiac structures (including cardiac muscles) and systems that alter cardiovascular hemodynamics. Hyperthyroidism increases virtually all cardiac functions including heart rate and contractility, diastolic relaxation, and rate of ventricular pressure development. This results to an increased cardiac output by as much as 250 percent. These physiological changes are (most likely) the consequences of an increase in the expression of ATP and a decrease in the expression of ATP’s inhibitor, phospholamban.
Another drawback of Cytomel is its catabolic ability. When Cytomel exerts this ability on stored fats, this is an asset. However, this becomes a liability when it exerts this on bones and muscles. The negative result is bone resorption and muscle wasting (mentioned above). Moreover, this drug also diminishes GH’s nitrogen retention ability (although it stimulates GH’s production, as mentioned earlier). There is consensus among Cytomel users that the dosage protocol with this drug is to ramp it up, which means you start at the lowest dosage then gradually move upward. However, there are divergent opinions on how long the ‘gradually’ part should be. There are those who say it should be every three days, and then some pharmacological studies endorse it from 1 to 2 weeks. However, the user’s tolerance level ultimately determines the time frame; that is, if the user reacts really well with Cytomel, then the dosage can gradually increase every three days. Users are advised not to ramp up and down the dosage during therapy as this causes fluctuations in hormone levels, which further results to hormonal imbalance. The more prudent practice is to taper off the dosage. The minimum daily dosage of T3 is 5mcg and the maximum is 100mcg.
Cytomel intake is not dependent on body weight or gender, but rather on the individual’s blood level. This means that females can take the same dosage volume and schedule as males.
No comments:
Post a Comment