- Feb 1, 2005
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Interesting thread from another board on Cytomel
First off – this is not as easy as most physiological functions to follow – but I am going to attempt to supply you with an easy to follow explanation of the thyroid function impact as well as how the thyroid functions. The thyroid is responsible for producing the hormones thyroxine (T4) and triiodothyronine (T3) (both of which are iodine containing hormones) which are incorporated into the protein thyroglobulin – which is stored in the thyroid follicles which is released into circulation following proteolysis which is the division of proteins by enzymes. These actions influence growth and metabolism. In normal thyroid function (meaning a healthy – normal operating thyroid) adequate amounts of thyroid hormone are maintained in the blood by a negative feedback mechanism in accordance with the metabolic demands of your body. Secretion of thyroid hormone is dependant on the amount of circulating TSH (thyroid stimulating hormone) also called thyrotropin – this is orchestrated in unison with volumes of TRH (thyroid releasing hormone) and TRF (thyroid releasing factor) as well as the level of circulating thyroid hormone. I hope you are getting that this is a very delicate and intricate balance. Since increased amounts of thyroid hormone suppress TSH release, a negative feedback mechanism is reached – thus maintaining a steady state of thyroid function and metabolism regulation.
Thyroid hormone in the blood is tightly bound to several serum binding proteins – TBG, TBPA and albumin. Iodine is absorbed in the small intestines as iodidie and carried into circulation to the thyroid under the direct influence of TSH where it is oxidized into a high energy state and bound to both free and thyroglobulin tyrosine forming mono and diiodotyrosine (MIT and DIT). The hormones T3 and T4 are formed by coupling MIT and DIT which are then entered into the blood where they are transported to the cell where it exerts its physiological function. Thyroid hormone bound to T4 – binding proteins is not able to enter the cell. T3 on the other hand is not bound by the same limiting physiological factors and is some 3 to 4 times more potent than T4 playing a larger impact role on metabolism relating to 2/3 of the thyroid hormone activity coming as a direct influence from T3. Basically to bodybuilders – this means that the conversion of T4 to T3 means a more dramatic impact on the metabolism.
Cytomel is Liothyronine used in the treatment of hypothyroidism – which is the an ailment or “disease” most commonly caused by iatrogenic factors (meaning usually induced or caused inadvertently by the medical treatment or procedures or activity of a physician) or other natural causes such as pituitary deficiency. Understanding that hypothyroidism results in most all cases as a result of autoimmunity against the thyroid gland, an immunity that destroys the gland rather than stimulates it (as hyperthyroidism is the exact opposite – it is an autoimmunity that over stimulates the thyroid). So here is where you need to listen up….let’s just figure you have a normal thyroid and thyroid function – and you take a drug like Cytomel to stimulate and promote T4/T3 conversion so you benefit from the increased metabolism…..the result will be some additional fat loss no doubt. BUT – the risk you are running (and it is more common than not) is that your thyroid – then is unable to find its natural balance and you then force an autoimmune reaction causing severe hyper or hypo reaction thus placing yourself in peril to regaining a normal thyroid function. Know for a fact that the end result may far outweigh the “immediate” benefits – as when you stop taking Cytomel – it is very common to experience a huge weight gain – due to your thyroid function being screwed up by your little stint with a “tiny little white pill”…..in the end the same thing can be accomplished with proper diet and caloric manipulation without the risk of sending a delicate balance astray. There are better avenues to explore for stimulating T3/T4 conversion and supporting proper thyroid function – say like when following a low calorie diet – when the body’s natural response is to slow T3/T4 conversion.
I did a ton of research in the field of phosphate supplementation for this very purpose. The rationale behind phosphate supplementation is that it will prevent the resting metabolic rate from decreasing on a low-calorie diet, allowing fat loss to continue at an increased rate, and even preventing the regain of body mass after discontinuation of the diet (Nazar et al. 1996). Nazar and colleagues (1996) suggest that phosphate increases the resting metabolic rate through the effects it has on the thyroid hormones. When the thyroid gland is stimulated, it releases a hormone called thyroxine (T4). Thyroxine increases the rates of chemical reactions in nearly all the cells of the body, thereby increasing the general level of body metabolism (Guyton and Hall 1997). Even more potent, is the hormone triiodothyronine (T3), which is what T4 is converted to by the removal of iodine (Nazar et al. 1996). When subjected to a low-calorie diet, the rate of conversion of T4 to T3 is decreased. Nazar and colleagues suggest that phosphate supplementation reverses this, increasing the rate of T3 production. Since T3 has a stronger effect on metabolism, the resting metabolic rate increases, ultimately resulting in a greater loss of fat mass. The theory that phosphate supplementation reverses the hindrance of the conversion of T4 to T3 during a low-calorie diet, brings into account the idea that phosphate also enhances the metabolism of glucose (sugar) in the body. The transformation of T4 to T3 requires NADPH, which is produced during the process of glucose degradation, more commonly referred to as glycolysis. Phosphate is believed to increase the concentration of certain enzymes that may ordinarily limit glycolysis, thus increasing the production of NADPH. When the concentration of NADPH is increased, so is the conversion of T4 to T3, which finally results in an increased metabolic rate leading to a greater loss of fat mass. In summary, Nazar and colleagues (1996) state that "the observed elevation in resting metabolic rate is casually connected with changes in the rate of thyroxine deiodination most probably associated with enhancement of glucose utilization and production of NADPH induced by addition of inorganic phosphates." In the first study, conducted by Nazar and colleagues (1996), thirty overweight women aged 31-46 years participated in an eight week weight-reduction program. The women were randomly divided into two groups. Group one received phosphate supplement during the first four weeks of the study and placebo (sugar pills) during the last four weeks, while group two received placebo the first four weeks and phosphate supplement the remaining four weeks. The study was conducted so that neither the subjects nor the investigators knew which group was receiving which treatment. The subjects were instructed to take two tablets three times per day (after meals), and they also took fiber pills in order to suppress their appetites. Resting metabolic rates and blood samples to determine hormone levels were taken before the study, after four weeks, and again at the end of the study. Results showed that both groups lost more body mass during the first four weeks than during the last four, and that there were no significant differences between groups in total body mass loss. However, both groups showed an elevated resting metabolic rate - approximately 12% in group one and 19% in group two (Nazar et al. 1996) - after their respective four weeks on the phosphate supplement. In group one, resting metabolic rate increased after the first four weeks when they were on the phosphate supplement, and then decreased even below initial values after the last four weeks when they were on the placebo. The same occurred in group two; resting metabolic rate decreased below initial values during the first four weeks when they were on the placebo, and then increased above initial values after the final four weeks when they were taking the phosphates. This information not only supports the idea that resting metabolic rate decreases during a restricted calorie diet, but also shows evidence of an increasing resting metabolic rate when supplementing with phosphates. In regards to the ratios of T4 to T3, the study showed that in both groups the ratio was significantly decreased at the conclusion of the periods of phosphate supplementation, supporting the idea that phosphates allow more T4 to be converted to T3, which causes the increased resting metabolic rate. In a second study, conducted by Kaciuba-Uscilko and colleagues (1993), a group of thirty-six obese women participated in a four week weight reduction program. All subjects were put on the same low fat, high carbohydrate and protein diet, amounting to a consumption of only 1000 calories per day. The subjects were randomly divided into two groups, where group one received mineral tablets containing phosphates, and group two received placebo (not containing phosphates). Subjects in both groups experienced a loss in body mass, but no significant differences were found between either group. This information suggests that the loss in body mass could have been the result of the diet alone rather than that of the phosphate supplement. However, it was noted that after four weeks on the phosphate treatment, the fasting blood glucose level in group one was significantly lowered, while remaining unchanged in group two. This data supports the theory that phosphate supplementation increases glucose degradation, eventually leading to an increased resting metabolic rate.
I just know that playing with your thyroid can be like playing with fire – some get away with it because they have experience and know how to handle themselves – they are educated in “fire”….say like a fireman…..but in most cases – you get burned…and the burn can be long enduring and painful – just wanted you to be well advised. The choice is ultimately up to you – just be advised.
First off – this is not as easy as most physiological functions to follow – but I am going to attempt to supply you with an easy to follow explanation of the thyroid function impact as well as how the thyroid functions. The thyroid is responsible for producing the hormones thyroxine (T4) and triiodothyronine (T3) (both of which are iodine containing hormones) which are incorporated into the protein thyroglobulin – which is stored in the thyroid follicles which is released into circulation following proteolysis which is the division of proteins by enzymes. These actions influence growth and metabolism. In normal thyroid function (meaning a healthy – normal operating thyroid) adequate amounts of thyroid hormone are maintained in the blood by a negative feedback mechanism in accordance with the metabolic demands of your body. Secretion of thyroid hormone is dependant on the amount of circulating TSH (thyroid stimulating hormone) also called thyrotropin – this is orchestrated in unison with volumes of TRH (thyroid releasing hormone) and TRF (thyroid releasing factor) as well as the level of circulating thyroid hormone. I hope you are getting that this is a very delicate and intricate balance. Since increased amounts of thyroid hormone suppress TSH release, a negative feedback mechanism is reached – thus maintaining a steady state of thyroid function and metabolism regulation.
Thyroid hormone in the blood is tightly bound to several serum binding proteins – TBG, TBPA and albumin. Iodine is absorbed in the small intestines as iodidie and carried into circulation to the thyroid under the direct influence of TSH where it is oxidized into a high energy state and bound to both free and thyroglobulin tyrosine forming mono and diiodotyrosine (MIT and DIT). The hormones T3 and T4 are formed by coupling MIT and DIT which are then entered into the blood where they are transported to the cell where it exerts its physiological function. Thyroid hormone bound to T4 – binding proteins is not able to enter the cell. T3 on the other hand is not bound by the same limiting physiological factors and is some 3 to 4 times more potent than T4 playing a larger impact role on metabolism relating to 2/3 of the thyroid hormone activity coming as a direct influence from T3. Basically to bodybuilders – this means that the conversion of T4 to T3 means a more dramatic impact on the metabolism.
Cytomel is Liothyronine used in the treatment of hypothyroidism – which is the an ailment or “disease” most commonly caused by iatrogenic factors (meaning usually induced or caused inadvertently by the medical treatment or procedures or activity of a physician) or other natural causes such as pituitary deficiency. Understanding that hypothyroidism results in most all cases as a result of autoimmunity against the thyroid gland, an immunity that destroys the gland rather than stimulates it (as hyperthyroidism is the exact opposite – it is an autoimmunity that over stimulates the thyroid). So here is where you need to listen up….let’s just figure you have a normal thyroid and thyroid function – and you take a drug like Cytomel to stimulate and promote T4/T3 conversion so you benefit from the increased metabolism…..the result will be some additional fat loss no doubt. BUT – the risk you are running (and it is more common than not) is that your thyroid – then is unable to find its natural balance and you then force an autoimmune reaction causing severe hyper or hypo reaction thus placing yourself in peril to regaining a normal thyroid function. Know for a fact that the end result may far outweigh the “immediate” benefits – as when you stop taking Cytomel – it is very common to experience a huge weight gain – due to your thyroid function being screwed up by your little stint with a “tiny little white pill”…..in the end the same thing can be accomplished with proper diet and caloric manipulation without the risk of sending a delicate balance astray. There are better avenues to explore for stimulating T3/T4 conversion and supporting proper thyroid function – say like when following a low calorie diet – when the body’s natural response is to slow T3/T4 conversion.
I did a ton of research in the field of phosphate supplementation for this very purpose. The rationale behind phosphate supplementation is that it will prevent the resting metabolic rate from decreasing on a low-calorie diet, allowing fat loss to continue at an increased rate, and even preventing the regain of body mass after discontinuation of the diet (Nazar et al. 1996). Nazar and colleagues (1996) suggest that phosphate increases the resting metabolic rate through the effects it has on the thyroid hormones. When the thyroid gland is stimulated, it releases a hormone called thyroxine (T4). Thyroxine increases the rates of chemical reactions in nearly all the cells of the body, thereby increasing the general level of body metabolism (Guyton and Hall 1997). Even more potent, is the hormone triiodothyronine (T3), which is what T4 is converted to by the removal of iodine (Nazar et al. 1996). When subjected to a low-calorie diet, the rate of conversion of T4 to T3 is decreased. Nazar and colleagues suggest that phosphate supplementation reverses this, increasing the rate of T3 production. Since T3 has a stronger effect on metabolism, the resting metabolic rate increases, ultimately resulting in a greater loss of fat mass. The theory that phosphate supplementation reverses the hindrance of the conversion of T4 to T3 during a low-calorie diet, brings into account the idea that phosphate also enhances the metabolism of glucose (sugar) in the body. The transformation of T4 to T3 requires NADPH, which is produced during the process of glucose degradation, more commonly referred to as glycolysis. Phosphate is believed to increase the concentration of certain enzymes that may ordinarily limit glycolysis, thus increasing the production of NADPH. When the concentration of NADPH is increased, so is the conversion of T4 to T3, which finally results in an increased metabolic rate leading to a greater loss of fat mass. In summary, Nazar and colleagues (1996) state that "the observed elevation in resting metabolic rate is casually connected with changes in the rate of thyroxine deiodination most probably associated with enhancement of glucose utilization and production of NADPH induced by addition of inorganic phosphates." In the first study, conducted by Nazar and colleagues (1996), thirty overweight women aged 31-46 years participated in an eight week weight-reduction program. The women were randomly divided into two groups. Group one received phosphate supplement during the first four weeks of the study and placebo (sugar pills) during the last four weeks, while group two received placebo the first four weeks and phosphate supplement the remaining four weeks. The study was conducted so that neither the subjects nor the investigators knew which group was receiving which treatment. The subjects were instructed to take two tablets three times per day (after meals), and they also took fiber pills in order to suppress their appetites. Resting metabolic rates and blood samples to determine hormone levels were taken before the study, after four weeks, and again at the end of the study. Results showed that both groups lost more body mass during the first four weeks than during the last four, and that there were no significant differences between groups in total body mass loss. However, both groups showed an elevated resting metabolic rate - approximately 12% in group one and 19% in group two (Nazar et al. 1996) - after their respective four weeks on the phosphate supplement. In group one, resting metabolic rate increased after the first four weeks when they were on the phosphate supplement, and then decreased even below initial values after the last four weeks when they were on the placebo. The same occurred in group two; resting metabolic rate decreased below initial values during the first four weeks when they were on the placebo, and then increased above initial values after the final four weeks when they were taking the phosphates. This information not only supports the idea that resting metabolic rate decreases during a restricted calorie diet, but also shows evidence of an increasing resting metabolic rate when supplementing with phosphates. In regards to the ratios of T4 to T3, the study showed that in both groups the ratio was significantly decreased at the conclusion of the periods of phosphate supplementation, supporting the idea that phosphates allow more T4 to be converted to T3, which causes the increased resting metabolic rate. In a second study, conducted by Kaciuba-Uscilko and colleagues (1993), a group of thirty-six obese women participated in a four week weight reduction program. All subjects were put on the same low fat, high carbohydrate and protein diet, amounting to a consumption of only 1000 calories per day. The subjects were randomly divided into two groups, where group one received mineral tablets containing phosphates, and group two received placebo (not containing phosphates). Subjects in both groups experienced a loss in body mass, but no significant differences were found between either group. This information suggests that the loss in body mass could have been the result of the diet alone rather than that of the phosphate supplement. However, it was noted that after four weeks on the phosphate treatment, the fasting blood glucose level in group one was significantly lowered, while remaining unchanged in group two. This data supports the theory that phosphate supplementation increases glucose degradation, eventually leading to an increased resting metabolic rate.
I just know that playing with your thyroid can be like playing with fire – some get away with it because they have experience and know how to handle themselves – they are educated in “fire”….say like a fireman…..but in most cases – you get burned…and the burn can be long enduring and painful – just wanted you to be well advised. The choice is ultimately up to you – just be advised.
