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Ruthless Supplements :: T-3 PCT - Ruthless Supplements
Cytomel is a synthetic thyroid agen that is usually a prescribed version of a specific thyroid hormone; that being T3 the biological form of the thyroid hormone sort of like the Vitamin D3 is to the Vitamin D2. Cytomel increases the way the body responds to many processes like the release of adrenaline. Even though it is synthetic, Cytomel is no doubting identical to the naturally occurring hormone liothyronine (also known as triiodothyronine/ T3). It is approved to treat an underactive thyroid gland which is medically defined as hypothyroidism and goiters. Cytomel is also used for specific thyroid investigative tests. The thyroid gland makes two distinct thyroid hormones: levothyroxine (T4) and triiodothyronine (T3). Even though T3 is much more active than T4, the thyroid will produce more T4 than T3. The body can convert the T4 hormone into T3 when necessary. If your thyroid does not make enough thyroid hormones, there are a few different options to increase your levels, one being to combine synthetic T3 and T4 hormones. Some people may not convert T4 into T3 properly, in which case a T3 product such as Cytomel would be implemented to help the individual correct their thyroid hormone level ratio. One might ask how does cytomel work within the body? The area of the brain called the hypothalamus creates thyrotropin-releasing hormone, or TRH, this signaling within the HPTA occurs when levels of thyroid hormone in the blood become noticeably low. This reaction stimulates the production of thyroid-stimulating hormone aka TSH, from the pituitary gland which located right below the brain and is also responsible for the creation of sex hormones such as testosterone. This process in turn will stimulate the thyroid gland to produce and release thyroid hormones. T4 is converted to T3 in tissues such as the liver. T3 only makes up 7 to 10 percent of total thyroid hormone which is obviously a very small amount. Realize that 70 percent of T3 is unfortunately bound to proteins called thyroxine-binding globulin and albumin as well. The other 30 percent of T3 is unbound or free, which is considered the active form. The levels of T3 and T4 are regulated by a feedback loop just as testosterone and estrogen are. Therefore, high levels of T3 and T4 suppress the release of TRH, leading to a suppression of TSH and consequently a suppression of thyroid hormone. On the oppositional side, low levels of T3 and T4 stimulate the release of TRH, which then stimulates the release of TSH, which then stimulates the release of thyroid hormone. T3 supplements increase the basal metabolic rate, stimulate the body's utilization of oxygen and promote the breaking down of proteins, carbohydrates and fats. Over 90 percent of T3 is absorbed into the tissues rapidly because it is not firmly bound to proteins.
As you see use of this drug will suppress your natural thyroid output hormones. Unless one plans to stay on this treatment for life, I highly recommend that they regulate and jumpstart their endogenous thyroid hormone production after using cytomel for bodybuilding purposes. Ruthless Supplements has developed a supplement that boosts natural thyroid hormones without the fear of overstimulating one’s thyroid hormone output. Ruthless’s T3 PCT was made to get one’s adrenals back in place as well while controlling cortisol levels.
Breakdown of ingredients
Vitamin B-12 also known as cyanocobalamine or cobalmin, is an essential vitamin that is required for the development of red blood cells. It is also used to make the protective coating surrounding nerves. There is a link between vitamin B-12 deficiency and hypothyroidism. Over 40% of autoimmune thyroid patients have low levels of Vitamin B-12. About 25 percent of people with thyroid issues will make antibodies that attack their thyroid also make antibodies that attack the parietal glands, and this can cause B-12 levels to drop significantly. Fatigue is a common symptom that both B-12 deficient and thyroid deficient patients experience. When researchers wanted to know why there was link between thyroid hormones and B-12 if most people in the U.S. have a high protein diet. Research showed that it’s the human’s lack of ability to digest the B-12 due to the negative effect that hypothyroidism has on the digestive tract, also realize that B-12 is a metylator and its has many functions in the body; one being that it regulates hormone production. (Ness-Abramof R, et al. Prevalence and evaluation of B12 deficiency in patients with autoimmune thyroid disease. Am J Med Sci, September 2006;332(3):119-22.)
Here are two excerpts on links of B-12 deficiency and hypothyroidism
“J Nutr 1988 Dec;118(12):1495-501
Effect of hypothyroidism on methylmalonate excretion and hepatic vitamin B-12 levels in rats.
Stokstad EL, Nair CP
Department of Nutritional Sciences, University of California, Berkeley 94720.
The effect of hypo- and hyperthyroidism on vitamin B-12 metabolism in the rat was studied by measuring methylmalonic acid excretion, B-12 content of liver and oxidation of 2-[14C]histidine. Ten percent pectin was added to increase severity of B-12 deficiency. The addition of thiouracil to a diet containing 10% pectin decreased the excretion of methylmalonic acid suggesting an amelioration of the B-12 deficiency. It was found that part of this decreased methylmalonic acid excretion was due to a decreased food consumption with a correspondingly decreased intake of branched-chain amino acids which are precursors of methylmalonic acid. When attempts were made to increase the protein intake of animals receiving thiouracil so their amino acid intake was equal to that of the control animals, methylmalonic acid excretion was still lower than that of the controls. It was also found that the vitamin B-12 content of the liver was higher in the animals receiving thiouracil than in the controls. Thyroidectomy had the same effect as feeding thiouracil. Liver B-12 levels are rapidly depleted on a B-12 deficient diet containing 10% pectin. It appears that hypothyroidism, induced either by thyroidectomy or by feeding thiouracil, slows the rate of depletion of hepatic B-12 which in turn facilitates the metabolism of methylmalonic acid and decreases its excretion in the urine.”
“Nuklearmedizin 1979;18(6):278-82
Serum vitamin B12 and folic acid levels in hyperthyroidism.
Gyftaki H, Kesse-Elias M, Koutras D, Pandos P, Papazoglou S, Moulopoulos S
Serum vitamin B12 and folic acid levels were measured in 48 hyperthyroid patients and in a group of euthyroid controls. The levels of vitamin B12 ranged from 120-900 pg/ml with a mean of 429.3 +/- 30.9 pg/ml (SE). The mean serum vitamin B12 level was lower in hyperthyroid patients than in normal controls, the difference being statistically significant (t = 2.584, p less than 0.025). Serum vitamin B12 levels showed a statistically significant negative correlation with the clinical index of Grooks et al. (r = 0.344, p less than 0.05). The findings, although not excluding the involvement of auto-immune gastritis in patients with low serum vitamin B12 levels, suggest a direct action of increased thyroid hormone concentrations. Serum folic acid levels ranged from 0.5-13.8 ng/ml with a mean of 6.8 +/- 0.46 ng/ml (SE). The mean serum folic acid levels were higher in the hyperthyroid patients than in normal controls but the difference was not statistically significant (t = 1.2, p greater than 0.2). The serum folic acid levels did not show any statistically significant correlation with the clinical index of Grooks et al. The fact that no statistically significant difference was found between the mean value in hyperthyroid patients and the mean value in normal controls is probably due to the high folic acid intake in Greece.”
Iodine is literally needed to produce thyroid hormones; it’s the major mineral involved in thyroid development. Iodine is transformed into its free elemental form referred to as iodide. Iodide enters the thyroid gland through a unique transport mechanism. Iodide then goes through a process called oxidation and is included into transitional hormones called MIT aka Monoiodotyrosine, which contains 1 iodide and the other hormone being DIT aka Diiodotyrosine, which contains 2 iodides. These compounds then combine to form the active hormones which are tri-iodothyronine (T3) and thyroxine (T4). Experts on iodine and thyroid production state that iodine deficienty is much more dangerous than excess iodine which can lead to toxic levels of thyroid. Children with iodine deficiency and its resulting hypothyroidism can suffer from stunted growth, with mental retardation and problems in movement capabilities, speech or hearing. A mere mild low thyroid function can cause an imbalance of other hormones, such as estrogens, progesterones, and EVEN ANDROGENS. These hormones are ones that play a fundamental role in sexual/reproductive health as well as in the prevention of cancerous tumors, which includes but is not limited; such as fibroids and even fibrocystic breast disease. Low thyroid function normally coincides with low adrenal function. Symptoms of iodine deficiency with low thyroid function are fatigue, low energy during the day, insomnia, low body temperature, very low blood pressure, low-grade depression, dry skin, dry hair, pear-shaped figure, weight gain, infertility, PMS, sensitivity to cold (particularly the extremities), calcification buildup, hardening of the arteries, cystic breasts and/or ovaries, and cancers of the breast and ovaries. (Herbal Medicine Healing Cancer by Donald R Yance Jr, page 161, 85)
Zinc deficiency was associated with decreased concentrations of T3 and free thyroxine in serum by approximately 30 percent when compared with zinc-adequate controls (Kralik A et al 1996). Zinc may play a role in thyroid hormone metabolism in patients with low T3 and may contribute to conversion of T4 to T3 in humans (Nishiyama S et al 1994). Science yet can explain the exact reason behind the correlation of adequate zinc and thyroid production but there are NUMEROUS studies showing how important zinc is in the maintenance of thyroid hormone production. One thing is for sure; zinc is CRUCIAL for hormone production in general. Another reason that zinc is a must for proper thyroid function is that it prevents estradiol from forming via testosterone aromatization. Estradiol is known to speed up thyroid issues. This explains why about 90 percent of people who suffer from thyroid deficiency are female. Here are just two scholar excerpts since there is a Ton of them:
“Drug Nutr Interact, 5(2):113-24 1987
Abstract
Interactive combinations of altered zinc and thyroid states were studied in rats to assess pathophysiologic effects. Clinical signs of zinc deficiency or thyroid alteration were limited to effects on growth rate. Changes in organ and glandular weights and serum thyrotropin levels reflected changes in serum thyroid hormone concentrations. Significantly (probability less than .001), zinc-deficient rats had enhanced hepatic thyroxine-5'-monodeiodinase activity. In addition, the zinc-deficient state was found to be protective against thiouracil-induced suppression of the microsomal-monooxygenase and thyroxine-5'-monodeiodinase enzyme complex. This protective effect was evident by greater thyroxine-5'-monodeiodinase and reduced nicotinamide-adenine dinucleotide phosphate cytochrome c reductase activities, as well as cytochrome P-450 content, in zinc-deficient/thiouracil-treated animals. Thus, the enzyme complex had increased triiodothyronine-generating capacity in conditions of zinc deficiency, which may be important because of the greater biological reactivity of triiodothyronine. Primary zinc deficiency conditions of the magnitude seen in this study and in this-age rat did not appear to alter serum thyroid hormone levels or organ/glandular function. However, concurrent zinc deficiency and altered thyroid status did change thyroid hormone response and disposition, which may be important to populations at risk because of thyroid dysfunctional states.”
“Am J Clin Nutr, 33(8):1767-70 1980 Aug(Zinc deficiency, chronic starvation, and hypothalamic-pituitary-thyroid function.)
Abstract
Male Sprague-Dawley rats were fed a zinc-deficient diet to study its effects on the hypothalamic-pituitary-thyroid axis. As zinc-deficient animals fail to gain weight, they were compared to pair-fed growth restricted animals as well as ad libitum fed controls. The growth velocity curves were superimposable for the zinc-deficient animals and the pair-fed controls; both were markedly reduced compared to the ad libitum controls. Both the zinc-deficient and the pair-fed controls had lower triiodothyronine (T3) and thyroxine levels compared to the ad libitum controls. In addition T3 values were lower in the zinc-deficient animals compared to the pair-fed controls (P < 0.05). Hypothalamic thyrotrophin-releasing hormone content was decreased in the zinc-deficient rats (162 +/- 32 pg/ml) compared to the ad libitum controls (305 +/- 102; P < 0.01). The 125I thyroidal uptakes were not significantly different between the zinc-deficient and the pair-fed controls. Zinc deficiency lowers T3 more than comparable caloric restriction; this suggests that zinc deficiency may impair extrathyroidal production of T3.”
Selenium is a factor of the enzyme that helps convert T4 to T3 peripherally, so deficiencies of selenium canimpair thyroid function and eventually cause hypothyroidism. It is also the most abount mineral in thyroid glands. According to the New England Journal, "selenium deficiency can result in thyroid injury and decreased extrathyroidal triiodothyronine production" (reduced peripheral T3 production.) Selenoenzymes are very vital to many thyroid passageways and also protects against oxidation of hydrogen peroxide which translates to a more stable thyroid gland. Selenium is also responsible for the conversion of iodine to thyroglobulin which is responsible for the conversion factor or T4 to T3. They key with selenium is not to over consume it because that can cause a negative effect which why Ruthless’s new T3 PCT contains only a sufficient dose of selenium without going into an excessive dose. Here is an excerpt on selenium’s positive effect on controlling ATT (a thyroid condition):
“Selenium and Thyroid Autoantibodies
Recently published biochemical data suggest the significant role of selenium compounds as the adjuvants combined with L: -thyroxine therapy, which can reduce antithyroid peroxidase antibodies’ (TPOAb) levels in patients with Hashimoto disease. The study was undertaken to document in a more detailed way the changes in parameters expressing the thyroid and ovarian function brought about by selenium supplementation (50-100 microg/day) in a woman undergoing autoimmune thyroiditis (AIT) therapy. This prospective observational case study lasted for 14 months plus additional 5 months as a follow-up period. Parameters reflecting selenium status, thyroid metabolism, and sex hormones secretion were determined at the onset and end of the study period, as well as in some of its middle points. During the supplementation trial, serum selenium (Se) increased by 45% and plasma glutathione peroxidase (GPX3) by 21%. TPOAb decreased by 76%. All other parameters also fluctuated during the supplementation period, but all results were always within normal physiological ranges. After withdrawal of the supplementation, the sharp fall of Se and GPX3 promptly occurred, and this phenomenon was accompanied with a marked increase in TPOAb. This report stresses the importance of selenium supplementation in AIT treatment. However, the efficiency and durability of the effect of Se supplementation on the TPOAb titer remain an open question. The clarification of mechanism(s) underlying Se interaction with autoimmune processes should throw new light on this issue. (Zagrodzki P, Ratajczak R. Selenium supplementation in autoimmune thyroiditis female patient--effects on thyroid and ovarian functions (case study). Biol Trace Elem Res. 2008 October Winter;126(1-3):76-82.
Department of Food Chemistry and Nutrition, Collegium Medicum Jagiellonian University, Medyczna 9, 30-688 Krakow, Poland.)”
Copper is what I like to call the mediator that makes sure that Zinc is not over abundanct causing excessive thyroid production by having a blunting effect on thyroxin. For some reason though, if one is deficient in copper it can induce low thyroid output.
“Interrelationships between athyroetic and copper-deficient states in rats.
Oliver JW
Am J Vet Res, 36(11):1649-53 1975 Nov
Abstract
Possible interrelationships of copper-deficient (copper-deficient ration) and hypothyroid (thiouracil treatment) states in rats were examined. Clinical signs, necropsy changes, and thyroxine concentrations were determined in 6 groups of rats treated as follows: group A--nontreated control; group B--thiouracil treated; group C--fed copper-deficient ration; group D--thiouracil treated and fed copper-deficient ration; group E--thyroid-stimulating hormone (TSH) treated; and group F--TSH treated and fed copper-deficient ration. Clinical signs occurred first and were most severe in the thiouracil-treated rats fed copper-deficient ration and included conformational changes and slower maturation, weakening of ear cartilage, middle ear changes (reflected by tilting of heads), and alopecia. Fatty infiltration of hepatic tissue was found in all rats fed copper-deficient rations, and considerable fluid retention occurred in rats fed copper-deficient ration and subjected to daily TSH treatment. Adrenal gland weights were 81% of control values (adjusted for body weight) in thiouracil-treated rats fed copper-deficient ration, and hypophysis weights were 114 and 154% of control values in thiouracil-treated rats and thiouracil-treated rats fed copper-deficient ration, respectively. Thyroid gland weights were 281% of control values in both thiouracil-treated rats and thiouracil-treated rats fed copper-deficient ration. Plasma thyroxine concentrations were markedly reduced (9% of control value) in thiouracil-treated rats fed copper-deficient ration. Thus, copper-deficient and hypothyroid states were considerably enhanced when the 2 existed concurrently, giving added meaning and necessity to close surveillance of trace mineral concentrations and thyroid gland status.”
“The effect of copper on the metabolism of iodine, carbohydrates and proteins in ratsEsipenko
BE; Marsakova NV
Fiziol Zh, 36(2):35-43 1990 Mar-Apr
Abstract
Experiments on 156 rats maintained at ration with copper deficiency have demonstrated a decrease in the values of iodine metabolism in organs and tissues excluding the liver where a sharp increase in the concentration and content of inorganic iodine was observed. A disturbance in indices of carbohydrate and proteins metabolism in the organism of animals is marked. A direct relationship with a correlation coefficient equaling 0.87-1.00 is determined between changes in the concentration of protein-bound iodine in blood and concentration of glycogen in the liver, skeletal muscles, albumins, alpha 1-, alpha 2-globulins, urea concentration; an inverse relationship with glucose, activity of blood lipo-dehydrogenase and liver mitochondria, aldolase, concentration of pyruvic and lactic acids is established as well. It is concluded that copper deficiency can exert both a direct effect on metabolic processes (as data from literature testify) and an indirect one disturbing iodine metabolism, i. e. sharply decreasing protein-bound iodine production by the thyroid gland.z”
Manganese can reduce thyroid activity if deficient. Manganese is one of the minerals required for T4 production. Manganese deficiency or lack of bioavailability is a very common condition. Adrenal fatigue causes manganese to become unavailable as the binding protein known as transmanganin; is not produced in sufficient quantity. Manganese is one of the minerals that is responsible for stimulating the parasympathetic nervous system which is needed in the process of producing thyroid hormones. When supplementing manganese, it must be taken with copper so that one nor the other mineral overrides each other as there must be balance, too low manganese will lead to hypothyroidism. Just as with copper more is less which is why T3 PCT contains only a specific amount per dose to help with thyroid function.
Molybdenum also acts very similar to copper in its role in regulating thyroid production along hormone production within hypothalamus.
L-Tyrosine is an non-essential amino acid that helps with the production of thyroid and thyroxin. Even though it first acts as a precursor to dopamine, norepinepherine, and epinephrine; it still acts as messenger to create hormones including thyroid hormones. Here is a study that shows the correlation of augmented levels of tyrosine increasing thyroid hormone ouput:
“Metabolism
Volume 37, Issue 1, January 1988, Pages 9-14
Abstract
A man with diabetes mellitus, chronic hepatitis, chronic pancreatitis, and blind loop syndrome but without and previous thyroid disease developed three episodes of transient primary hypothyroidism associated with protein-calorie malnutrition (PCM). Clinical examinations suggested that this primary hypothyroidism was not caused by chronic thyroiditis, iodine deficiency, or iodine excess. Since the three times association of primary hypothyroidism with PCM suggested the possibility that the primary hypothyroidism was caused by PCM, we have tried to clarify its mechanism. For this purpose we have investigated the change of thyroid functions during protein-calorie repletion and the effect of amino acid deficiency. Total parenteral nutrition with full supplementation of amino acids resulted in a rapid increase in serum thyroxine (T4), triiodothyronine (T3), free T4, and reverse T3, and subsequently, a rapid decrease in TSH in several days after the nutrition was begun. When amino acid solution was changed to that depleted of phenylalanine and tyrosine after the restoration of thyroid functions, serum T4 and T3 showed a gradual decrease, but serum free T4 and TSH remained within normal range. However, resupplementation of phenylalanine and tyrosine after 8 weeks of depletion gave a rapid increase in serum T4, T3, free T4, and reverse T3. These results suggested that the primary hypothyroidism was caused by an impaired T4 production and that the deficiency of amino acids in PCM partly contributed to the impairment of T4 production.”
Ashwagandha is an adaptogen that contains in its roots a certain extract that increases glucose-6-phosphatase within the liver. When this occurs, the body is able to produce more thyroid hormones. There is documentation that shows how ashwagandha increases thyroid hormone production especially T4, and for some reason it also has a high conversion from T4 to T3. Since it adaptogen it also aids in adrenal fatigue which is one of the symptoms associated with thyroid deficiency. It is also a great aid for preventing anxiety which also associated with thyroid deficiency. Due to its potency, not much of ashwagandha is needed to give results which is why we only implemented 200mgs per serving, too much of this herb can actually cause hyperthyroidism due its effectiveness on boosting thyroid hormone production. Here is the extract of the study I read which obtains information on how ashwagandha root boost thyroid function:
“J Pharm Pharmacol. 1998 Sep;50(9):1065-8.
Changes in thyroid hormone concentrations after administration of ashwagandha root extract to adult male mice.
Panda S, Kar A.
School of Life Sciences, D.A. University, Indore, India.
Abstract
The importance of ashwagandha root extract in the regulation of thyroid function with special reference to type-I iodothyronine 5'-monodeiodinase activity in mice liver has been investigated. Although the root extract (1.4 g kg(-1)) administered daily for 20 days by gastric intubation increased serum 3,3',5-triiodothyronine (T3) and tetraiodothyronine (T4) concentrations and hepatic glucose-6-phosphatase activity, hepatic iodothyronine 5'-monodeiodinase activity did not change significantly. Furthermore, ashwagandha root extract significantly reduced hepatic lipid peroxidation, whereas the activity of antioxidant enzymes such as superoxide dismutase and catalase were increased. These findings reveal that the ashwagandha root extract stimulates thyroidal activity and also enhances the antiperoxidation of hepatic tissue.”
Schizandra is also part of the formula for its ability to help with chronic fatigue. Coming off of Cytomel can be a real miserable time for some due to the lack of energy. This herb will give one that up lifting mood that gets one going as soon as it’s digested. It provides clean energy while cleaning the liver which also in return helps the body produce more hormones including thyroid hormones. It also helps the body control stress and cortisol which in return WILL promote better thyroid function.
Bladderwrack is a form of seaweed which is usually used as a source of iodine. For many years medicine practitioners prescribed bladderwrack for idodine deficiency in patients suffering from hypothyroidism and goiter. Dosage also should not be excessive since this formula contains iodine, also Bladderwrack may possibly induce hyperthyroidism if taken at an excessive dosage. Bladderwrack also contains anti fatigue properties which makes it even easier for someone to cope with the down mood of thyroid deficiency. Schizandra and bladderwrack make quite the combo for relieving fatigue in those coming off a cytomel cycle. Bladderwrack has also been documented to possess anti-estrogenic properties (decreased 17-beta estradiol), which translates to healthier thyroid function. (BMC Complement Altern Med. 2004 Aug 4;4:10.)
Cayenne Pepper was implemented in this formula for a couple of reasons. The first being that coming off of cytomel cycle, one’s metabolism will clearly be suffering; an oxford study showed that cayenne pepper increased the patients metabolism by over 20 percent. There is also some literature that suggests cayenne has the ability to help combat fatigue through its anti-inflammatory effects. This translates to more energy and less stress. Cayenne contains a high amount of iron which is also vital to proper thyroid function; iron deficiency has been linked to thyroid deficiency. Cayenne aka piperine is also ideal for absorption of nutrients or supplement ingredients which is another outstanding reason to include it in this formula.
T3 PCT was formulated to revive proper thyroid function/thyroid hormone production and help battle chronic fatigue. This formula has PLENTY of documentation as you can see which lets you know that we did our homework to come out with the most potent thyroid hormone revitalizer to the market.
Cytomel is a synthetic thyroid agen that is usually a prescribed version of a specific thyroid hormone; that being T3 the biological form of the thyroid hormone sort of like the Vitamin D3 is to the Vitamin D2. Cytomel increases the way the body responds to many processes like the release of adrenaline. Even though it is synthetic, Cytomel is no doubting identical to the naturally occurring hormone liothyronine (also known as triiodothyronine/ T3). It is approved to treat an underactive thyroid gland which is medically defined as hypothyroidism and goiters. Cytomel is also used for specific thyroid investigative tests. The thyroid gland makes two distinct thyroid hormones: levothyroxine (T4) and triiodothyronine (T3). Even though T3 is much more active than T4, the thyroid will produce more T4 than T3. The body can convert the T4 hormone into T3 when necessary. If your thyroid does not make enough thyroid hormones, there are a few different options to increase your levels, one being to combine synthetic T3 and T4 hormones. Some people may not convert T4 into T3 properly, in which case a T3 product such as Cytomel would be implemented to help the individual correct their thyroid hormone level ratio. One might ask how does cytomel work within the body? The area of the brain called the hypothalamus creates thyrotropin-releasing hormone, or TRH, this signaling within the HPTA occurs when levels of thyroid hormone in the blood become noticeably low. This reaction stimulates the production of thyroid-stimulating hormone aka TSH, from the pituitary gland which located right below the brain and is also responsible for the creation of sex hormones such as testosterone. This process in turn will stimulate the thyroid gland to produce and release thyroid hormones. T4 is converted to T3 in tissues such as the liver. T3 only makes up 7 to 10 percent of total thyroid hormone which is obviously a very small amount. Realize that 70 percent of T3 is unfortunately bound to proteins called thyroxine-binding globulin and albumin as well. The other 30 percent of T3 is unbound or free, which is considered the active form. The levels of T3 and T4 are regulated by a feedback loop just as testosterone and estrogen are. Therefore, high levels of T3 and T4 suppress the release of TRH, leading to a suppression of TSH and consequently a suppression of thyroid hormone. On the oppositional side, low levels of T3 and T4 stimulate the release of TRH, which then stimulates the release of TSH, which then stimulates the release of thyroid hormone. T3 supplements increase the basal metabolic rate, stimulate the body's utilization of oxygen and promote the breaking down of proteins, carbohydrates and fats. Over 90 percent of T3 is absorbed into the tissues rapidly because it is not firmly bound to proteins.
As you see use of this drug will suppress your natural thyroid output hormones. Unless one plans to stay on this treatment for life, I highly recommend that they regulate and jumpstart their endogenous thyroid hormone production after using cytomel for bodybuilding purposes. Ruthless Supplements has developed a supplement that boosts natural thyroid hormones without the fear of overstimulating one’s thyroid hormone output. Ruthless’s T3 PCT was made to get one’s adrenals back in place as well while controlling cortisol levels.
Breakdown of ingredients
Vitamin B-12 also known as cyanocobalamine or cobalmin, is an essential vitamin that is required for the development of red blood cells. It is also used to make the protective coating surrounding nerves. There is a link between vitamin B-12 deficiency and hypothyroidism. Over 40% of autoimmune thyroid patients have low levels of Vitamin B-12. About 25 percent of people with thyroid issues will make antibodies that attack their thyroid also make antibodies that attack the parietal glands, and this can cause B-12 levels to drop significantly. Fatigue is a common symptom that both B-12 deficient and thyroid deficient patients experience. When researchers wanted to know why there was link between thyroid hormones and B-12 if most people in the U.S. have a high protein diet. Research showed that it’s the human’s lack of ability to digest the B-12 due to the negative effect that hypothyroidism has on the digestive tract, also realize that B-12 is a metylator and its has many functions in the body; one being that it regulates hormone production. (Ness-Abramof R, et al. Prevalence and evaluation of B12 deficiency in patients with autoimmune thyroid disease. Am J Med Sci, September 2006;332(3):119-22.)
Here are two excerpts on links of B-12 deficiency and hypothyroidism
“J Nutr 1988 Dec;118(12):1495-501
Effect of hypothyroidism on methylmalonate excretion and hepatic vitamin B-12 levels in rats.
Stokstad EL, Nair CP
Department of Nutritional Sciences, University of California, Berkeley 94720.
The effect of hypo- and hyperthyroidism on vitamin B-12 metabolism in the rat was studied by measuring methylmalonic acid excretion, B-12 content of liver and oxidation of 2-[14C]histidine. Ten percent pectin was added to increase severity of B-12 deficiency. The addition of thiouracil to a diet containing 10% pectin decreased the excretion of methylmalonic acid suggesting an amelioration of the B-12 deficiency. It was found that part of this decreased methylmalonic acid excretion was due to a decreased food consumption with a correspondingly decreased intake of branched-chain amino acids which are precursors of methylmalonic acid. When attempts were made to increase the protein intake of animals receiving thiouracil so their amino acid intake was equal to that of the control animals, methylmalonic acid excretion was still lower than that of the controls. It was also found that the vitamin B-12 content of the liver was higher in the animals receiving thiouracil than in the controls. Thyroidectomy had the same effect as feeding thiouracil. Liver B-12 levels are rapidly depleted on a B-12 deficient diet containing 10% pectin. It appears that hypothyroidism, induced either by thyroidectomy or by feeding thiouracil, slows the rate of depletion of hepatic B-12 which in turn facilitates the metabolism of methylmalonic acid and decreases its excretion in the urine.”
“Nuklearmedizin 1979;18(6):278-82
Serum vitamin B12 and folic acid levels in hyperthyroidism.
Gyftaki H, Kesse-Elias M, Koutras D, Pandos P, Papazoglou S, Moulopoulos S
Serum vitamin B12 and folic acid levels were measured in 48 hyperthyroid patients and in a group of euthyroid controls. The levels of vitamin B12 ranged from 120-900 pg/ml with a mean of 429.3 +/- 30.9 pg/ml (SE). The mean serum vitamin B12 level was lower in hyperthyroid patients than in normal controls, the difference being statistically significant (t = 2.584, p less than 0.025). Serum vitamin B12 levels showed a statistically significant negative correlation with the clinical index of Grooks et al. (r = 0.344, p less than 0.05). The findings, although not excluding the involvement of auto-immune gastritis in patients with low serum vitamin B12 levels, suggest a direct action of increased thyroid hormone concentrations. Serum folic acid levels ranged from 0.5-13.8 ng/ml with a mean of 6.8 +/- 0.46 ng/ml (SE). The mean serum folic acid levels were higher in the hyperthyroid patients than in normal controls but the difference was not statistically significant (t = 1.2, p greater than 0.2). The serum folic acid levels did not show any statistically significant correlation with the clinical index of Grooks et al. The fact that no statistically significant difference was found between the mean value in hyperthyroid patients and the mean value in normal controls is probably due to the high folic acid intake in Greece.”
Iodine is literally needed to produce thyroid hormones; it’s the major mineral involved in thyroid development. Iodine is transformed into its free elemental form referred to as iodide. Iodide enters the thyroid gland through a unique transport mechanism. Iodide then goes through a process called oxidation and is included into transitional hormones called MIT aka Monoiodotyrosine, which contains 1 iodide and the other hormone being DIT aka Diiodotyrosine, which contains 2 iodides. These compounds then combine to form the active hormones which are tri-iodothyronine (T3) and thyroxine (T4). Experts on iodine and thyroid production state that iodine deficienty is much more dangerous than excess iodine which can lead to toxic levels of thyroid. Children with iodine deficiency and its resulting hypothyroidism can suffer from stunted growth, with mental retardation and problems in movement capabilities, speech or hearing. A mere mild low thyroid function can cause an imbalance of other hormones, such as estrogens, progesterones, and EVEN ANDROGENS. These hormones are ones that play a fundamental role in sexual/reproductive health as well as in the prevention of cancerous tumors, which includes but is not limited; such as fibroids and even fibrocystic breast disease. Low thyroid function normally coincides with low adrenal function. Symptoms of iodine deficiency with low thyroid function are fatigue, low energy during the day, insomnia, low body temperature, very low blood pressure, low-grade depression, dry skin, dry hair, pear-shaped figure, weight gain, infertility, PMS, sensitivity to cold (particularly the extremities), calcification buildup, hardening of the arteries, cystic breasts and/or ovaries, and cancers of the breast and ovaries. (Herbal Medicine Healing Cancer by Donald R Yance Jr, page 161, 85)
Zinc deficiency was associated with decreased concentrations of T3 and free thyroxine in serum by approximately 30 percent when compared with zinc-adequate controls (Kralik A et al 1996). Zinc may play a role in thyroid hormone metabolism in patients with low T3 and may contribute to conversion of T4 to T3 in humans (Nishiyama S et al 1994). Science yet can explain the exact reason behind the correlation of adequate zinc and thyroid production but there are NUMEROUS studies showing how important zinc is in the maintenance of thyroid hormone production. One thing is for sure; zinc is CRUCIAL for hormone production in general. Another reason that zinc is a must for proper thyroid function is that it prevents estradiol from forming via testosterone aromatization. Estradiol is known to speed up thyroid issues. This explains why about 90 percent of people who suffer from thyroid deficiency are female. Here are just two scholar excerpts since there is a Ton of them:
“Drug Nutr Interact, 5(2):113-24 1987
Abstract
Interactive combinations of altered zinc and thyroid states were studied in rats to assess pathophysiologic effects. Clinical signs of zinc deficiency or thyroid alteration were limited to effects on growth rate. Changes in organ and glandular weights and serum thyrotropin levels reflected changes in serum thyroid hormone concentrations. Significantly (probability less than .001), zinc-deficient rats had enhanced hepatic thyroxine-5'-monodeiodinase activity. In addition, the zinc-deficient state was found to be protective against thiouracil-induced suppression of the microsomal-monooxygenase and thyroxine-5'-monodeiodinase enzyme complex. This protective effect was evident by greater thyroxine-5'-monodeiodinase and reduced nicotinamide-adenine dinucleotide phosphate cytochrome c reductase activities, as well as cytochrome P-450 content, in zinc-deficient/thiouracil-treated animals. Thus, the enzyme complex had increased triiodothyronine-generating capacity in conditions of zinc deficiency, which may be important because of the greater biological reactivity of triiodothyronine. Primary zinc deficiency conditions of the magnitude seen in this study and in this-age rat did not appear to alter serum thyroid hormone levels or organ/glandular function. However, concurrent zinc deficiency and altered thyroid status did change thyroid hormone response and disposition, which may be important to populations at risk because of thyroid dysfunctional states.”
“Am J Clin Nutr, 33(8):1767-70 1980 Aug(Zinc deficiency, chronic starvation, and hypothalamic-pituitary-thyroid function.)
Abstract
Male Sprague-Dawley rats were fed a zinc-deficient diet to study its effects on the hypothalamic-pituitary-thyroid axis. As zinc-deficient animals fail to gain weight, they were compared to pair-fed growth restricted animals as well as ad libitum fed controls. The growth velocity curves were superimposable for the zinc-deficient animals and the pair-fed controls; both were markedly reduced compared to the ad libitum controls. Both the zinc-deficient and the pair-fed controls had lower triiodothyronine (T3) and thyroxine levels compared to the ad libitum controls. In addition T3 values were lower in the zinc-deficient animals compared to the pair-fed controls (P < 0.05). Hypothalamic thyrotrophin-releasing hormone content was decreased in the zinc-deficient rats (162 +/- 32 pg/ml) compared to the ad libitum controls (305 +/- 102; P < 0.01). The 125I thyroidal uptakes were not significantly different between the zinc-deficient and the pair-fed controls. Zinc deficiency lowers T3 more than comparable caloric restriction; this suggests that zinc deficiency may impair extrathyroidal production of T3.”
Selenium is a factor of the enzyme that helps convert T4 to T3 peripherally, so deficiencies of selenium canimpair thyroid function and eventually cause hypothyroidism. It is also the most abount mineral in thyroid glands. According to the New England Journal, "selenium deficiency can result in thyroid injury and decreased extrathyroidal triiodothyronine production" (reduced peripheral T3 production.) Selenoenzymes are very vital to many thyroid passageways and also protects against oxidation of hydrogen peroxide which translates to a more stable thyroid gland. Selenium is also responsible for the conversion of iodine to thyroglobulin which is responsible for the conversion factor or T4 to T3. They key with selenium is not to over consume it because that can cause a negative effect which why Ruthless’s new T3 PCT contains only a sufficient dose of selenium without going into an excessive dose. Here is an excerpt on selenium’s positive effect on controlling ATT (a thyroid condition):
“Selenium and Thyroid Autoantibodies
Recently published biochemical data suggest the significant role of selenium compounds as the adjuvants combined with L: -thyroxine therapy, which can reduce antithyroid peroxidase antibodies’ (TPOAb) levels in patients with Hashimoto disease. The study was undertaken to document in a more detailed way the changes in parameters expressing the thyroid and ovarian function brought about by selenium supplementation (50-100 microg/day) in a woman undergoing autoimmune thyroiditis (AIT) therapy. This prospective observational case study lasted for 14 months plus additional 5 months as a follow-up period. Parameters reflecting selenium status, thyroid metabolism, and sex hormones secretion were determined at the onset and end of the study period, as well as in some of its middle points. During the supplementation trial, serum selenium (Se) increased by 45% and plasma glutathione peroxidase (GPX3) by 21%. TPOAb decreased by 76%. All other parameters also fluctuated during the supplementation period, but all results were always within normal physiological ranges. After withdrawal of the supplementation, the sharp fall of Se and GPX3 promptly occurred, and this phenomenon was accompanied with a marked increase in TPOAb. This report stresses the importance of selenium supplementation in AIT treatment. However, the efficiency and durability of the effect of Se supplementation on the TPOAb titer remain an open question. The clarification of mechanism(s) underlying Se interaction with autoimmune processes should throw new light on this issue. (Zagrodzki P, Ratajczak R. Selenium supplementation in autoimmune thyroiditis female patient--effects on thyroid and ovarian functions (case study). Biol Trace Elem Res. 2008 October Winter;126(1-3):76-82.
Department of Food Chemistry and Nutrition, Collegium Medicum Jagiellonian University, Medyczna 9, 30-688 Krakow, Poland.)”
Copper is what I like to call the mediator that makes sure that Zinc is not over abundanct causing excessive thyroid production by having a blunting effect on thyroxin. For some reason though, if one is deficient in copper it can induce low thyroid output.
“Interrelationships between athyroetic and copper-deficient states in rats.
Oliver JW
Am J Vet Res, 36(11):1649-53 1975 Nov
Abstract
Possible interrelationships of copper-deficient (copper-deficient ration) and hypothyroid (thiouracil treatment) states in rats were examined. Clinical signs, necropsy changes, and thyroxine concentrations were determined in 6 groups of rats treated as follows: group A--nontreated control; group B--thiouracil treated; group C--fed copper-deficient ration; group D--thiouracil treated and fed copper-deficient ration; group E--thyroid-stimulating hormone (TSH) treated; and group F--TSH treated and fed copper-deficient ration. Clinical signs occurred first and were most severe in the thiouracil-treated rats fed copper-deficient ration and included conformational changes and slower maturation, weakening of ear cartilage, middle ear changes (reflected by tilting of heads), and alopecia. Fatty infiltration of hepatic tissue was found in all rats fed copper-deficient rations, and considerable fluid retention occurred in rats fed copper-deficient ration and subjected to daily TSH treatment. Adrenal gland weights were 81% of control values (adjusted for body weight) in thiouracil-treated rats fed copper-deficient ration, and hypophysis weights were 114 and 154% of control values in thiouracil-treated rats and thiouracil-treated rats fed copper-deficient ration, respectively. Thyroid gland weights were 281% of control values in both thiouracil-treated rats and thiouracil-treated rats fed copper-deficient ration. Plasma thyroxine concentrations were markedly reduced (9% of control value) in thiouracil-treated rats fed copper-deficient ration. Thus, copper-deficient and hypothyroid states were considerably enhanced when the 2 existed concurrently, giving added meaning and necessity to close surveillance of trace mineral concentrations and thyroid gland status.”
“The effect of copper on the metabolism of iodine, carbohydrates and proteins in ratsEsipenko
BE; Marsakova NV
Fiziol Zh, 36(2):35-43 1990 Mar-Apr
Abstract
Experiments on 156 rats maintained at ration with copper deficiency have demonstrated a decrease in the values of iodine metabolism in organs and tissues excluding the liver where a sharp increase in the concentration and content of inorganic iodine was observed. A disturbance in indices of carbohydrate and proteins metabolism in the organism of animals is marked. A direct relationship with a correlation coefficient equaling 0.87-1.00 is determined between changes in the concentration of protein-bound iodine in blood and concentration of glycogen in the liver, skeletal muscles, albumins, alpha 1-, alpha 2-globulins, urea concentration; an inverse relationship with glucose, activity of blood lipo-dehydrogenase and liver mitochondria, aldolase, concentration of pyruvic and lactic acids is established as well. It is concluded that copper deficiency can exert both a direct effect on metabolic processes (as data from literature testify) and an indirect one disturbing iodine metabolism, i. e. sharply decreasing protein-bound iodine production by the thyroid gland.z”
Manganese can reduce thyroid activity if deficient. Manganese is one of the minerals required for T4 production. Manganese deficiency or lack of bioavailability is a very common condition. Adrenal fatigue causes manganese to become unavailable as the binding protein known as transmanganin; is not produced in sufficient quantity. Manganese is one of the minerals that is responsible for stimulating the parasympathetic nervous system which is needed in the process of producing thyroid hormones. When supplementing manganese, it must be taken with copper so that one nor the other mineral overrides each other as there must be balance, too low manganese will lead to hypothyroidism. Just as with copper more is less which is why T3 PCT contains only a specific amount per dose to help with thyroid function.
Molybdenum also acts very similar to copper in its role in regulating thyroid production along hormone production within hypothalamus.
L-Tyrosine is an non-essential amino acid that helps with the production of thyroid and thyroxin. Even though it first acts as a precursor to dopamine, norepinepherine, and epinephrine; it still acts as messenger to create hormones including thyroid hormones. Here is a study that shows the correlation of augmented levels of tyrosine increasing thyroid hormone ouput:
“Metabolism
Volume 37, Issue 1, January 1988, Pages 9-14
Abstract
A man with diabetes mellitus, chronic hepatitis, chronic pancreatitis, and blind loop syndrome but without and previous thyroid disease developed three episodes of transient primary hypothyroidism associated with protein-calorie malnutrition (PCM). Clinical examinations suggested that this primary hypothyroidism was not caused by chronic thyroiditis, iodine deficiency, or iodine excess. Since the three times association of primary hypothyroidism with PCM suggested the possibility that the primary hypothyroidism was caused by PCM, we have tried to clarify its mechanism. For this purpose we have investigated the change of thyroid functions during protein-calorie repletion and the effect of amino acid deficiency. Total parenteral nutrition with full supplementation of amino acids resulted in a rapid increase in serum thyroxine (T4), triiodothyronine (T3), free T4, and reverse T3, and subsequently, a rapid decrease in TSH in several days after the nutrition was begun. When amino acid solution was changed to that depleted of phenylalanine and tyrosine after the restoration of thyroid functions, serum T4 and T3 showed a gradual decrease, but serum free T4 and TSH remained within normal range. However, resupplementation of phenylalanine and tyrosine after 8 weeks of depletion gave a rapid increase in serum T4, T3, free T4, and reverse T3. These results suggested that the primary hypothyroidism was caused by an impaired T4 production and that the deficiency of amino acids in PCM partly contributed to the impairment of T4 production.”
Ashwagandha is an adaptogen that contains in its roots a certain extract that increases glucose-6-phosphatase within the liver. When this occurs, the body is able to produce more thyroid hormones. There is documentation that shows how ashwagandha increases thyroid hormone production especially T4, and for some reason it also has a high conversion from T4 to T3. Since it adaptogen it also aids in adrenal fatigue which is one of the symptoms associated with thyroid deficiency. It is also a great aid for preventing anxiety which also associated with thyroid deficiency. Due to its potency, not much of ashwagandha is needed to give results which is why we only implemented 200mgs per serving, too much of this herb can actually cause hyperthyroidism due its effectiveness on boosting thyroid hormone production. Here is the extract of the study I read which obtains information on how ashwagandha root boost thyroid function:
“J Pharm Pharmacol. 1998 Sep;50(9):1065-8.
Changes in thyroid hormone concentrations after administration of ashwagandha root extract to adult male mice.
Panda S, Kar A.
School of Life Sciences, D.A. University, Indore, India.
Abstract
The importance of ashwagandha root extract in the regulation of thyroid function with special reference to type-I iodothyronine 5'-monodeiodinase activity in mice liver has been investigated. Although the root extract (1.4 g kg(-1)) administered daily for 20 days by gastric intubation increased serum 3,3',5-triiodothyronine (T3) and tetraiodothyronine (T4) concentrations and hepatic glucose-6-phosphatase activity, hepatic iodothyronine 5'-monodeiodinase activity did not change significantly. Furthermore, ashwagandha root extract significantly reduced hepatic lipid peroxidation, whereas the activity of antioxidant enzymes such as superoxide dismutase and catalase were increased. These findings reveal that the ashwagandha root extract stimulates thyroidal activity and also enhances the antiperoxidation of hepatic tissue.”
Schizandra is also part of the formula for its ability to help with chronic fatigue. Coming off of Cytomel can be a real miserable time for some due to the lack of energy. This herb will give one that up lifting mood that gets one going as soon as it’s digested. It provides clean energy while cleaning the liver which also in return helps the body produce more hormones including thyroid hormones. It also helps the body control stress and cortisol which in return WILL promote better thyroid function.
Bladderwrack is a form of seaweed which is usually used as a source of iodine. For many years medicine practitioners prescribed bladderwrack for idodine deficiency in patients suffering from hypothyroidism and goiter. Dosage also should not be excessive since this formula contains iodine, also Bladderwrack may possibly induce hyperthyroidism if taken at an excessive dosage. Bladderwrack also contains anti fatigue properties which makes it even easier for someone to cope with the down mood of thyroid deficiency. Schizandra and bladderwrack make quite the combo for relieving fatigue in those coming off a cytomel cycle. Bladderwrack has also been documented to possess anti-estrogenic properties (decreased 17-beta estradiol), which translates to healthier thyroid function. (BMC Complement Altern Med. 2004 Aug 4;4:10.)
Cayenne Pepper was implemented in this formula for a couple of reasons. The first being that coming off of cytomel cycle, one’s metabolism will clearly be suffering; an oxford study showed that cayenne pepper increased the patients metabolism by over 20 percent. There is also some literature that suggests cayenne has the ability to help combat fatigue through its anti-inflammatory effects. This translates to more energy and less stress. Cayenne contains a high amount of iron which is also vital to proper thyroid function; iron deficiency has been linked to thyroid deficiency. Cayenne aka piperine is also ideal for absorption of nutrients or supplement ingredients which is another outstanding reason to include it in this formula.
T3 PCT was formulated to revive proper thyroid function/thyroid hormone production and help battle chronic fatigue. This formula has PLENTY of documentation as you can see which lets you know that we did our homework to come out with the most potent thyroid hormone revitalizer to the market.
