levoxyl?

[builtbig]

do you guys think I could use my girlfriends levoxyl instead of t3 it is a t2 and I am not sure of the differance in the chemical chain. do you think it would be the same or even if I could use it? She doesn't need it anymore and i thought what the hell so tell me what you edamacated peeeps think

thanks bros
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[builtbig]

Levothyroxine sodium tablets and injection contain synthetic crystalline L-3,3¢,5, 5¢-tetraiodothyronine sodium salt [levothyroxine (T4) sodium]. Synthetic T4 is identical to that produced in the human thyroid gland.

this is the chemical compound and weight

C15H10I4NNaO4xH2O, and molecular weight of 798.86 (anhydrous).


Cytomel (liothyronine sodium) Tablets contain liothyronine (L-triiodothryonine or LT3), a synthetic form of a natural thyroid hormone, and is available as the sodium salt.

The empirical formula and molecular weight of liothyronine sodium are given below.

C15H11I3NNaO4 M.W. 672.96


the only differance is 1 more hydrogen 1 more iodine and some water!!

what do you think I think it is ok

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/;

[builtbig]

the mg of the pills are 75mg how much should I take and how often also with clen?
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[builtbig]

no buddy can help me out here?
builtbig:help:

[preist943]

never used it bro ,i know t-3 is stronger than t-4 but ive never read a thing on t-2

[preist943]

heres what i found bro i looked at a bunch of differnt sites and there all pretty much the same hope this helps
Levoxyl®
(levothyroxine sodium tablets, USP)

DESCRIPTION
LEVOXYL® (levothyroxine sodium tablets,USP) contain synthetic crystalline L-3,3’,5,5 ’-tetraiodothyronine sodium salt [levothyroxine (T4) sodium]. Synthetic T4 is identical to that produced in the human thyroid gland. Levothyroxine (T4) sodium has an empirical formula of C15H10 I4 N NaO4 • H2O, molecular weight of 798.86 g/mol (anhydrous), and structural formula as shown:


Inactive Ingredients
Microcrystalline cellulose, croscarmellose sodium and magnesium stearate. The following are the coloring additives per tablet strength:

Strength
(mcg) Color additive(s)
25 FD&C Yellow No.6 Aluminum Lake
50 None
75 FD&C Blue No.1 Aluminum Lake, D&C Red No.30 Aluminum Lake
88 FD&C Yellow No.6 Aluminum Lake, FD&C Blue No.1 Aluminum Lake, D&C Yellow No.10 Aluminum Lake
100 FD&C Yellow No.6 Aluminum Lake, D&C Yellow No.10 Aluminum Lake
112 FD&C Yellow No.6 Aluminum Lake, FD&C Red No.40 Aluminum Lake, D&C Red No.30 Aluminum Lake
125 FD&C Red No.40 Aluminum Lake, D&C Yellow No.10 Aluminum Lake
137 FD&C Blue No.1 Aluminum Lake
150 FD&C Blue No.1 Aluminum Lake, D&C Red No.30 Aluminum Lake
175 FD&C Blue No.1 Aluminum Lake, D&C Yellow No.10 Aluminum Lake
200 D&C Red No.30 Aluminum Lake, D&C Yellow No.10 Aluminum Lake
300 FD&C Yellow No.6 Aluminum Lake, FD&C Blue No.1 Aluminum Lake, D&C Yellow No.10 Aluminum Lake
Thyroid hormone synthesis and secretion is regulated by the hypothalamic-pituitary-thyroid axis. Thyrotropin-releasing hormone (TRH) released from the hypothalamus stimulates secretion of thyrotropin-stimulating hormone, TSH, from the anterior pituitary. TSH, in turn, is the physiologic stimulus for the synthesis and secretion of thyroid hormones, L-thyroxine (T4) and L-triiodothyronine (T3), by the thyroid gland. Circulating serum T3 and T4 levels exert a feedback effect on both TRH and TSH secretion. When serum T3 and T4 levels increase, TRH and TSH secretion decrease. When thyroid hormone levels decrease, TRH and TSH secretion increase.

The mechanisms by which thyroid hormones exert their physiologic actions are not completely understood, but it is thought that their principal effects are exerted through control of DNA transcription and protein synthesis. T3 and T4 diffuse into the cell nucleus and bind to thyroid receptor proteins attached to DNA. This hormone nuclear receptor complex activates gene transcription and synthesis of messenger RNA and cytoplasmic proteins.

Thyroid hormones regulate multiple metabolic processes and play an essential role in normal growth and development, and normal maturation of the central nervous system and bone. The metabolic actions of thyroid hormones include augmentation of cellular respiration and thermogenesis, as well as metabolism of proteins, carbohydrates and lipids. The protein anabolic effects of thyroid hormones are essential to normal growth and development.

The physiologic actions of thyroid hormones are produced predominately by T3, the majority of which (approximately 80%) is derived from T4 by deiodination in peripheral tissues.

Levothyroxine, at doses individualized according to patient response, is effective as replacement or supplemental therapy in hypothyroidism of any etiology, except transient hypothyroidism during the recovery phase of subacute thyroiditis.

Levothyroxine is also effective in the suppression of pituitary TSH secretion in the treatment or prevention of various types of euthyroid goiters, including thyroid nodules, Hashimoto’s thyroiditis, multinodular goiter and, as adjunctive therapy in the management of thyrotropin-dependent well-differentiated thyroid cancer (see INDICATIONS AND USAGE, PRECAUTIONS, DOSAGE AND ADMINISTRATION).

Pharmacokinetics

Absorption – Absorption of orally administered T4 from the gastrointestinal (GI) tract ranges from 40% to 80%. The majority of the levothyroxine dose is absorbed from the jejunum and upper ileum. The relative bioavailability of LEVOXYL® tablets, compared to an equal nominal dose of oral levothyroxine sodium solution, is approximately 98%. T4 absorption is increased by fasting, and decreased in malabsorption syndromes and by certain foods such as soybean infant formula. Dietary fiber decreases bioavailability of T4. Absorption may also decrease with age. In addition, many drugs and foods affect T4 absorption (see PRECAUTIONS, Drug Interactions and Drug-Food Interactions).

Distribution – Circulating thyroid hormones are greater than 99% bound to plasma proteins, including thyroxine-binding globulin (TBG), thyroxine-binding prealbumin (TBPA), and albumin (TBA), whose capacities and affinities vary for each hormone. The higher affinity of both TBG and TBPA for T4 partially explains the higher serum levels, slower metabolic clearance, and longer half-life of T4 compared to T3. protein-bound thyroid hormones exist in reverse equilibrium with small amounts of free hormone. Only unbound hormone is metabolically active. Many drugs and physiologic conditions affect the binding of thyroid hormones to serum proteins (see PRECAUTIONS, Drug Interactions and Drug-Laboratory Test Interactions). Thyroid hormones do not readily cross the placental barrier (see PRECAUTIONS, Pregnancy).

Metabolism –T4 is slowly eliminated (see TABLE 1). The major pathway of thyroid hormone metabolism is through sequential deiodination. Approximately eighty-percent of circulating T3 is derived from peripheral T4 by monodeiodination. The liver is the major site of degradation for both T4 and T3, with T4 deiodination also occurring at a number of additional sites, including the kidney and other tissues. Approximately 80%of the daily dose of T4 is deiodinated to yield equal amounts of T3 and reverse T3 (rT3). T3 and rT3 are further deiodinated to diiodothyronine. Thyroid hormones are also metabolized via conjugation with glucuronides and sulfates and excreted directly into the bile and gut where they undergo enterohepatic recirculation.

Elimination – Thyroid hormones are primarily eliminated by the kidneys. A portion of the conjugated hormone reaches the colon unchanged and is eliminated in the feces. Approximately 20% of T4 is eliminated in the stool. Urinary excretion of T4 decreases with age.

Table 1:
Pharmacokinetic Parameters of Thyroid Hormones in Euthyroid Patients
Hormone Ratio in
Thyroglobulin Biologic
Potency
t1/2 (days) protein
Binding (%)2
Levothyroxine
(T4)
Liothyronine
(T3) 10 –20

1
1

4
6–71

2 99.96

99.5

13 to 4 days in hyperthyroidism, 9 to 10 days in hypothyroidism;
2Includes TBG, TBPA, and TBA

INDICATIONS AND USAGE
Levothyroxine sodium is used for the following indications:

Hypothyroidism – As replacement or supplemental therapy in congenital or acquired hypothyroidism of any etiology, except transient hypothyroidism during the recovery phase of subacute thyroiditis. Specific indications include: primary (thyroidal), secondary (pituitary), and tertiary (hypothalamic) hypothyroidism and subclinical hypothyroidism. Primary hypothyroidism may result from functional deficiency, primary atrophy, partial or total congenital absence of the thyroid
Drugs that may decrease T4 5’-deiodinase activity
Amiodarone
Beta-adrenergic
antagonists
- (e.g., Propranolol
> 160 mg/day)
Glucocorticoids
- (e.g., Dexamethasone
> 4 mg/day)
Propylthiouracil (PTU) Administration of these enzyme inhibitors decreases the peripheral conversion of T4 to T3, leading to decreased T3 levels. However, serum T4 levels are usually normal but may occasionally be slightly increased. In patients treated with large doses of propranolol (> 160 mg/day), T3 and T4 levels change slightly, TSH levels remain normal, and patients are clinically euthyroid. It should be noted that actions of particular beta-adrenergic antagonists may be impaired when the hypothyroid patient is converted to the euthyroid state. Short-term administration of large doses of glucocorticoids may decrease serum T3 concentrations by 30% with minimal change in serum T4 levels. However, long term glucocorticoid therapy may result in slightly decreased T3 and T4 levels due to decreased TBG production (see above).

[stackdizzy]

are you sure it isn't 75 mcg

[builtbig]

the pills are 75mcg

thanks for posting do you think it is ok to take I think it would be!
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[crackerjack414]

t3 is around 4 times as strong as t4. Iam on 250mg t4 year round due to a medical condition

[builtbig]

what is the differance between MCG and MG? I can't find any info on it?
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[preist943]

1000mcg-1mg 1000mg-1g