Serm = selective estrogen receptor mechanism, tamoxifen is a serm and is not an AI.
I just saw that CNW now has research Raloxifene. I read on Lilly's cite about what the medical application is, but what is it's application as far as we are concerned? I read that it is a SERM, and I don't remember exactly what that means. Does that mean it is an AI?
5'8 1/2, 225lbs
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Serm = selective estrogen receptor mechanism, tamoxifen is a serm and is not an AI.
John Defendis has AMAZING stories to tell but he hides them with a code - send him a fanmail or something to get it if you wish
Bench form Charles Poliquin When I let go of what I am, I become what I might be. Lao-Tzu
Check out this thread on AM which includes some clinical studies - http://anabolicminds.com/forum/showt...9&page=1&pp=30
From breastcancer.org:-
Drugs called SERMs—selective estrogen receptor modulators—block the actions of estrogen in breast tissues and certain other tissues by "occupying" the estrogen receptors on cells. With a SERM sitting in the estrogen receptor, there is no place for the real estrogen to "sit down"—like a game of musical chairs. The SERM fits in the estrogen receptor, but it does NOT send messages to the cell nucleus to grow and divide.
So will the standard dose be 40mg? This sounds promising, being as how I have gyno from my last cycle that is giving me some problems.
5'8 1/2, 225lbs
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Dream as though you'll live forever,
Live each day like it's you last.
Love like you've never been hurt.
Tomorrow is never promised.
If you have gyno now then you need Arimidex...and post cycle 60-40mg nolvadex...20mg is nowhere near enough.Originally Posted by Purdue Power
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I read where Dr. D on AM said that 120-240 mg should be the dose range. If that is the case, I don't know why CNW made it 40 mg/mL unless that is the highest conentration he could get in solution--which is very possible, since that seems to be the max concentration for tamoxifen citrate. Search on AM for more info about it.Originally Posted by Purdue Power
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Could I take Arimidex off-cycle? I still have some Letro around, but I was told that it messes with your lipid profiles hardcore if you aren't on-cycle.Originally Posted by ForemanRules
5'8 1/2, 225lbs
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Dream as though you'll live forever,
Live each day like it's you last.
Love like you've never been hurt.
Tomorrow is never promised.
both arimidex and letro lowers your HDL levels. taking an AI does nothing for pre-existing gyno. you may want to try a topical DHT application for your situation. try to find some Andractim GelOriginally Posted by Purdue Power
William F. Buckley describes a conservative as, "someone who stands athwart history, yelling Stop." - and then proceeds to drag civilization back to times best left in history's dungheap.
Since Nolva only blocks estrogen, I have read that arimidex is good to get rid of circulating estrogen at the end of the cycle to prevent rebound.
Disclaimer: All health, fitness, diet, nutrition, anabolic steroid & supplement information posted here is intended for educational and informational purposes only, and is not intended as a substitute for proper medical advice from a medical doctor. We do not condone the use of anabolic steroids (AAS), all information about AAS is for educational and entertainment purposes only. If you choose to use AAS it's your responsibility to know the laws of the country that you live in. Consult your physician or health care professional before performing any of the exercises, or following any diet, nutrition or supplement advice described on this website.
AI's don't effect the levels of free estrogen
William F. Buckley describes a conservative as, "someone who stands athwart history, yelling Stop." - and then proceeds to drag civilization back to times best left in history's dungheap.
Effects of Long-Term Use of Raloxifene, a Selective Estrogen Receptor Modulator, on Thyroid Function Test Profiles
Sandy H.-J. Hsu, Wern-Cherng Cheng, Men-Wang Jang and Keh-Sung Tsai
Estrogen (1)(2)(3)(4)(5) may increase hepatic production of thyroxine-binding globulin (TBG) and decrease TBG clearance (6), thus increasing serum total thyroxine (tT4) (3)(4) and, to a lesser extent, total triiodothyronine (tT3) (3)(4). As a result, increased tT4 and tT3 are seen in states of excessive estrogen and/or progestin, such as pregnancy, estrogen replacement therapy (HRT) (5), and oral contraceptive usage (1). This phenomenon may cause problems in clinical diagnoses when tT4 or tT3 is used for these patients. On the other hand, estrogen has been shown to increase thyroid-stimulating hormone (TSH) and to decrease free thyroxine (fT4) through a mild inhibitory effect on the thyroid gland (4). Compound that are analogs of estrogens, such as tamoxifen, have been shown to increase TSH without decreasing fT4 (7)(8). Recently, a new category of therapeutic agents, collectively termed selective estrogen receptor modulators (SERMs), has been developed to treat patients with postmenopausal osteoporosis (9). Raloxifene is one SERM. It decreases bone resorption (9)(10) and serum LDL-cholesterol (9)(11)(12), but it does not stimulate breast (13) or endometrium (14) at the recommended dosage of 60 mg daily. This agent is becoming one of the first-line pharmaceutical agents for postmenopausal osteoporosis and is currently administered to a large number of patients. However, the effect of long-term raloxifene usage on TBG, T3 uptake, tT3, tT4, fT4, and TSH has not been well documented. To investigate whether raloxifene causes changes in serum concentrations of these markers, we compared the effects of 1 year of treatment with either raloxifene or combined continuous estrogen and progesterone (CCEP) on the thyroid function test profiles, estradiol 2 (E2), and follicle-stimulating hormone (FSH).
We studied 60 euthyroid postmenopausal women (age range, 40–75 years) with relatively low bone mineral density. The t-score, using the mean and SD of healthy premenopausal Taiwanese women as reference (15), ranged from +1 to -2.49. These 60 women were divided into two groups in a double-blind, randomized fashion. Fifty women received raloxifene (60 mg daily) before breakfast, and 10 women received combined conjugated equine estrogen (premarin®; 0.625 mg) and medroxyprogesterone acetate (provera®; 5 mg) daily. Fasting serum samples were collected for all participants at baseline and after 1 year of treatment. All of the serum samples were stored at -70 °C, thawed simultaneously, and measured on the same day. All participants completed the treatment program. The compliance was good for both groups. Pill counting showed that each patient consumed 85–100% of the tablets/capsules.
Serum tT3, tT4, fT4, TBG, third-generation TSH, T3 uptake, E2, and FSH were all measured using commercial chemiluminescent immunoassays and instruments (Immulite; DPC). The within-day imprecision (CVs) of these assays was 3–7%.
We used two-way ANOVA for repeated measures to compare the concentrations of E2 and FSH and the thyroid function profiles between the two therapeutic groups, before and after treatment. The data were analyzed by the general linear model procedure (PROG GLM) included in the SAS package (SAS, Ver. 6.12; SAS Institute).
The anthropometric data and the mean value (± SE) for each thyroid function test item before and after treatment in the CCEP and raloxifene groups are shown in Table 1 . At baseline, there was no significant difference in height, weight, age, years since menopause, or thyroid function test items between these two groups. CCEP significantly increased serum TBG (17%), tT3 (5.7%), and tT4 (19%) and decreased T3 uptake (9%), whereas it did not change TSH. The mean fT4 concentration decreased by 3%, but the change was not statistically significant. Raloxifene also increased serum TBG (7.8%), tT3 (4.4%), and tT4 (5.7%) and decreased T3 uptake (3.7%). The mean fT4 concentration decreased by 3%, but this change was not statistically significant (Table 1 ). The changes in these five markers were apparently smaller than those caused by CCEP but did not reach statistical significance.
http://www.clinchem.org/cgi/content/full/47/10/1865
William F. Buckley describes a conservative as, "someone who stands athwart history, yelling Stop." - and then proceeds to drag civilization back to times best left in history's dungheap.
An AI is to prevent or lower the creation of estrogen through aromatase action inhibition, not block what already exists - thats where nolvadex comes in since it occupies the receptor site. Clomiphene does the same thing, replace the action of a stronger estrogen with its own molecule at the site.
John Defendis has AMAZING stories to tell but he hides them with a code - send him a fanmail or something to get it if you wish
Bench form Charles Poliquin When I let go of what I am, I become what I might be. Lao-Tzu
Originally Posted by ForemanRules
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If you dont know the answer to a question, why would you just post false and harmful information????Originally Posted by ForemanRules