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Generic Nolvadex

vitor

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I can get a tub of 1000 Generic 50mg Nolvadex's from a friend of mine for around 100$. I was thinking of using them instead of liquiddex/arimidex. Any thoughts comments on using them instead. I figured taking 20-30mgs a day would be ok?? ALso is Nolvadex Liver toxic. Any help appreciated.
 

dpsquat

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hey yea

Ill take 200 off your hands for half of what you have in it if ther real
 

balplayer

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i was just thinking about this the other day because i can get it cheap also and wondered if higher doses would be a substitute for arimidex/liquidex.
 

bignipps

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nolvadex has a 10 fold lower affinity for the ER than estrogen. you will need to take a massive amount to block all E.
 

xcelbeyond

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I've always been told to not use Nolva unless you "have to." It can hinder gains from AAS.

In today's world we have such xcelent anti-e's like letrozole and anastrozole that it seems like like using nolva or proviron is taking two steps backwards? I believe those 2 products still have their use but not as a "daily" anti-e preventitives. Anyone - please feel free to correct me :)

xcelbeyond
 

balplayer

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i agree with your statement excell, but i cant always afford arimidex. wish i could
 

eatcrow

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xcelbeyond said:
I've always been told to not use Nolva unless you "have to." It can hinder gains from AAS.

In today's world we have such xcelent anti-e's like letrozole and anastrozole that it seems like like using nolva or proviron is taking two steps backwards? I believe those 2 products still have their use but not as a "daily" anti-e preventitives. Anyone - please feel free to correct me :)

xcelbeyond
I've heard that Nolva increases bone density in oestoperosis sufferers whereas Arimidex doesnt, plus, IGF levels are decreased a lot more with arimidex.

as anti e's, arimidex and Letrozole are better but I believe that Nolva has more benefits ( I think). :confused:
 
Last edited:

BCC

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xcelbeyond said:
I've always been told to not use Nolva unless you "have to." It can hinder gains from AAS.

In today's world we have such xcelent anti-e's like letrozole and anastrozole that it seems like like using nolva or proviron is taking two steps backwards? I believe those 2 products still have their use but not as a "daily" anti-e preventitives. Anyone - please feel free to correct me :)

xcelbeyond
I'll have to disagree. As excellent as arimidex is, you run the risk of driving estrogen too low and playing havoc on your lipids. Nolvadex does an excellent job of balancing out cholesterol and I make it a part of every cycle.
 

Dave_19

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balplayer said:
i agree with your statement excell, but i cant always afford arimidex. wish i could
you should just get some liquid letro from kaotic then, I cannot afford arimidex myself either..
 

leapfrog

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FYI

nolvadex knocks growth down 70%,so if your on gh your shooting yourself in the foot.also when i was getting all my AS from the doc (when i had insurance)he told me the only time your should take nolvadex was for pct-hcg,clomid,nolvadex.at first he would perscribe me arimidex but then he switched to femara,he said it was a better anti-E.

leap
 

Dave_19

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leapfrog said:
nolvadex knocks growth down 70%,so if your on gh your shooting yourself in the foot.also when i was getting all my AS from the doc (when i had insurance)he told me the only time your should take nolvadex was for pct-hcg,clomid,nolvadex.at first he would perscribe me arimidex but then he switched to femara,he said it was a better anti-E.

leap
this is a good point, its probably why people often say that nolva/clomid is "on hand" when writing their cycle layout..
 

Snarf

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I don't take Nolvadex as a part of my cycles becuase it does inhibit IGF production which can limit gains.

It is easier to dose correctly without totally crashing your estrogen, but it also is not as effective at preventing gyno as an aromatase inhibitor.

If you are prone to bloat, high blood pressure or gyno, then an aromatase inhibitor is your best bet. Just play with the dose and take as little as possible. For me, I only take it when my nips get sore. If I use too much my estrogen drops too low and my sex drive goes to nothing. (you need some estrogen for sex drive. A lot of people blame their tren or deca, when really they are just running too much anti-e).

It is a good idea to keep some Nolvadex on hand in case you get a gyno flare up. The aromatase inhibitor will not help short term as much becuase it does not block estrogen binding to the receptor site, it just prevents your body from making estrogen. So, if you already have too much estrogen in your body, you don't want to wait for the aromatase inhibitor to work, you need Nolvadex to block the binding and then wait for the aromatase inhibitor to drop your estrogen levels over time.

Hope this makes sense.
 

Starkraven

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the new thing is aromasin. it doesnt drive estro too low or mess up your lipid profile and works better than letro/l-dex. just what i have been reading though. in a future cycle, ill use it and then do aromasin + nolva for PCT.
 

eatcrow

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Snarf said:
I don't take Nolvadex as a part of my cycles becuase it does inhibit IGF production which can limit gains.
Would it be possible to combine Nolva with Femara to overcome this.
 

Phrmdude

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eatcrow said:
Would it be possible to combine Nolva with Femara to overcome this.
There really is no need to do this, unless you are getting some serious gyno symptoms. There is no way to know if the Femara IGF boosting affect is enough to cancel out the Nolvadex inhibiting affect. Nobody is going to do that study.

I think we all started to use the aromatase inhibitor with the best inhibition, but it looks like partial aromatase inhibition might be better as Starkraven mentioned.
 

eatcrow

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Phrmdude said:
There really is no need to do this, unless you are getting some serious gyno symptoms. There is no way to know if the Femara IGF boosting affect is enough to cancel out the Nolvadex inhibiting affect. Nobody is going to do that study.

I think we all started to use the aromatase inhibitor with the best inhibition, but it looks like partial aromatase inhibition might be better as Starkraven mentioned.
Can't remember where I nabbed this one from but here are a few interesting studies.

Remember all studies were conducted on women with breast cancer, which can raise IGF-1 markers.

Different anti-estrogens effect IGF-1 level to a different degree. How really important is IGF-1 level for us? Does it matter?
It certainly does for natural athletes, but what about steroids users?
I did a little comparison of different anti-estrogens, in relation to IGF-1.
Those are:

Femara(letrozole) - potent aromatise inhibitor, easily available, slightly less expensive then Arimidex, but cost a little more then Liquidex.

The aromatase inhibitor letrozole in advanced breast cancer: effects on serum insulin-like growth factor (IGF)-I and IGF-binding protein-3 levels.
J Steroid Biochem Mol Biol 1997 Nov-Dec;63(4-6):261-7 (ISSN: 0960-0760)
Bajetta E; Ferrari L; Celio L; Mariani L; Miceli R; Di Leo A; Zilembo N; Buzzoni R; Spagnoli I; Martinetti A; Bichisao E; Seregni E [Find other articles with these Authors]
Medical Oncology B Division, Istituto Nazionale per lo Studio e la Cura dei Tumori, Milan, Italy.
Serum insulin-like growth factor (IGF)-I and IGF-binding protein-3 levels were measured in two groups of postmenopausal women with advanced breast cancer, who received the aromatase inhibitor letrozole 0.5 or 2.5 mg p.o. once daily. Blood samples were obtained from 15 patients in each dose group at baseline, and one and three months after starting therapy. Circulating IGF-I and IGFBP-3 concentrations were determined by means of radioimmunoassay. In both dosage groups a statistically significant increase in the IGF-I levels was observed during three months of letrozole treatment (P=0.003). In addition, the multiple testing procedure yielded in the whole patient population a significant result in the comparison between mean IGF-I values after three months of therapy and those observed at baseline (P=0.004), the estimated average increase being of 24%. No significant result was obtained in the analysis for the dose effect (P=0.077) and for the time x dose interaction (P=0.208). Circulating IGFBP-3 levels did not appear to be affected by letrozole treatment in either of the dose groups. This is the first report concerning the short-term effects of letrozole on components of the IGF system in breast cancer patients; further investigations are warranted in order to confirm these preliminary data.
-------------------------------------------------
Arimidex(anastrozole) - We all know this one.

Estrogen suppression in males: metabolic effects.
J Clin Endocrinol Metab 2000 Jul;85(7):2370-7 (ISSN: 0021-972X)
Mauras N; O'Brien Karomatase inhibitor letrozole 0.5 or 2.5 mg p.o. once daily. Blood samples were obtained from 15 patients in each dose group at baseline, and one and three months after starting therapy. Circulating IGF-I and IGFBP-3 concentrations were determined by means of radioimmunoassay. In both dosage groups a statistically significant increase in the IGF-I levels was observed during three months of letrozole treatment (P=0.003). In addition, the multiple testing procedure yielded in the whole patient population a significant result in the comparison between mean IGF-I values after three months of therapy and those observed at baseline (P=0.004), the estimated average increase being of 24%. No significant result was obtained in the analysis for the dose effect (P=0.077) and for the time x dose interaction (P=0.208). Circulating IGFBP-3 levels did not appear to be affected by letrozole treatment in either of the dose groups. This is the first report concerning the short-term effects of letrozole on components of the IGF system in breast cancer patients; further investigations are warranted in order to confirm these preliminary data.
-------------------------------------------------
Arimidex(anastrozole) - We all know this one.

Estrogen suppression in males: metabolic effects.
J Clin Endocrinol Metab 2000 Jul;85(7):2370-7 (ISSN: 0021-972X)
Mauras N; O'Brien KO; Klein KO; Hayes V [Find other articles with these Authors]
Nemours Research Programs at the Nemours Children's Clinic, Jacksonville, Florida 32207, USA. [email protected].
We have shown that testosterone (T) deficiency per se is associated with marked catabolic effects on protein, calcium metabolism, and body composition in men independent of changes in GH or insulin-like growth factor I production. It is not clear,,however, whether estrogens have a major role in whole body anabolism in males. We investigated the metabolic effects of selective estrogen suppression in the male using a potent aromatase inhibitor, Arimidex (Anastrozole). First, a dose-response study of 12 males (mean age, 16.1 +/- 0.3 yr) was conducted, and blood withdrawn at baseline and after 10 days of oral Arimidex given as two different doses (either 0.5 or 1 mg) in random order with a 14-day washout in between. A sensitive estradiol (E2) assay showed an approximately 50% decrease in E2 concentrations with either of the two doses; hence, a 1-mg dose was selected for other studies. Subsequently, eight males (aged 15-22 yr; four adults and four late pubertal) had isotopic infusions of [(13)C]leucine and (42)Ca/(44)Ca, indirect calorimetry, dual energy x-ray absorptiometry, isokinetic dynamometry, and growth factors measurements performed before and after 10 wO; Klein KO; Hayes V [Find other articles with these Authors]
Nemours Research Programs at the Nemours Children's Clinic, Jacksonville, Florida 32207, USA. [email protected].
We have shown that testosterone (T) deficiency per se is associated with marked catabolic effects on protein, calcium metabolism, and body composition in men independent of changes in GH or insulin-like growth factor I production. It is not clear,,however, whether estrogens have a major role in whole body anabolism in males. We investigated the metabolic effects of selective estrogen suppression in the male using a potent aromatase inhibitor, Arimidex (Anastrozole). First, a dose-response study of 12 males (mean age, 16.1 +/- 0.3 yr) was conducted, and blood withdrawn at baseline and after 10 days of oral Arimidex given as two different doses (either 0.5 or 1 mg) in random order with a 14-day washout in between. A sensitive estradiol (E2) assay showed an approximately 50% decrease in E2 concentrations with either of the two doses; hence, a 1-mg dose was selected for other studies. Subsequently, eight males (aged 15-22 yr; four adults and four late pubertal) had isotopic infusions of [(13)C]leucine and (42)Ca/(44)Ca, indirect calorimetry, dual energy x-ray absorptiometry, isokinetic dynamometry, and growth factors measurements performed before and after 10 weeks of daily doses of Arimidex. Contrary to the effects of T withdrawal, there were no significant changes in body composition (body mass index, fat mass, and fat-free mass) after estrogen suppression or in rates of protein synthesis or degradation; carbohydrate, lipid, or protein oxidation; muscle strength; calcium kinetics; or bone growth factors concentrations. However, E2 concentrations decreased 48% (P = 0.006), with no significant change in mean and peak GH concentrations, but with an 18% decrease in plasma insulin-like growth factor I concentrations. There was a 58% increase in serum T (P = 0.0001), sex hormone-binding globulin did not change, whereas LH and FSH concentrations increased (P < 0.02, both). Serum bone markers, osteocalcin and bone alkaline phosphatase concentrations, and rates of bone calcium deposition and resorption did not change. In conclusion, these data suggest that in the male 1) estrogens do not contribute significantly to the changes in body composition and protein synthesis observed with changing androgen levels; 2) estrogen is a main regulator of the gonadal-pituitary feedback for the gonadotropin axis; and 3) this level of aromatase inhibition does not negatively impact either kinetically measured rates of bone calcium turnover or indirect markers of bone calcium turnover, at least in the short term. Further studies will provideeeks of daily doses of Arimidex. Contrary to the effects of T withdrawal, there were no significant changes in body composition (body mass index, fat mass, and fat-free mass) after estrogen suppression or in rates of protein synthesis or degradation; carbohydrate, lipid, or protein oxidation; muscle strength; calcium kinetics; or bone growth factors concentrations. However, E2 concentrations decreased 48% (P = 0.006), with no significant change in mean and peak GH concentrations, but with an 18% decrease in plasma insulin-like growth factor I concentrations. There was a 58% increase in serum T (P = 0.0001), sex hormone-binding globulin did not change, whereas LH and FSH concentrations increased (P < 0.02, both). Serum bone markers, osteocalcin and bone alkaline phosphatase concentrations, and rates of bone calcium deposition and resorption did not change. In conclusion, these data suggest that in the male 1) estrogens do not contribute significantly to the changes in body composition and protein synthesis observed with changing androgen levels; 2) estrogen is a main regulator of the gonadal-pituitary feedback for the gonadotropin axis; and 3) this level of aromatase inhibition does not negatively impact either kinetically measured rates of bone calcium turnover or indirect markers of bone calcium turnover, at least in the short term. Further studies will provide valuable information on whether timed aromatase inhibition can be useful in increasing the height potential of pubertal boys with profound growth retardation without the confounding negative effects of gonadal androgen suppression.
-------------------------------------------------
Nolvadex(tamoxifen) - The least expensive and most available, until recently, the most popular as well. Far not as effective as previous two, sinse it's not inhibitor, but selective antagonist.


Effect of tamoxifen on lipoprotein(a) and insulin-like growth factor-I (IGF-I) in healthy women.
Eur J Cancer 1999 Apr;35(4):596-600 (ISSN: 0959-8049)
Decensi A; Robertson C; Ballardini B; Paggi D; Guerrieri-Gonzaga A; Bonanni B; Manetti L; Johansson H; Barreca A; Bettega D; Costa A [Find other articles with these Authors]
FIRC Chemoprevention Unit, European Institute of Oncology, Milan, Italy. [email protected].
Studies in breast cancer patients have shown that tamoxifen decreases circulating levels of lipoprotein(a) (Lp(a)), an independent risk factor for premature coronary heart disease, and insulin-like growth factor-I (IGF-I), a promising surrogate biomarker for breast cancer. Since a common hormone regulatory pathway has been suggested for both biomarkers, we measured Lp(a) levels for 6 months in 68 healthy women participati valuable information on whether timed aromatase inhibition can be useful in increasing the height potential of pubertal boys with profound growth retardation without the confounding negative effects of gonadal androgen suppression.
-------------------------------------------------
Nolvadex(tamoxifen) - The least expensive and most available, until recently, the most popular as well. Far not as effective as previous two, sinse it's not inhibitor, but selective antagonist.


Effect of tamoxifen on lipoprotein(a) and insulin-like growth factor-I (IGF-I) in healthy women.
Eur J Cancer 1999 Apr;35(4):596-600 (ISSN: 0959-8049)
Decensi A; Robertson C; Ballardini B; Paggi D; Guerrieri-Gonzaga A; Bonanni B; Manetti L; Johansson H; Barreca A; Bettega D; Costa A [Find other articles with these Authors]
FIRC Chemoprevention Unit, European Institute of Oncology, Milan, Italy. [email protected].
Studies in breast cancer patients have shown that tamoxifen decreases circulating levels of lipoprotein(a) (Lp(a)), an independent risk factor for premature coronary heart disease, and insulin-like growth factor-I (IGF-I), a promising surrogate biomarker for breast cancer. Since a common hormone regulatory pathway has been suggested for both biomarkers, we measured Lp(a) levels for 6 months in 68 healthy women participating in a chemoprevention trial of tamoxifen and correlated its changes with IGF-I. After 1 month, mean Lp(a) levels decreased by 23% with tamoxifen and increased by 6% with placebo (P = 0.033). No further change was observed after 2 and 6 months. Women with abnormal values at baseline (i.e. > 30 mg/dl) showed the highest reduction. The mean levels of IGF-I decreased by 23.5% with tamoxifen and remained stable with placebo, but the changes induced by tamoxifen in Lp(a) and IGF-I levels were uncorrelated. Our results support the observation that tamoxifen may be a suitable preventive option for women with multiple disease risk factors.
-------------------------------------------------

Faslodex(ICI 182, 780)[/b] - next generation of anti-esterogens, not available yet, is due next year. Should be at least as potent as Arimidex, but has different mechanism of action, it acts by decreasing the # of ER on cell, or decreasing their level of responsiveness to E.

Regulation of insulin-like growth factor I receptor expression by the pure antiestrogen ICI 182780.

Clin Cancer Res 1996 Dec;2(12):2037-42 (ISSN: 1078-0432)

Huynh H; Nickerson T; Pollak M; Yang X [Find other articles with these Authors]
Lady Davis Research Institute, and Department of Medicine, McGill University, 3755 Cote St. Catherine Roang in a chemoprevention trial of tamoxifen and correlated its changes with IGF-I. After 1 month, mean Lp(a) levels decreased by 23% with tamoxifen and increased by 6% with placebo (P = 0.033). No further change was observed after 2 and 6 months. Women with abnormal values at baseline (i.e. > 30 mg/dl) showed the highest reduction. The mean levels of IGF-I decreased by 23.5% with tamoxifen and remained stable with placebo, but the changes induced by tamoxifen in Lp(a) and IGF-I levels were uncorrelated. Our results support the observation that tamoxifen may be a suitable preventive option for women with multiple disease risk factors.
-------------------------------------------------

Faslodex(ICI 182, 780)[/b] - next generation of anti-esterogens, not available yet, is due next year. Should be at least as potent as Arimidex, but has different mechanism of action, it acts by decreasing the # of ER on cell, or decreasing their level of responsiveness to E.

Regulation of insulin-like growth factor I receptor expression by the pure antiestrogen ICI 182780.

Clin Cancer Res 1996 Dec;2(12):2037-42 (ISSN: 1078-0432)

Huynh H; Nickerson T; Pollak M; Yang X [Find other articles with these Authors]
Lady Davis Research Institute, and Department of Medicine, McGill University, 3755 Cote St. Catherine Road, Montreal, Quebec H3T 1E2, Canada.

Insulin-like growth factor I (IGF-I) is a mitogen for human breast cancer cells both in vivo and in vitro. We demonstrate here that the antiestrogen ICI 182780 (ICI) at 10(-8) m decreases IGF-I receptor (IGF-IR) mRNA levels by 70% after treatment for 48 h. Measurements of mRNA stability indicate that the half-life of IGF-IR mRNA is approximately 3 h. Estradiol treatment increases the half-life of the IGF-IR mRNA to approximately 6 h and the level of IGF-IR gene transcription by 1.8-fold, whereas ICI treatment not only decreases the IGF-IR transcription rate by 50% but also decreases the IGF-IR mRNA half-life to less than 3 h. Affinity labeling studies with [125I]-IGF-I show 35% increased labeled IGF-I to MCF-7 cell membrane following estradiol treatment and 40% decreased labeling following ICI treatment. We also demonstrate that ICI attenuates IGF-I-stimulated growth. Our data suggest that attenuation of IGF-I responsivity by ICI may be due in part to reducing the IGF-IR expression.
------------------------------------------------

Femara - increases IGF-1 by 24%
Arimidex - decreases IGF-1 by 18%
Nolvadex - decreases IGF-1 by 23.5%
Faslodex - decreases IGF-1 by 70%

a 0.5% increase is better than nothing.
 
Last edited:

xcelbeyond

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This post was almost 3 Years Old!

BCC said:
I'll have to disagree. As excellent as arimidex is, you run the risk of driving estrogen too low and playing havoc on your lipids. Nolvadex does an excellent job of balancing out cholesterol and I make it a part of every cycle.
I have learned "more" since this was originally posted :eek: ;)

If you read what Snarf said (and Starkraven) posted recently, this is my thinking nowadays on this issue.

I really don't care if you disagree with me, just disagree with my thoughts as they are today, not 3 years ago :p ;) :)
 

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