IGF and Nolva

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    IGF and Nolva


    ok i herd that nolva counters gh. does it do the same with the igf?

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    Were did you hear that? Does it counterract it completely?
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    from what i heard it counters it completely...
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    i am not 100% at all but i thought it just supressed "natural" igf production..

    again i am not at all sure about this.. please research this.. i probably shouldnt have even posted
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    lol its ok man even if your not sure post... cus im not 100% but almost 90%...sure if it completely counters gh either.
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    This is some pretty good info I found googling around. You can skip to the bottom if you just want the nolva/igf info. It says 23% reduction in women who were tested. So a male who lifts and takes PH's or AAS, maybe less I would think.


    Anti-e's and IGF-1

    --------------------------------------------------------------------------------

    Can't remember where I nabbed this one from

    Here a few interesting studies originally posted by small on anabolex.
    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. nmauras@nemours.org.
    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. nmauras@nemours.org.
    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. adecensi@ieo.it.
    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. adecensi@ieo.it.
    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.

    [i]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.

    [i]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%

    Does it matter at all, for us?


    It would also be wise to note that aas may compensate for reductions in IGF-1.


    , 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.
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    I don't think you are correct.. but I will have to do a search later..
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    I'm not saying it's correct, it's just some data I found. I don't know the reliability. If you find different data please post.
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    enash , what u posted is for endogenous igf-1 . i remember someone saying igf-1 isnt effected by nolva when injected ? but i'm not sure either .
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    bump-- Iwould love to have this info before I start PCT
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    What causes muscle growth is Igf-1EA, which is expressed in the skeletal muscle. Nolva on the other hand lowers systemic IGF-1, therefore it shouldn't effect gains.
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    Reading that last study they did not use nolva but the anti-estrogen they used some how decrease serum IGF-1 and decreased the affinity of the the Igf-1 binding receptors, yet somehow increased Igf-1 induced growth. In all of the studies using nolva there is no mention of affect on igf binding receptors which you would think would be the main determining factor for whether it would affect injected igf-1 but since that other anti-estrogen decreased the affinity of the receptor yet increased igf-1 induced growth. Does anyone no of any studies of the effectiveness of igf-1 while on nolva, because the effect of serum levels really make no difference when it comes to injecting.
  

  
 

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