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Aifm Rash Poll
- Thread starter Zuperman
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DieselGunz
New member
we can not see all this shady stuff going on behind the scenes because we are not mods. This is a level playing field with X and company because both of them can see eveything being done.
M
Mr.X
Guest
DieselGunz said:
Don't worry you'll get PMs from macro in a second telling you about posting here. They'll give you a refund, shut you up, and then they'll injure some more members with this dangerous product.
A
Anthony Roberts
Guest
Remember my friend who suffered cognitive impairment from A transdermal AI? Because brain aromatase is necessary to avoid cognitive impairment? He came here and shared his experience, remember? Well...Then Macro said it was because he used Letro Transdermally, not ATD? Here's a study showing ATD inhibits brain aromatase:
J Clin Endocrinol Metab. 1993 Dec;77(6):1529-34.
Differential effects of aromatase inhibition on luteinizing hormone secretion in intact and castrated male cynomolgus macaques.
Resko JA, Connolly PB, Roselli CE, Abdelgadir SE, Choate JV.
Department of Physiology, Oregon Health Sciences University, Portland 97201-3098.
To understand the role of central aromatization in feedback regulation of LH in nonhuman primates, we treated adult male cynomolgus monkeys with the aromatase inhibitor, 1,4,6-androstatriene-3,17-dione (ATD). We measured LH, testosterone (T), and ATD in systemic sera of blood samples drawn on a diurnal schedule (0900 and 2100 h). Each animal was bled for 4 pretreatment days from a femoral catheter after which they were divided into the following treatment groups: castrated (Cx), n = 2; Cx + T, n = 6; Cx + T + ATD, n = 6; Cx + ATD, n = 3; and sham operated + ATD, n = 3. Silastic capsules or packets containing T or ATD, respectively, were placed sc between the scapulae at the time of Cx or sham treatment. In T-treated animals, T (20 micrograms/kg body weight) dissolved in propylene glycol was injected im at 2100 h to mimic the diurnal rise of T observed in nonhuman primates. Animals were bled for 2 weeks after which they were killed, and selected brain areas were analyzed for aromatase activity and cytosolic and nuclear androgen receptors. Animals treated with ATD had significantly reduced levels of aromatase activity in selected regions of the hypothalamus, preoptic area, and the amygdala (P < 0.05). Even though ATD inhibited brain aromatase activity, it did not prevent the negative feedback actions of T on LH secretion after Cx. In addition, ATD by itself inhibited LH secretion after Cx and activated brain androgen receptors. These latter effects of ATD seemed to have been mediated through a metabolite. In sham-operated intact males, ATD produced variable surges of LH that were accompanied by elevations of T in the systemic circulation. These differential effects of ATD in intact vs. castrated animals demonstrate the importance of selecting the proper model system to study LH control mechanisms. In the intact animal, aromatization seems to play a role in regulating LH secretion, but the postcastration rise of LH seems to be regulated differently.
PMID: 8263136 [PubMed - indexed for MEDLINE]
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My verdict? ATD is dangerous. Avoid.
J Clin Endocrinol Metab. 1993 Dec;77(6):1529-34.
Differential effects of aromatase inhibition on luteinizing hormone secretion in intact and castrated male cynomolgus macaques.
Resko JA, Connolly PB, Roselli CE, Abdelgadir SE, Choate JV.
Department of Physiology, Oregon Health Sciences University, Portland 97201-3098.
To understand the role of central aromatization in feedback regulation of LH in nonhuman primates, we treated adult male cynomolgus monkeys with the aromatase inhibitor, 1,4,6-androstatriene-3,17-dione (ATD). We measured LH, testosterone (T), and ATD in systemic sera of blood samples drawn on a diurnal schedule (0900 and 2100 h). Each animal was bled for 4 pretreatment days from a femoral catheter after which they were divided into the following treatment groups: castrated (Cx), n = 2; Cx + T, n = 6; Cx + T + ATD, n = 6; Cx + ATD, n = 3; and sham operated + ATD, n = 3. Silastic capsules or packets containing T or ATD, respectively, were placed sc between the scapulae at the time of Cx or sham treatment. In T-treated animals, T (20 micrograms/kg body weight) dissolved in propylene glycol was injected im at 2100 h to mimic the diurnal rise of T observed in nonhuman primates. Animals were bled for 2 weeks after which they were killed, and selected brain areas were analyzed for aromatase activity and cytosolic and nuclear androgen receptors. Animals treated with ATD had significantly reduced levels of aromatase activity in selected regions of the hypothalamus, preoptic area, and the amygdala (P < 0.05). Even though ATD inhibited brain aromatase activity, it did not prevent the negative feedback actions of T on LH secretion after Cx. In addition, ATD by itself inhibited LH secretion after Cx and activated brain androgen receptors. These latter effects of ATD seemed to have been mediated through a metabolite. In sham-operated intact males, ATD produced variable surges of LH that were accompanied by elevations of T in the systemic circulation. These differential effects of ATD in intact vs. castrated animals demonstrate the importance of selecting the proper model system to study LH control mechanisms. In the intact animal, aromatization seems to play a role in regulating LH secretion, but the postcastration rise of LH seems to be regulated differently.
PMID: 8263136 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
My verdict? ATD is dangerous. Avoid.
A
Anthony Roberts
Guest
At least it is an anti-androgen too...so it'll help you avoid any of that nasty testosterone you have floating around making you bigger or stronger...
Effects of ATD on male sexual behavior and androgen receptor binding: a reexamination of the aromatization hypothesis.
Kaplan ME, McGinnis MY.
Department of Anatomy, Mount Sinai School of Medicine, CUNY, New York 10029.
The aromatization hypothesis asserts that testosterone (T) must be aromatized to estradiol (E2) to activate copulatory behavior in the male rat. In support of this hypothesis, the aromatization inhibitor, ATD, has been found to suppress male sexual behavior in T-treated rats. In our experiment, we first replicated this finding by peripherally injecting ATD (15 mg/day) or propylene glycol into T-treated (two 10-mm Silastic capsules) or control castrated male rats. In a second experiment, we bilaterally implanted either ATD-filled or blank cannulae into the medial preoptic area (MPOA) of either T-treated or control castrated male rats. With this more local distribution of ATD, a lesser decline in sexual behavior was found, suggesting that other brain areas are involved in the neurohormonal activation of copulatory behavior in the male rat. To determine whether in vivo ATD interacts with androgen or estrogen receptors, we conducted cell nuclear androgen and estrogen receptor binding assays of hypothalamus, preoptic area, amygdala, and septum following treatment with the combinations of systemic T alone. ATD plus T, ATD alone, and blank control. In all four brain areas binding of T to androgen receptors was significantly decreased in the presence of ATD, suggesting that ATD may act both as an androgen receptor blocker and as an aromatization inhibitor. Competitive binding studies indicated that ATD competes in vitro for cytosol androgen receptors, thus substantiating the in vivo antiandrogenic effects of ATD. Cell nuclear estrogen receptor binding was not significantly increased by exposure to T in the physiological range. No agonistic properties of ATD were observed either behaviorally or biochemically. Thus, an alternative explanation for the inhibitory effects of ATD on male sexual behavior is that ATD prevents T from binding to androgen receptors.
PMID: 2925181 [PubMed - indexed for MEDLINE]
Effects of ATD on male sexual behavior and androgen receptor binding: a reexamination of the aromatization hypothesis.
Kaplan ME, McGinnis MY.
Department of Anatomy, Mount Sinai School of Medicine, CUNY, New York 10029.
The aromatization hypothesis asserts that testosterone (T) must be aromatized to estradiol (E2) to activate copulatory behavior in the male rat. In support of this hypothesis, the aromatization inhibitor, ATD, has been found to suppress male sexual behavior in T-treated rats. In our experiment, we first replicated this finding by peripherally injecting ATD (15 mg/day) or propylene glycol into T-treated (two 10-mm Silastic capsules) or control castrated male rats. In a second experiment, we bilaterally implanted either ATD-filled or blank cannulae into the medial preoptic area (MPOA) of either T-treated or control castrated male rats. With this more local distribution of ATD, a lesser decline in sexual behavior was found, suggesting that other brain areas are involved in the neurohormonal activation of copulatory behavior in the male rat. To determine whether in vivo ATD interacts with androgen or estrogen receptors, we conducted cell nuclear androgen and estrogen receptor binding assays of hypothalamus, preoptic area, amygdala, and septum following treatment with the combinations of systemic T alone. ATD plus T, ATD alone, and blank control. In all four brain areas binding of T to androgen receptors was significantly decreased in the presence of ATD, suggesting that ATD may act both as an androgen receptor blocker and as an aromatization inhibitor. Competitive binding studies indicated that ATD competes in vitro for cytosol androgen receptors, thus substantiating the in vivo antiandrogenic effects of ATD. Cell nuclear estrogen receptor binding was not significantly increased by exposure to T in the physiological range. No agonistic properties of ATD were observed either behaviorally or biochemically. Thus, an alternative explanation for the inhibitory effects of ATD on male sexual behavior is that ATD prevents T from binding to androgen receptors.
PMID: 2925181 [PubMed - indexed for MEDLINE]
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Mr.X
Guest
anthony roberts said:
Wasn't macro PMing him trying to keep him from posting his results on the open forums?
I bet macro will try to spin this now. He will insult you, and try to discredit you, instead of facing the reality of AIFM.
M
Mr.X
Guest
Guvna said:
AIFM was being sold on the AS forum as something you use instead of all other anti-estrogens. It's being shown here to be nothing more then a marketing trick.
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