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bicepts101
New member
where is the addy for it i cant find it in your store
MACRO/ULTER........Testing a new Aromatese Inhibitor Formula:
- Thread starter swordfish151
- Start date
A
Anthony Roberts
Guest
macrophage69alpha said:
And testosterone, has a transdermal delivery rate (from the largest pharmaceutical companies best formula) of up to 10%. So we can assume your blend is no better than the best effort put forth by pharmaceutical companies. I think that's reasonable. So...we can now say with confidence that 90% of the ATD in your product...never makes it into the body, right?
Sounds like a waste...
SO even if there was a 90% inhibition of Aromatase possible by the amount in your product...how much does someone actually get of that aromatase inhibition when only 10% of the ATD ever makes it into the body?
1: J Clin Endocrinol Metab. 2000 Dec;85(12):4500-10.
Long-term pharmacokinetics of transdermal testosterone gel in hypogonadal men.
Swerdloff RS, Wang C, Cunningham G, Dobs A, Iranmanesh A, Matsumoto AM, Snyder PJ, Weber T, Longstreth J, Berman N.
Divisions of Endocrinology, Departments of Medicine/Pediatrics, Harbor-University of California-Los Angeles Medical Center, Torrance, California 90509, USA.
Transdermal delivery of testosterone (T) represents an effective alternative to injectable androgens. Transdermal T patches normalize serum T levels and reverse the symptoms of androgen deficiency in hypogonadal men. However, the acceptance of the closed system T patches has been limited by skin irritation and/or lack of adherence. T gels have been proposed as delivery modes that minimize these problems. In this study we examined the pharmacokinetic profiles after 1, 30, 90, and 180 days of daily application of 2 doses of T gel (50 and 100 mg T in 5 and 10 g gel, delivering 5 and 10 mg T/day, respectively) and a permeation-enhanced T patch (2 patches delivering 5 mg T/day) in 227 hypogonadal men. This new 1% hydroalcoholic T gel formulation when applied to the upper arms, shoulders, and abdomen dried within a few minutes, and about 9-14% of the T applied was bioavailable. After 90 days of T gel treatment, the dose was titrated up (50 mg to 75 mg) or down (100 mg to 75 mg) if the preapplication serum T levels were outside the normal adult male range. Serum T rose rapidly into the normal adult male range on day 1 with the first T gel or patch application. Our previous study showed that steady state T levels were achieved 48-72 h after first application of the gel. The pharmacokinetic parameters for serum total and free T were very similar on days 30, 90, and 180 in all treatment groups. After repeated daily application of the T formulations for 180 days, the average serum T level over the 24-h sampling period (C(avg)) was highest in the 100 mg T gel group (1.4- and 1.9-fold higher than the C(avg) in the 50 mg T gel and T patch groups, respectively). Mean serum steady state T levels remained stable over the 180 days of T gel application. Upward dose adjustment from T gel 50 to 75 mg/day did not significantly increase the C(avg), whereas downward dose adjustment from 100 to 75 mg/day reduced serum T levels to the normal range for most patients. Serum free T levels paralleled those of serum total T, and the percent free T was not changed with transdermal T preparations. The serum dihydrotestosterone C(avg) rose 1.3-fold above baseline after T patch application, but was more significantly increased by 3.6- and 4.6-fold with T gel 50 and 100 mg/day, respectively, resulting in a small, but significant, increase in the serum dihydrotestosterone/T ratios in the two T gel groups. Serum estradiol rose, and serum LH and FSH levels were suppressed proportionately with serum T in all study groups; serum sex hormone-binding globulin showed small decreases that were significant only in the 100 mg T gel group. We conclude that transdermal T gel application can efficiently and rapidly increase serum T and free T levels in hypogonadal men to within the normal range. Transdermal T gel provided flexibility in dosing with little skin irritation and a low discontinuation rate.
Publication Types:
Clinical Trial
Multicenter Study
Randomized Controlled Trial
But here's something I find interesting...it would seem that ATD is an androgen receptor blocker...meaning it prevents testosterone from attaching to the receptor and thus would eliminate some of it's genomic (Receptor Mediated) effects, such as an increase in protein synthesis, etc...basically slowing down muscle building. Here's a study:
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]
macrophage69alpha
New member
anthony roberts said:
this study done in 1989 proposed a theory, that effects were due to AR binding, a theory that was later refuted and dismissed.. by studies like this one.
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.
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with respect to AR binding, ATD has the same binding affinity as exemestane (Aromasin) between .2% and .25% of DHT.
macrophage69alpha
New member
anthony roberts said:
1. poor assumption
2. not really best effort- even at the time of conception
3. not reasonable
4. such confidence is not justified
do you even know what the base for androgel is?
alcohol and a single permeation enhancer IPM (isopropyl myristate). (relevant ingredients)
this technology is not only OLD it has a low efficiency, what it does have is FDA approval for that prescription use. developed in this case over 20 years ago. Hey old technologies can be good, this is just not one of them.
EVEN IF ALL THE CLAIMS YOU MADE WERE TRUE---- which they are NOT.
its irrelevant, dosing is not based on delivery percent. Those percentages, while interesting and somewhat prideful are just estimates of delivery based on the delivery vehichle. Dosing is based on suppression of aromatase activity.
How much of the active that is "wasted" is also irrelevant, sure its interesting to the developer of the delivery platform- in a prideful way, but to the end user suppression of aromatase is what matters. Whether you waste 100mg or 30mg to deliver 10mg but the cost and effects to the end user are the same- what does it matter to them?
Tux
Well-known member
Well I just started using my sample one pump on each forearm, morning and night, for 4 pumps per day total. This will be with over a gram of test and around 80mg/day of dbol. If don't become a total blimp, I'll say it's pretty good. I'll know in about 10-14 days. Smells kinda like orange pine-sol.. kinda nice 
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