Dermacrine !??

Ok, I followed the link under MR X's signature to read about this Dermacrine stuff. One heck of an impressive website. So is this a version of AIFM or something. Does anyone have any unbiased opinions. Don't bash so the thread doesn't get shut down.

Twoguns said:

Ok, I followed the link under MR X's signature to read about this Dermacrine stuff. One heck of an impressive website. So is this a version of AIFM or something. Does anyone have any unbiased opinions. Don't bash so the thread doesn't get shut down.

Click to expand...

Hello,

First of all, Id like to introduce myself as the primary owner of Primordial Performance. As you have been reading, our current flag-ship product is our testosterone boosting topical --Dermacrine, along with the saliva kits we sell to test your hormones.

After about 12 months of product development, cross referencing of thousands of scientific studies of different hormones & aromatase inhibitors, and performing dozens saliva hormone analysis’s on testers we feel have reached the pinnacle point in designing one of the most advanced formulas on the market.

I know some of you are curious about what makes our product different from other topical based testosterone booster / anti-estrogen based products. Let me take a moment to explain the unique properties of Dermacrine –

Dermacrine contains both DHEA and pregenolone. The DHEA was included for the obvious benefit of boosting testosterone. The pregnenolone was included for several neurological reasons, but also for its conversion to progesterone. Progesterone is crucial for preventing excessive conversion of testosterone > DHT. This makes dermacrine a great choice those concerned with prostate of hair loss issues.

Our choice of resveratrol, benzoflavone and chrysin (our phyto-AI complex) as estrogen reducers stem from the studies which show these natural polyphenols to be incredible fertility enhancers, meaning they have positive effects on the HTPA, LH and FSH. The research even points out that another undiscovered mechanism is involved, and estrogen inhibition is only half the story. Furthermore, our Phyto-AI complex also has various hearth health benefits, related to the vaso-relaxant properties, as well as being powerful anti-oxidants. Make no mistake, these are some powerful components, some of which have shown to bind to aromatase stronger than formestane (the reference standard) You can find this material referenced on our site - http://www.primordialperformance.com/benefits.cfm

The reason we didn’t include ATD is because it is a steroidal-based aromatase inhibitor which means it was designed off of the testosterone platform. Since ATD resembles testosterone’s structure, it competes for the aromatase enzyme, only it cannot be converted to estrogen like testosterone can. However, all steroidal based inhibitors tend to mimic the action of there parent compound, which means they can inhibit steroidogenesis from the hypothalamus and testis by directly interacting with the androgen receptor (AR) and lowering LH & FSH release. All related compounds, including ATD, formestane, aromasin, ect follow the same rules. They look like androgens, so they act like androgens… and therefore suppress testosterone production via the AR. IMO, these steroidal based inhibitors would not suite our type of product designed for PCT. For more referenced info on this visit here - http://www.primordialperformance.com/benefits.cfm

You may ask. Why include DHEA and pregnenolone if our phyto AI complex is so effective? Well, the answer is not simple. Basically if you don’t use your testis they shrink. The same rules apply to your steroidogenic enzymes. If you don’t use em, you lose em. DHEA and pregnenolone make your body use these steroidogenic enzymes that where inhibited and degraded during your massive steroid cycle. See our hormone tree page for more info on this. http://www.primordialperformance.com/hormone_tree.cfm

The combination of The Phyto-AI complex and the well balanced hormones in Dermacrine make it one hell of a PCT product, and we plan to prove this with our soon-to-be testers whom will be testing the product and there hormones before and after.

Stay tuned.

-Pp

bump

Primordial Performance said:

Hello,

First of all, Id like to introduce myself as the primary owner of Primordial Performance. As you have been reading, our current flag-ship product is our testosterone boosting topical --Dermacrine, along with the saliva kits we sell to test your hormones.

After about 12 months of product development, cross referencing of thousands of scientific studies of different hormones & aromatase inhibitors, and performing dozens saliva hormone analysis’s on testers we feel have reached the pinnacle point in designing one of the most advanced formulas on the market.

I know some of you are curious about what makes our product different from other topical based testosterone booster / anti-estrogen based products. Let me take a moment to explain the unique properties of Dermacrine –

Dermacrine contains both DHEA and pregenolone. The DHEA was included for the obvious benefit of boosting testosterone. The pregnenolone was included for several neurological reasons, but also for its conversion to progesterone. Progesterone is crucial for preventing excessive conversion of testosterone > DHT. This makes dermacrine a great choice those concerned with prostate of hair loss issues.

Our choice of resveratrol, benzoflavone and chrysin (our phyto-AI complex) as estrogen reducers stem from the studies which show these natural polyphenols to be incredible fertility enhancers, meaning they have positive effects on the HTPA, LH and FSH. The research even points out that another undiscovered mechanism is involved, and estrogen inhibition is only half the story. Furthermore, our Phyto-AI complex also has various hearth health benefits, related to the vaso-relaxant properties, as well as being powerful anti-oxidants. Make no mistake, these are some powerful components, some of which have shown to bind to aromatase stronger than formestane (the reference standard) You can find this material referenced on our site - http://www.primordialperformance.com/benefits.cfm

The reason we didn’t include ATD is because it is a steroidal-based aromatase inhibitor which means it was designed off of the testosterone platform. Since ATD resembles testosterone’s structure, it competes for the aromatase enzyme, only it cannot be converted to estrogen like testosterone can. However, all steroidal based inhibitors tend to mimic the action of there parent compound, which means they can inhibit steroidogenesis from the hypothalamus and testis by directly interacting with the androgen receptor (AR) and lowering LH & FSH release. All related compounds, including ATD, formestane, aromasin, ect follow the same rules. They look like androgens, so they act like androgens… and therefore suppress testosterone production via the AR. IMO, these steroidal based inhibitors would not suite our type of product designed for PCT. For more referenced info on this visit here - http://www.primordialperformance.com/benefits.cfm

You may ask. Why include DHEA and pregnenolone if our phyto AI complex is so effective? Well, the answer is not simple. Basically if you don’t use your testis they shrink. The same rules apply to your steroidogenic enzymes. If you don’t use em, you lose em. DHEA and pregnenolone make your body use these steroidogenic enzymes that where inhibited and degraded during your massive steroid cycle. See our hormone tree page for more info on this. http://www.primordialperformance.com/hormone_tree.cfm

The combination of The Phyto-AI complex and the well balanced hormones in Dermacrine make it one hell of a PCT product, and we plan to prove this with our soon-to-be testers whom will be testing the product and there hormones before and after.

Stay tuned.

-Pp

Click to expand...

nice

good info...

it does sound promising.

I just want to make it clear that no one is suggesting, that I can see, that this product is the same or is to be used like AIFM is currently being used for cycling. They are recommending their product for PCT, NOT for use on a gram of test. At least that's what I'm reading.

this is going to be a good thread =]

Ulter said:

I just want to make it clear that no one is suggesting, that I can see, that this product is the same or is to be used like AIFM is currently being used for cycling. They are recommending their product for PCT, NOT for use on a gram of test. At least that's what I'm reading.

Click to expand...

To answer your question; Yes, we are promoting Dermacrine as a PCT product.

If Dermacrine was used during a heavy cycle of test I would suggest the use of an additional aromatase inhibitor or SERM if one was especially sensitive to estrogenic side effects.

However, I think the estrogenic side effects of testosterone are generally overstated. We must remember that testosterone is a big boy, and generally prefers the man pathway over the female pathway. More specifically, about 6-8% of testosterone interacts with the 5a-reductase enzyme (man pathway), while only about 0.3% is being converted to estradiol.(female pathway) As we know, the 5-alpha reduced metabolites of testosterone are strong antagonizers of estrogen and can usually ward off gyno, water bloat, ect. Those that suffer estrogenic side effects from a gram of testosterone are usually those with a higher aromatase concentration (higher body fat), or are using it in combination with other drugs such as trenbolone, deca, d-bol, hGH, IGF-1, finestride, ect.

-Pp

The things you're posting are wrong on so many levels I don't even know where to start. AI's are a poor choice for hypogonadism because they surpress T production? See: below
Test will inhibit Estrogen, and therefore water retention, and gyno, enough all by itself so men don't need an anti E while on cycles of test? That's um... revolutionary.

However, all steroidal based inhibitors tend to mimic the action of there parent compound, which means they can inhibit steroidogenesis from the hypothalamus and testis by directly interacting with the androgen receptor (AR) and lowering LH & FSH release. All related compounds, including ATD, formestane, aromasin, ect follow the same rules. They look like androgens, so they act like androgens… and therefore suppress testosterone production via the AR. IMO, these steroidal based inhibitors would not suite our type of product designed for PCT.

Click to expand...

Maybe you can explain why testolactone (steroidal-based AI) didn't inhibit but rather ignited test, LH, FSH production in these studies. This seems to argue that your statements are incorrect.

1: Metabolism. 2003 Sep;52(9):1126-8. Links
Reversal of the hypogonadotropic hypogonadism of obese men by administration of the aromatase inhibitor testolactone.Zumoff B, Miller LK, Strain GW.
Division of Endocrinology and Metabolism, Beth Israel Medical Center, New York, NY 10003, USA.

Studies from this laboratory have shown that obese men have elevated serum estrogen levels and diminished levels of follicle-stimulating hormone (FSH) and free and total testosterone, all in proportion to their degree of obesity. The decreases in testosterone and FSH constitute a state of hypogonadotropic hypogonadism (HHG), and we have hypothesized that it results from feedback suppression of the pituitary by the elevated estrogen levels. We tested this hypothesis by lowering the serum estrogens of 6 health obese men (body mass index [BMI], 38 to 73) by administering the aromatase inhibitor testolactone (1 g daily for 6 weeks). Twenty-four-hour mean serum testosterone rose in every subject, from a mean of 290 +/- 165 ng/dL to a mean of 403 +/- 170 (P <.0003); 24-hour mean serum estradiol decreased in every subject, from a mean of 40 +/- 10.8 pg/mL to a mean of 29 +/- 6.7 (P <.004); and 24-hour mean serum luteinizing hormone (LH) increased in every subject, from a mean of 14.3 +/- 4.1 mIU/mL to a mean of 19.3 +/- 5.1 (P <.004). The rise in mean LH was due to an increase in the amplitude of the individual secretory pulses, especially at night. Twenty-four-hour mean serum estrone decreased nonsignificantly, from 48 +/- 14 pg/mL to 39 +/- 6.4, and 24-hour mean serum FSH increased nonsignificantly, from 13.5 +/- 5.3 mIU/mL to 15.0 +/- 5.4. The results are in accordance with the hypothesis, in that inhibition of estrogen biosynthesis (through administration of the aromatase inhibitor testolactone) results in alleviation of the HHG of our obese male subjects.


: J Urol. 2002 Feb;167(2 Pt 1):624-9. Links
Comment in:
J Urol. 2002 Oct;168(4 Pt 1):1509.
Aromatase inhibitors for male infertility.Raman JD, Schlegel PN.
Department of Urology, James Buchanan Brady Urology Foundation, Center for Male Reproductive Medicine and Microsurgery, New York Presbyterian Hospital, Weill Medical College of Cornell University, New York, New York, USA.

PURPOSE: Testosterone-to-estradiol ratio levels in infertile men improve during treatment with the aromatase inhibitor, testolactone, and resulting changes in semen parameters. We evaluated the effect of anastrozole, a more selective aromatase inhibitor, on the hormonal and semen profiles of infertile men with abnormal baseline testosterone-to-estradiol ratios. MATERIALS AND METHODS: A total of 140 subfertile men with abnormal testosterone-to-estradiol ratios were treated with 100 to 200 mg. testolactone daily or 1 mg. anastrozole daily. Changes in testosterone, estradiol, testosterone-to-estradiol ratios and semen parameters were evaluated during therapy. The effect of obesity, diagnosis of the Klinefelter syndrome, and presence of varicocele and/or history of varicocele repair on treatment results was studied. RESULTS: Men treated with testolactone had an increase in testosterone-to-estradiol ratios during therapy (mean plus or minus standard error of the mean 5.3 +/- 0.2 versus 12.4 +/- 1.1, p <0.001). This change was confirmed in subgroups of men with the Klinefelter syndrome, a history of varicocele repair and those with varicocele. A total of 12 oligospermic men had semen analysis before and during testolactone treatment with an increase in sperm concentration (5.5 versus 11.2 million sperm per ml., p <0.01), motility (14.7% versus 21.0%, p <0.05), morphology (6.5% versus 12.8%, p = 0.05), and motility index (606.3 versus 1685.2 million motile sperm per ejaculate, respectively, p <0.05) appreciated. During anastrozole treatment, similar changes in the testosterone-to-estradiol ratios were seen (7.2 +/- 0.3 versus 18.1 +/- 1.0, respectively, p <0.001). This improvement of hormonal parameters was noted for all subgroups except those patients with the Klinefelter syndrome. A total of 25 oligospermic men with semen analysis before and during anastrozole treatment had an increase in semen volume (2.9 versus 3.5 ml., p <0.05), sperm concentration (5.5 versus 15.6 million sperm per ml., p <0.001) and motility index (832.8 versus 2930.8 million motile sperm per ejaculate, respectively, p <0.005). These changes were similar to those observed in men treated with testolactone. No significant difference in serum testosterone levels during treatment with testolactone and anastrozole was observed. However, the anastrozole treatment group did have a statistically better improvement of serum estradiol concentration and testosterone-to-estradiol ratios (p <0.001). CONCLUSIONS: Men who are infertile with a low serum testosterone-to-estradiol ratio can be treated with an aromatase inhibitor. With treatment, an increase in testosterone-to-estradiol ratio occurred in association with increased semen parameters. Anastrozole and testolactone have similar effects on hormonal profiles and semen analysis. Anastrazole appears to be at least as effective as testolactone for treating men with abnormal testosterone-to-estradiol ratios, except for the subset with the Klinefelter syndrome, who appeared to be more effectively treated with testolactone.