Why Alphamine and Erase DESTROY Stubborn Fat
- 08-18-2013, 10:10 PM
Why Alphamine and Erase DESTROY Stubborn Fat
I know many people who have used Alphamine + Erase in a stack and noticed the now famous "leaning out" or "drying out" effect. In essence, these individuals lose fat in regions which no other product (or lack thereof) can replicate. Indeed, it's shockingly obvious when you're on these products vs off of them.
There's more to this story than just anecdote though. The science actually supports the combination for stubborn fat loss:
Estrogen controls lipolysis by up-regulating alpha2A-adrenergic receptors directly in human adipose tissue through the estrogen receptor alpha. Implications for the female fat distribution.
Pedersen SB, Kristensen K, Hermann PA, Katzenellenbogen JA, Richelsen B.
Source
Department of Endocrinology and Metabolism, Aarhus Amtssygehus, Aarhus University Hospital, Denmark. [email protected]
Abstract
Estrogen seems to promote and maintain the typical female type of fat distribution that is characterized by accumulation of adipose tissue, especially in the sc fat depot, with only modest accumulation of adipose tissue intraabdominally. However, it is completely unknown how estrogen controls the fat accumulation. We studied the effects of estradiol in vivo and in vitro on human adipose tissue metabolism and found that estradiol directly increases the number of antilipolytic alpha2A-adrenergic receptors in sc adipocytes. The increased number of alpha2A-adrenergic receptors caused an attenuated lipolytic response of epinephrine in sc adipocytes; in contrast, no effect of estrogen on alpha2A-adrenergic receptor mRNA expression was observed in adipocytes from the intraabdominal fat depot. These findings show that estrogen lowers the lipolytic response in sc fat depot by increasing the number of antilipolytic alpha2A-adrenergic receptors, whereas estrogen seems not to affect lipolysis in adipocytes from the intraabdominal fat depot. Using estrogen receptor subtype-specific ligands, we found that this effect of estrogen was caused through the estrogen receptor subtype alpha. These findings demonstrate that estrogen attenuates the lipolytic response through up-regulation of the number of antilipolytic alpha2A-adrenergic receptors only in sc and not in visceral fat depots. Thus, our findings offer an explanation how estrogen maintains the typical female sc fat distribution because estrogen seems to inhibit lipolysis only in sc depots and thereby shifts the assimilation of fat from intraabdominal depots to sc depots.
For those unaware, the alpha2A receptor causes retention of stubborn fat. By reducing estrogen with Erase, we reduce the number of alpha2A receptors in the gender-specific region of stubborn fat (for us men, it's the belly). Then alphamine takes things a step further by blocking the remaining alpha2A receptors. Ever notice how the yohimbe blend in Alphamine is termed "SA2A?" Now you know why...because all along, it's been targeting the alpha2A receptor.
So the next time you notice the really strong leaning out effect of alphamine + erase, rest assured, it's not in your head...it's totally real.
- 08-18-2013, 10:13 PM
Currently using ras lemon and nolvadren-xt....so far so good
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- 08-18-2013, 10:18 PM
- 08-18-2013, 10:21 PM
I've been cutting for 3 months. Picked up helladrol and a few finaflex 1alphas
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nutra-innovations.com - 08-18-2013, 10:36 PM
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- 08-18-2013, 10:40 PM
- 08-18-2013, 11:01 PM
You don't say..
http://www.****************/product/p....html?sel=5947 - 08-18-2013, 11:14 PM
- 08-19-2013, 12:09 AM
Thanks for this coop. Awesome information.
PEScience Representativehttp://www.pescience.com/insiderInstagram: kylebayne23 - 08-19-2013, 05:39 AM
I decided to go against my usual stack and run ABE without EP so I can use it when I hop back on Alphamine.
Alphamine and EP for the lean and hard physique.PEScience Representative
http://pescience.com/insider
http://selectprotein.com - 08-19-2013, 07:18 AM
Why Alphamine and Erase DESTROY Stubborn Fat
So what about the international version without the SA2A yohimbe blend?
- 08-19-2013, 08:48 AM
- 08-20-2013, 12:50 AM
And here's why Enhanced would round out the stack:
Nitric oxide inhibits aromatase activity: mechanisms of action.
Snyder GD, Holmes RW, Bates JN, Van Voorhis BJ.
Source
Department of Obstetrics and Gynecology, University of Iowa College of Medicine, Iowa City 52242, USA. [email protected]-edu
Abstract
NO synthase is present in human ovarian granulosa-luteal cells and NO inhibits estradiol secretion by granulosa cells in culture. These findings suggest that NO is an autocrine regulator of ovarian steroidogenesis. The purpose of this investigation was to explore the mechanisms through which NO exerts an inhibitory effect on cytochrome P450 aromatase activity. To examine the effect of NO on aromatase mRNA levels, human granulosa-luteal cells were cultured in the presence or absence of the NO donor SNAP for 16 h. Using a probe for human aromatase, Northern blots revealed a 26% decrease in aromatase mRNA in cells exposed to SNAP. Because this modest decrease in mRNA is unlikely to explain a rapid and profound reduction in estradiol secretion that we have observed, we looked for direct effects of NO on cytochrome P450 aromatase activity. Aromatase activity was assayed in placental microsomes and granulosa-luteal cells by measuring the release of 3H2O from [1 beta-3H] androstenedione. NO (10(-4)-10(-3)M), added as a saturated saline solution, reduced aromatase activity by as much as 90% in a concentration-dependent, non-competitive manner. In contrast, carbon monoxide (CO), a gas known to bind to the heme iron in aromatase, had no effect on aromatase activity when added alone nor could CO reverse the NO-induced inhibition of aromatase. These data suggest that NO binding to the heme is insufficient to inhibit aromatase activity. NO has been reported to alter protein function by reacting with the sulfhydryl group of cysteines, forming a nitrosothiol group. Because a cysteine sulfhydryl group is thought to participate in the catalytic mechanism of all P450 enzymes, experiments were designed to test whether NO might inhibit aromatase via such a mechanism. Addition of increasing amounts of mercaptoethanol, a chemical with free sulfhydryl groups, blocked the NO-induced inhibition of aromatase in microsomes. N-Ethylmaleimide, a chemical which covalently modifies sulfhydryl groups, reduced aromatase activity in a concentration-dependent manner. We conclude that NO inhibits aromatase both by decreasing mRNA for the enzyme and by an acute, direct inhibition of enzyme activity. We hypothesize that the direct inhibition occurs as a result of the formation of a nitrosothiol on the cysteine residue adjacent to the heme in aromatase.
Enhanced + Alphamine + Erase = maximizing fat loss, testosterone production, and estrogen reduction - 08-20-2013, 12:58 AM
- 08-20-2013, 08:35 AM
Its all starting to make sense. Great info, Coop.
E-Pharm Rep... PM me with any questions or concerns - 08-20-2013, 08:56 AM
Nice to see some research showing what many have experienced. Solid read.
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- 08-20-2013, 09:29 AM
- 08-20-2013, 06:10 PM
- 08-20-2013, 06:14 PM
- 08-21-2013, 12:21 AM
- 08-21-2013, 03:56 AM
You aren't allowed to name other retailers on this forum.
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http://selectprotein.com - 08-21-2013, 02:57 PM
- 08-22-2013, 11:25 PM
- 08-25-2013, 04:41 PM
- 08-30-2013, 01:03 AM
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