mr.cooper69
Legend
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:
[h=1]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.[/h]Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed.
[h=3]Source[/h]Department of Endocrinology and Metabolism, Aarhus Amtssygehus, Aarhus University Hospital, Denmark. [email protected]
[h=3]Abstract[/h]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.
There's more to this story than just anecdote though. The science actually supports the combination for stubborn fat loss:
[h=1]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.[/h]Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed.
[h=3]Source[/h]Department of Endocrinology and Metabolism, Aarhus Amtssygehus, Aarhus University Hospital, Denmark. [email protected]
[h=3]Abstract[/h]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.
