Thanks Big D,
What do you think about- D Aspartic-acid? -DAA
Testosterone being converted to 17ß Estradiol
In animal studies (boar, lizard), D-Aspartic Acid was shown to increase gonadal (testes, ovary) aromatase activity which is an enzyme responsible for the conversion of testosterone to 17ß Estradiol (an estrogen).
Whether this aromatase activity is increased in humans is uncertain. However, in Western obesogenic societies where abdominal fat is a major concern in countless millions of individuals, we know this deep visceral fat is very active tissue and we also know this active fatty tissue has significant aromatase activity.
Increased testosterone levels induced in overweight individuals by D-Aspartic Acid, will indeed drive the conversion of testosterone to estrogen in this abdominal fat store thus increasing 17ß Estradiol.
http://www.nutridesk.com.au/d_aspartic_acid_daa_testosterone-21.phtml
http://www.biology.arizona.edu/biochemistry/problem_sets/aa/aspartate.html
Concerning the effect of D-Asp on the induction of testosterone release, after 12 days of D-Asp treatment, the levels of testosterone in the serum of the participants were significantly increased compared with basal levels. Out of 23 participants, 20 had increased testosterone. From a mean of 4.5 ± 0.6 ng/ml serum at zero time, it rose to 6.4 ± 0.8 ng/ml, a 42% increase (Table 1). Statistical analyses indicated a significant effect [ANOVA with repeated measures: treatment effect: F(1,82) = 7.724, p < 0.0082] and a significant interaction between treatment and days [F(2,82) = 32.599; P < 0.0001]. As with LH, so also with testosterone, the effect of D-aspartate was time dependent. When subjects were treated with sodium-D-aspartate for only 6 days, testosterone was found of 1.15-fold higher than basal levels, but this increase was not statistically significant (Table 1). Interestingly 3 days after the suspension of D-Asp treatment, testosterone was still increased 1.22-fold compared with the basal levels (5.8 ± 0.6 ng/ml against 4.5 ± 0.6 ng/ml).
What do you think about- D Aspartic-acid? -DAA
Testosterone being converted to 17ß Estradiol
In animal studies (boar, lizard), D-Aspartic Acid was shown to increase gonadal (testes, ovary) aromatase activity which is an enzyme responsible for the conversion of testosterone to 17ß Estradiol (an estrogen).
Whether this aromatase activity is increased in humans is uncertain. However, in Western obesogenic societies where abdominal fat is a major concern in countless millions of individuals, we know this deep visceral fat is very active tissue and we also know this active fatty tissue has significant aromatase activity.
Increased testosterone levels induced in overweight individuals by D-Aspartic Acid, will indeed drive the conversion of testosterone to estrogen in this abdominal fat store thus increasing 17ß Estradiol.
http://www.nutridesk.com.au/d_aspartic_acid_daa_testosterone-21.phtml
http://www.biology.arizona.edu/biochemistry/problem_sets/aa/aspartate.html
Concerning the effect of D-Asp on the induction of testosterone release, after 12 days of D-Asp treatment, the levels of testosterone in the serum of the participants were significantly increased compared with basal levels. Out of 23 participants, 20 had increased testosterone. From a mean of 4.5 ± 0.6 ng/ml serum at zero time, it rose to 6.4 ± 0.8 ng/ml, a 42% increase (Table 1). Statistical analyses indicated a significant effect [ANOVA with repeated measures: treatment effect: F(1,82) = 7.724, p < 0.0082] and a significant interaction between treatment and days [F(2,82) = 32.599; P < 0.0001]. As with LH, so also with testosterone, the effect of D-aspartate was time dependent. When subjects were treated with sodium-D-aspartate for only 6 days, testosterone was found of 1.15-fold higher than basal levels, but this increase was not statistically significant (Table 1). Interestingly 3 days after the suspension of D-Asp treatment, testosterone was still increased 1.22-fold compared with the basal levels (5.8 ± 0.6 ng/ml against 4.5 ± 0.6 ng/ml).