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The role and molecular mechanism of D-aspartic acid in the release and synthesis of LH and testosterone in humans and rats, Enza Topo, Reproductive Biology and Endocrinology 2009, 7:120
Dose:
"Every morning at breakfast for 12 consecutive days subjects in the first group were invited to consume, by mouth a solution of 10 ml of 2.0 M sodium D-aspartate (3.12 g/10 ml) supplemented with vitamin B6, folic acid and vitamin B12 and diluted in half a glass of water or fruit juice. This solution is marketed in Italy under the name DADAVIT"
Result:
Concerning the LH pattern, the results demonstrated that after 12 days of D-Asp treatment, 20 out of 23 (87%) participants had significantly increased concentrations of LH in their blood with respect to basal values (the value of LH found in the same subjects before starting treatment). Statistical analysis demonstrated that the value (mean ± SEM) of serum calculated for all the 23 subjects treated with D-Asp increased by 33.3%. From a basal-level mean of 4.2 ± 0.5 mIU/ml, LH rose to a mean value of 5.6 ± 0.9 mIU/ml (Table 1). The increase was statistically significant (ANOVA with repeated measures: [F(2,82) = 24.279, p < 0.0001]). LH concentration determined in the placebo group after D-Asp treatment compared with the level before treatment had not increased [ANOVA: F(1,82) = 0.643, p > 0.427]), thus indicating that the increase of LH due to D-aspartate treatment was authentic. The effect of D-aspartate on LH increase was time dependent. When subjects drank sodium D-aspartate for 6 days, LH increased only 1.07-fold, and this value was not statistically significant (Table 1). However, when the treatment of D-Asp was continued for 12 consecutive days, the LH concentration in the serum increased significantly (benefit effects). In order to know how long LH remained increased in the blood after the suspension of the treatment, we measured the concentration of LH in the serum 3 days after the D-Asp treatment or the placebo treatment was suspended. The results indicated that 3 days after suspension of D-Asp treatment, LH was still found at a 1.14-fold increased levels compared with the respect of basal level, but not statistically significant (Table 1).
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). Fisher's post-hoc analysis also revealed a significant difference in the testosterone concentration in the serum 3 days after the end of the treatment (p < 0.01) (Table 1). One plausible explanation of this phenomenon is that since in rats ingested D-Asp remains accumulated in the testes in significant amounts until 3 days after the suspension of D-Asp treatment (see below), if it is assumed that in humans D-Asp also remains significantly increased in the testes 3 days after the suspension of D-Asp treatment, we can deduce that in humans as in rats, D-Asp had remained accumulated in significant amounts in the testes and consequently it continued to stimulate testosterone release.
Dose:
"Every morning at breakfast for 12 consecutive days subjects in the first group were invited to consume, by mouth a solution of 10 ml of 2.0 M sodium D-aspartate (3.12 g/10 ml) supplemented with vitamin B6, folic acid and vitamin B12 and diluted in half a glass of water or fruit juice. This solution is marketed in Italy under the name DADAVIT"
Result:
Concerning the LH pattern, the results demonstrated that after 12 days of D-Asp treatment, 20 out of 23 (87%) participants had significantly increased concentrations of LH in their blood with respect to basal values (the value of LH found in the same subjects before starting treatment). Statistical analysis demonstrated that the value (mean ± SEM) of serum calculated for all the 23 subjects treated with D-Asp increased by 33.3%. From a basal-level mean of 4.2 ± 0.5 mIU/ml, LH rose to a mean value of 5.6 ± 0.9 mIU/ml (Table 1). The increase was statistically significant (ANOVA with repeated measures: [F(2,82) = 24.279, p < 0.0001]). LH concentration determined in the placebo group after D-Asp treatment compared with the level before treatment had not increased [ANOVA: F(1,82) = 0.643, p > 0.427]), thus indicating that the increase of LH due to D-aspartate treatment was authentic. The effect of D-aspartate on LH increase was time dependent. When subjects drank sodium D-aspartate for 6 days, LH increased only 1.07-fold, and this value was not statistically significant (Table 1). However, when the treatment of D-Asp was continued for 12 consecutive days, the LH concentration in the serum increased significantly (benefit effects). In order to know how long LH remained increased in the blood after the suspension of the treatment, we measured the concentration of LH in the serum 3 days after the D-Asp treatment or the placebo treatment was suspended. The results indicated that 3 days after suspension of D-Asp treatment, LH was still found at a 1.14-fold increased levels compared with the respect of basal level, but not statistically significant (Table 1).
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). Fisher's post-hoc analysis also revealed a significant difference in the testosterone concentration in the serum 3 days after the end of the treatment (p < 0.01) (Table 1). One plausible explanation of this phenomenon is that since in rats ingested D-Asp remains accumulated in the testes in significant amounts until 3 days after the suspension of D-Asp treatment (see below), if it is assumed that in humans D-Asp also remains significantly increased in the testes 3 days after the suspension of D-Asp treatment, we can deduce that in humans as in rats, D-Asp had remained accumulated in significant amounts in the testes and consequently it continued to stimulate testosterone release.
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