CobbledPath
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I stopped taking DAA when I started having episodes of anxiety..
Because that's the most that was shown in an actual human study (and the number pimped by supp companies... if it were bigger, you'd definitely gear about it, LOL). What is the max number you have seen in a human study?
BTW, for some reason, I have ZERO thread notifications after being gone for a few days, so If anyone replied to me in any others, I'll have to go searching. Board glitch?
And what kind of variation was there in the baseline levels? Of 40% is a absolute max increase, then baselines should be all over the place. Or was the baseline numbers kind of similar so the increase is a relative one?I haven't seen anything over 40% in any study either. And as you pointed out, a 40% increase for 14 days isn't going to create a T level capable of any noticeable difference.
As far as your original question, below is a blurb from the '09 study, and then a linkIn order to verify if D-aspartate treatment could induce
unwanted side effects, each patient that had been treated
with D-aspartate underwent a full blood clinical analysis
(as previously detailed in the methods section). None of
the blood metabolites as well as the complete blood and
platelets count was outside the physiological range. The
only variation was observed in the LH and testosterone
concentrations that were found to be increased between
1.3 - 1.6 fold compared to their basal levels in the D-
aspartate group. However, the increased levels of LH and
testosterone observed in this study were in agreement
with the previously reported results [18] (The 2009 Study - T.O.G.)
Found here: rbej.com/content/7/1/120 <--- That's the 2009 Italian "42%" study.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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