DAA reduces testosterone at 3 and 6 g

[CobbledPath]

I stopped taking DAA when I started having episodes of anxiety..

 

[NeoNewfie]

From my understanding, testosterone spikes in the early morning and nadirs in the evening, varying up to a max of -- you guessed it -- 40%. Could the 40% increase noted in the DAA study be simply the result of diurnal variation rather than supplementation?

 

[NeoNewfie]

found the site where i read this originally -- not sure about rules governing references to other sites, so will cut and paste:

"The last factor that makes a direct quantitative comparison of the effects "naturally" and "artificially" elevated testosterone levels questionable, to say the least, is the absence of the natural diurnal rhythm with exogenous testosterone administration. In the course of 24h the testosterone levels fluctuate by +/-40% with a spike in the morning (around 6-7am) and a trough in the early evening. Contrary to the "artificially enhanced" testosterone levels, the ones on the printout from your lab thusly represent either the daily max (if the blood was drawn early in the morning), an average (blood drawn around noon) or the nadir (blood drawn in the evening) of your 24h testosterone level.
Just as an aside: Imagine you wanted to sell a "natural test booster". What would be the best way to get a "clinically proven" rise in testosterone? Right! You just get your "study" participants tested in the evening for baseline and in the morning for post-intervention levels and *bang* you got your "clinically proven" +40% increase in testosterone ;-)"

 

[storm 011]

this study is not conclusive. and very vague

1st - the original study done in Italy for the first time, showed that the DAA increases testosterone within the first 6 days up to a maximum of 12 days with only 3.12 grams with the Sodium D-Aspartate (Na + D-Aspartate )

2nd - the DAA raises testosterone only in individuals who are deficient, in individuals who have a hormonal drop because of advanced age, or in individuals who have taken steroid / hormone precursors that are suppressive

3 ^ - the DAA has no effect on individuals with normal hormone levels, indeed in many people could lead to an imbalance hormone because of aromatase enzyme

the DAA you must run in PULS Cycles, for example: 4 days ON - 3 days OFF or at most for 5 days ON and 4 days OFF etc .... this applies to those who not have low testosterone ***

sorry for my english :lol5:

ps. the SNS Daa caps is a good one, as the old TCF-1 and the old DAA-HCG or AsparTest... IMO

 

[JudoJosh]

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?

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.

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?


BTW, they observed a 60% increase in this one -> Invalid Link Removed

So is 40% a absolute max increase or a relative one?

 

[The_Old_Guy]

I just read the full .pdf at the link you gave - the one for people with Asthenozoospermia. Correct me if I'm wrong, but that's all that study looked at as far as I can tell - sperm count and motility. They do quote the *gold standard* 2009:

The role and molecular mechanism of D-aspartic acid in the release and synthesis of LH and testosterone in humans and rats

Enza Topo, Andrea Soricelli, Antimo D'Aniello, Salvatore Ronsini and Gemma D'Aniello



...using the Notation (18) when taking about LH and T. But where is the 60% Testosterone increase you spoke of? Not saying it's not there, I just read it once. For example when they discuss testosterone and safety here:

In 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.)

As far as your original question, below is a blurb from the '09 study, and then a link

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.

Found here: rbej.com/content/7/1/120 <--- That's the 2009 Italian "42%" study.