hmmm, its funny you should mention that i actually have noticed that when i’ve gone running lately my legs have been a bit sore. i wonder if it’s connected to the d-aspartic acid.
any update regarding a reply back from PP regarding brain damage co-relation??
No response…I’m gonna press the issue.
hmm… dam! i was gona get 1 and get another free… but now the offer is gna finish!! 
I got two more bottles at buy one get one free because they were cheap enough. If I can’t get good answers I just wont use the stuff. We now have a bunch of people over at the PP site wondering and asking about the studies I posted over there. Hopefully we get an answer soon.
This isn’t a response from the person we are waiting on, but some other dude who decided to throw his two cents in. Figured I’d post it.
don’t have the answers you are looking for, but I want to point out a few things.
Wikipedia is a wiki, which means that I can create an account and edit the pages above to read “aspartate tastes like chicken”. The point is that one can easily disseminate misinformation via Wikipedia. At least source the studies cited on wikipedia before drawing conclusions. Wikipedia often has useful information, but it often has conflicting, misleading, and misinterpreted information on it as well (as well as information without references). Thus, Wikipedia isn’t a reliable source and isn’t a “study”.
Quote:
it says directly on Wikipedia that the conjugate base of this substance can cause nerve damage…
Here is what I see directly stated on “Wiki” on the excitoxicity page which you mentioned. Aspartate is mentioned twice, both times in the context of traumatic brain injury. The NMDA link you provided doesn’t mention aspartate:
Quote:
Brain trauma or stroke can cause ischemia, in which blood flow is reduced to inadequate levels. Ischemia is followed by accumulation of glutamate and aspartate in the extracellular fluid, causing cell death, which is aggravated by lack of oxygen and glucose…
Inadequate ATP production resulting from brain trauma can eliminate electrochemical gradients of certain ions. Glutamate transporters require the maintenance of these ion gradients to remove glutamate from the extracellular space. The loss of ion gradients results not only in the halting of glutamate uptake, but also in the reversal of the transporters, causing them to release glutamate and aspartate into the extracellular space. This results in a buildup of glutamate and further damaging activation of glutamate receptors.[11]
I tried to source study [11] above, and the “item was not found”.
What Wiki has to say about Aspartic Acid and Aspartate:
Aspartic acid - Wikipedia, the free encyclopedia
Quote:
Aspartate (the conjugate base of aspartic acid) stimulates NMDA receptors, though not as strongly as the amino acid neurotransmitter glutamate does.[5] It serves as an excitatory neurotransmitter in the brain and is an excitotoxin.
And what does study [5] cited by Wikipedia say?
Structural Features of the Glutamate Binding Site in Recombinant NR1/NR2A N-Methyl-d-aspartate Receptors Determined by Site-Directed Mutagenesis and Molecular Modeling ? Molecular Pharmacology
Quote:
We investigated the effects of mutations in the S1 and S2 regions on the potencies of the agonists l-glutamate, l-aspartate, (R,S)-tetrazol-5yl-glycine, and NMDA.
Aspartate can refer to D-AA, L-AA, or D,L-AA. In this case, it refers to L-AA which is not present in TCF-1.
Now, some interesting studies about D-aspartate:
D-aspartate exerts an opposing role upon age-dependent NMDAR-related synaptic plasticity and memory decay : Nature Precedings
Quote:
In the present study, we demonstrated that D-aspartate acts as an in vitro and in vivo neuromodulatory molecule upon hippocampal NMDAR transmission. Accordingly, we showed that this D-amino acid, widely expressed during embryonic phase, was able to strongly influence hippocampus-related functions at adulthood. Thus, while up-regulated levels of D-aspartate increased LTP and spatial memory in four-month old adult mice, the prolonged deregulation of this molecule in thirteen-month old animals induced a substantial acceleration of age-dependent decay of synaptic plasticity and cognitive functions. Moreover, we highlighted a role for D-aspartate in enhancing NMDAR-dependent synaptic plasticity through an inducible “turn-on/turn-off-like mechanism”. Strikingly, we also showed that D-aspartate, when administered to aged mice, strongly rescued their physiological synaptic decay and attenuated their cognitive deterioration. In conclusion, our data suggest a tantalizing hypothesis for which this in-embryo-occurring D-amino acid, might disclose plasticity windows in the aging brain.
Aspartate racemase, generating neuronal D-aspartate, regulates adult neurogenesis ? PNAS
Quote:
D-Aspartic acid is abundant in the developing brain. We have identified and cloned mammalian aspartate racemase (DR), which converts L-aspartate to D-aspartate and colocalizes with D-aspartate in the brain and neuroendocrine tissues. Depletion of DR by retrovirus-mediated expression of short-hairpin RNA in newborn neurons of the adult hippocampus elicits profound defects in the dendritic development and survival of newborn neurons and survival. Because D-aspartate is a potential endogenous ligand for NMDA receptors, the loss of which elicits a phenotype resembling DR depletion, D-aspartate may function as a modulator of adult neurogenesis.
I’m not Eric, and I probably haven’t answered your questions, but I encourage you to dig a little bit deeper than wikipedia before jumping to conclusions.
3PM:
This is what the owner asked:
Where specifically are you seeing the bit about nerve damage from actual NMDA? On the link you posted Im seeing;
“activation of synaptic NMDA receptors only activated the CREB pathway, which activates BDNF (brain-derived neurotrophic factor), not activating apoptosis.”
and further stating in the other link;
“in lower quantities NMDA is not neurotoxic”
Besides, injecting high amounts of anything into the brain is going to have toxic effects. Injecting acetyl-choline into the brain will probably cause toxic effects too, but that doesn’t mean we shouldn’t take efforts to increase endogenous production of it within a reasonable physiological means.
-Eric
en.wikipedia.org/wiki/Aspartic_acid
en.wikipedia.org/wiki/Excitotoxin
I’m just saying be careful what you consume. I’m not about to get into a chemistry war with someone defending their product.
My left eye kept twitching the other day. That used to happen to me when I chewed certain gums that had Aspartame in it. I’m sure that’s not a good a thing.
That happens to me every once in awhile regardless of what I take…
I get that too, though I’m not convinced propecia has any link to it to be honest, if anything it points to a magnesium deficiency.
So no one knows if this stuff is safe or not? I have a bottle of it, but I am afraid to use it because popping pills is how I got myself into this mess in the first place.
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I’m now on my second day on DAA. Started yesterday with a dose of 2.6 g. Definitely felt when it kicked in, earlier I felt depressed and burned out like even existing was a hard work, then suddenly feeling of joy and excitement. Later I noticed that my balls hurt.
Today, took 3.0 g in the morning and have been quite energetic and positive today, but that aching feeling have stayed with me the whole day. It’s quite disturbing.
edit: Day 4: Dropped my dosage to about 2.0 g’s two days ago, and no hurting genitals anymore. I’m going to titrate upwards to the maximum dose that doesn’t have side effects. But even with this dosage I feel really good. This is great stuff.
edit2: The ballpain seemed to be only temporary side effect, 3,0g didn’t do that later on. DAA seemed to make be a bit easily irritated though.
Is anyone using this?
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bump
bump
has anyone tried d-aspartic acid, i was reading about it and sounds pretty safe for raising t levels by 40 percent
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Has anyone else tried this lately?
How about the guys who were trying it back then at the beginning of the thread? Would you mind giving us an update on long term improvements and letting us know how sustainable those were once you stop taking it?
Thanks!
Tried to use it about 2-3 years ago. It just gave me gyno. Pretty much any substance that is supposed to raise testosterone levels converts straight to estrogens in me, even when I use high doses of AIs.
Thanks for the update moonman1.
My hormone levels have always been ‘within range’ but my most persistent symptoms are low libido and mild ED along with high billirubin.
I seem to be having some luck in raising my libido levels and getting it up with gym supplements which are supposed to raise Testosterone and DHT.
Test booster: Zeus
DHT: Creatine Monohydrate (Purple K)
I’ve done short cycles of it for the past month and 1/2 or so and can clearly tell the difference in libido and quality of erections when I’m off of it. The initial boost seems to be wearing off slowly over time though.
No Gyno so far, so I guess excess E is not one of my main issues. I think I will give D-aspartic acid a try once I’m off of Zeus/Purple-K.
On a side note: Purple K seems to increase my hair loss quite a bit and there has been some reports of bad reactions to creatine on this forum so it is probably not for everyone.