D Aspartic Acid & Negative side effects
- 03-11-2011, 01:07 PM
Thanks for answering my questions - I didn't understand all of it but I got enough of it to understand exactly what the big deal might be.
I will ease off the DAA I think - until there is more evidence on it's short and long term toxic effects. I use test boosters occasionally - but I really don't need to even though I'm 49 - my body still responds to training pretty well.
Which kind of "segways" into another discussion - and that is this crazy quest (by many) to reach a free testosterone level of 10,000 or something like that. I think people forget - that there is a lot more to the equation than testosterone ...
Now me - I have always responded to training - even if I eat badly - I can still build lean muscle. There have been times when I had to leave the gym (for whatever reason) and I stayed away for three, four years even - and I'd get fat as pig and you'd swear my muscle was totally gone - but whenever I came back I was able to quickly regain (within months) what I lost - and lose all the fat I had gained. It amazes me ...
I don't think I am the only one like this. I think a lot of people on this board are like me.
Does this mean I have high testosterone? Well, I don't know - because I have never paid attention to the blood tests when given one. But - I don't think so - because I have to WORK HARD to get down to 13% BF or lower. I can get under 18 no problem - but going under 13 is a trick for me!
I think it means something else.
I had a friend in the Navy who was the biggest horn-dog I've ever seen. He ****ed everything that moved - and when he wasn't ****ing with it he was yanking it - guy thought about nothing but sex. He couldn't help it - and felt a bit tormented by it - so he went to a psyche and the psyche actually tested his hormone profile. He came back on the high end for everything male related - which explained a lot concerning his sex drive.
And he was a lean mother ****er too - not an ounce of fat on him. However - when we'd drag him into the gym to get his mind off shagging - he'd work like hell, eat like hell - and not gain an ounce of muscle.
And I think - my dumb theory - is that the guy just didn't have it on the other end - the part where your muscles actually RESPOND to the presence of hormones and training and nutrition.
I think many guys have "so-so" test levels - but their muscles just respond disproportionally to the presence of test and training - and they get big because of that.
So I don't think testosterone is the "be all / end all".
Then again - I'm pretty stupid and prolly should go lift something right now before I start thinking I'm smart.
- 03-11-2011, 01:15 PM
- 03-11-2011, 01:36 PM
03-11-2011, 02:03 PM
03-11-2011, 02:19 PM
I would go give my input there but don't have time or attention for multiple forums.. There are some obvious problems with their input, as well as, the aspartame studies quoted..
1. Aspartame is %40 L-DAA, given a 165lb person at 75mg/kg that is still only 2/3 of the dose of DAA that people are taking.
2. Aspartame requires metabolism which is a rate limiting step for DAA production. This means that taking equal amounts of DAA and % wise of Aspartame are going to cause far different blood concentrations of DAA. Aspartame will not reach the same blood plasma level that straight DAA does even if you take the equivilant same amount
3. DAA is an NMDA agonist itself
4. Because of the higher blood concentrations of DAA, more is free to convert to NMDA at any given time. Addionally, given the secretion rate of DAA it is possible that you would never reach the blood acumulation level of DAA with Aspartame that you would with DAA supplementation
Comparing Aspartame to DAA is like comparing L-lysine-D-amphetamine to D-amphetamine. It is far easier to reach nerotoxicity with an equivilant dose of D-amphet than with L-lysine-D-amphetamine
03-11-2011, 02:34 PM
03-11-2011, 04:10 PM
Thanks everyone for the input!
03-11-2011, 06:09 PM
I'm kind of surprised that no one has mentioned the protective effects that have been seen when pairing DHEA supplementation with that of NMDA agonists:
The experiments reported here show that the neurosteroid DHEA has powerful ameliorating effects on excitatory amino acid-induced neurotoxicity. This conclusion is strengthened by this effect being demonstrated both in vitro and in vivo for NMDA.Dehydroepiandrosterone (DHEA) and DHEA-sulfate (DHEAS) protect hippocampal neurons against excitatory amino acid-induced neurotoxicityDHEA, together with DHEAS, is the most abundant steroid in the blood of young adult humans. Levels in humans decline with age and during certain types of illness or stress. We have found that DHEA(S) can prevent or reduce the neurotoxic actions in the hippocampus of the glutamate agonists N-methyl-D-aspartic acid (NMDA) both in vitro and in vivo or a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainic acid in vitro.
Pre-treatment with DHEA (10–100 nM for 6–8 h) protected primary hippocampal cultures from embryonic day 18 (E18) embryos against NMDA-induced toxicity (0.1, 1, 10, and 50 mM). DHEA added either with NMDA (1 mM) or 1 h later had lesser, but still significant, protective actions. DHEAS also reduced NMDA-induced toxicity (1 mM), although the lowest effective dose of DHEAS (100 nM) was higher than that of DHEA (10 nM).
DHEA (100 nM) protected cultured neurons against the neurotoxic actions of either AMPA (25 mM) or kainic acid (1 mM) as well. In vivo, s.c. pellets of DHEA, which resulted in plasma levels that resembled those in young adult humans, protected hippocampal CA1y2 neurons against unilateral infusions of 5 or 10 nmol of NMDA.
Because the release of glutamate has been implicated in the neural damage after cerebral ischemia and other neural insults, these results suggest that decreased DHEA levels may contribute significantly to the increased vulnerability of the aging or stressed human brain to such damage.
V. G. Kimonides, N. H. Khatibi, C. N. Svendsen, M. V. Sofroniew, and J. Herbert
PNAS, Feb 1998; 95: 1852 - 1857.
Maybe taking Erase or another DHEA product a couple of hours before taking your dose of DAA is a good idea, if you're going to take it. Just another thing to consider.
03-11-2011, 06:38 PM
There is also no evidence as to the effect of anything major happening in the brain or making its way though the BBB and thus having a negative response. There is no scientific fact on this. There are some obscure studies that people are trying their best to link together. There is NO CONCLUSIVE STUDY ON THIS!
By the way NDMA is a proven excitotoxin, not DAA itself. There are no studies on this as yet so it can not be proven.
03-11-2011, 06:49 PM
03-11-2011, 06:53 PM
03-11-2011, 07:01 PM
im already a recovering addict... lol ive put plenty of holes in my brain already.... so on one hand, i could say fu*ck it, but that never seems to work out the way i plan......
if this stuff is actually potentially dangerous for my brain(or whats left of it), i think i should stop
i read ur first post in this thread when u started it... im assuming you stopped taking it?
03-11-2011, 07:05 PM
03-11-2011, 07:07 PM
03-11-2011, 07:14 PM
I can't believe this thread is still going. The only one that keeps stating that DAA is an excitotoxin (btw, learn to spell the big words if you are going to toss them around) is bubs here. I'm not sure what his definition of excitotoxicty or an agonist is, but DAA has NOT been shown to be excitotoxic at any orally ingested level and if you have a single paper...JUST ONE!!!...then show it.
Using your logic, every agonist of the NMDA receptor including glutamate should cause excitotoxicity. I wrote an entire PhD thesis on the role of nitric oxide in glutamatergic transmission as it pertains to schizophrenia. I was earlier told I was lying about being a neuroscientist and I don't wish to post my personal info on here, but if you want a copy of my thesis, PM your email and I will gladly send it. That isn't to say everything I say is fact, but I would think I have a better grasp on this topic than somebody who just copies and pastes from wikipedia.
DAA has not been show to be excitotoxic. Doesn't mean it isn't, but it has not been shown to be even though this person keeps saying it does.
My challenge still stands. Got a paper? Show it! Really not that complicated.
03-11-2011, 07:20 PM
03-11-2011, 07:21 PM
Alek, I'm just trying to play safe. I don't think at any time I was rude or unprofessional with you so I don't think you're talking about me, lol. I do know, i don't know how to spell half the sh!t we're talking about let alone even know what any of it means. Which is the reason I have stopped supplementing with DAA.
PM is on it's way. Even tho the chance of me comprehending it is close to none...
03-11-2011, 07:22 PM
03-11-2011, 07:27 PM
03-11-2011, 07:33 PM
03-11-2011, 09:00 PM
And I probably could, but the wife being a federal prosecutor would not appreciate it lol.
03-11-2011, 09:06 PM
03-15-2011, 06:48 AM
03-15-2011, 08:44 AM
03-15-2011, 09:34 AM
I am using it as a bridge between a Osta-sarm cycle and a S4 cycle. I like it. No negative sides yet for me.
03-15-2011, 09:36 AM
this is something that does the opposite, and after discontinuation i would expect levels to simply return to normal. just like with SERMs and AIs which also work via upregulation of the HPTa
03-15-2011, 09:43 AM
the term excititoxin is really a misnomer. It assumes that all agonists of the NMDA receptor are neurotoxic no matter what the concentration. That obvoiusly is not true
Lack of NMDA agonists would surely **** your brain up as you can well imagine. Too much can be kill neurons. The question here is are we reaching the level of d-aspartic acid in the brain that is dangerous. There is no evidence that we are
03-15-2011, 09:57 AM
03-15-2011, 10:03 AM
second of all, he is not a chemist. neuroscientists cant synthesize jack squat in the lab, that is not what they do. that is more up my alley
03-15-2011, 10:08 AM
dont expect anyone to do a study to see what DAA usage does to someone after 50 years. and if someone does this study I will be dead by the time the results are in anyway.
03-15-2011, 10:10 AM
03-15-2011, 10:19 AM
03-15-2011, 10:25 AM
Amino Acids. 2010 May;38(5):1561-9. Epub 2009 Nov 5.
Evidence for the involvement of D-aspartic acid in learning and memory of rat.
Topo E, Soricelli A, Di Maio A, D'Aniello E, Di Fiore MM, D'Aniello A.
Laboratory of Animal Physiology and Evolution, Stazione Zoologica Anton Dohrn, Villa Comunale, 80121, Naples, Italy. firstname.lastname@example.org
D-Aspartic acid (D-Asp) is an endogenous amino acid present in neuroendocrine systems. Here, we report evidence that D-Asp in the rat is involved in learning and memory processes. Oral administration of sodium D-aspartate (40 mM) for 12-16 days improved the rats' cognitive capability to find a hidden platform in the Morris water maze system. Two sessions per day for three consecutive days were performed in two groups of 12 rats. One group was treated with Na-D-aspartate and the other with control. A significant increase in the cognitive effect was observed in the treated group compared to controls (two-way ANOVA with repeated measurements: F ((2, 105)) = 57.29; P value < 0.001). Five further sessions of repeated training, involving a change in platform location, also displayed a significant treatment effect [F ((2, 84)) = 27.62; P value < 0.001]. In the hippocampus of treated rats, D-Asp increased by about 2.7-fold compared to controls (82.5 +/- 10.0 vs. the 30.6 +/- 5.4 ng/g tissue; P < 0.0001). Moreover, 20 randomly selected rats possessing relatively high endogenous concentrations of D-Asp in the hippocampus were much faster in reaching the hidden platform, an event suggesting that their enhanced cognitive capability was functionally related to the high levels of D-Asp. The correlation coefficient calculated in the 20 rats was R = -0.916 with a df of 18; P < 0.001. In conclusion, this study provides corroborating evidence that D-aspartic acid plays an important role in the modulation of learning and memory.
03-15-2011, 10:26 AM
03-15-2011, 10:29 AM
i used it for about 6 months straight then cycled off because i started taking something else that in conjunction with the daa caused stomach upset. now i am back taking the daa. glad you reminded me cuz i forgot to mix my morning dose (must be those dead neurons, eh?)
03-15-2011, 10:37 AM
03-15-2011, 10:38 AM
Could someone please correct me if I am wrong. I glossed over some posts in this thread as the banter was getting a little boring. Despite that I did find the term "E-resume" funny. I will summarise when I think has been concluded in this thread.
- It seems the arguments in this thread have been down to the definitions. NMDA agonist and excitotoxin have been used interchangeably when they definitely aren't.
- How much DAA would it take to go from something that stimulates the NMDA receptor to something that is toxic? Nobody knows.
- Some people prefer not to take a known NMDA receptor agonist in fears of excitoxicity and side effects i.e., guilty until proven innocent.
- Some don't mind taking it until something proves it is unsafe at x dosage per day i.e., innocent until proven guilty.
Conclusion, nobody is going to know until more studies are completed. Even if studies were completed they would have to be long term to assess damage on the brain unless the damage showed up a lot sooner than anticipated.
So, it is simple. User discretion with this type of compound.
03-15-2011, 11:22 AM
03-15-2011, 07:49 PM
03-15-2011, 09:03 PM
Studies haven't been shown that daa causes excitotoxicity, but yes, studies have also not shown that it doesn't. Because of that I don't think it is right to keep calling it an excitotoxin. One can easily make the argument that increased protein, and therefore amino acid, consumption could increase neurotransmitter synthesis which should cause increased excitotoxicity. And with no studies proving that wrong, I think we should all stop taking protein
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