I have used daa both ways as part of pct and on its own. The bulk powder is very cheap. As part of pct it gets the test production going good. Before a hot date I use 1 scoop is a glass of grape juice to get test up. At 55 I need all the help I can get
Im using DAA now with my pct. Been on it for 3 weeks and its great stuff. My strength is still increasing and I actually gain 2 lbs. Now keep in mind im also taking erase and anabeta so im sute these helped As well. I would recommend it.
I need more ifo about daa,anybody can give me?thanks.
Per Patrick Arnold:
When d-aspartic acid (DAA) is ingested it is absorbed into the body and taken up preferentially by endocrine tissues such as the hypothalamus, pituitary, and testicles. There it stimulates the activity of what are known as NMDA receptors. NMDA receptors are located on neurons and they regulate neuronal activity. DAA binds to a specific docking site (receptor) located on the NMDA receptor known as NMDA binding site.
In the hypothalamus the stimulation of NMDA receptors leads to the production of gonadotropin releasing hormone (GnRH). GnRH then stimulates the pituitary gland to release luteinizing hormone (LH) and follicle stimulating hormone (FSH). LH and FSH then in turn travel to the testicles to initiate the process of steroidogenesis, which leads eventually to the release of testosterone into the blood stream. Stimulation of NMDA receptors in the hypothalamus also leads to the release of growth hormone releasing hormone (GHRH) which in turn promotes the release of growth hormone from the pituitary gland.
So the key here is the NMDA receptor. The more you activate this receptor in the hypothalamus the greater the release of GnRH and GHRH, and ultimately testosterone and growth hormone.
The NMDA receptor is somewhat unique in that it requires activaton by two ligands (a ligand is like a “key” to a receptor). In the hypothalamus the main ligand for the NMDA receptor is d-aspartic acid. The secondary ligand (or co-activator) is the amino acid glycine. Both DAA and glycine have specific binding sites on the NMDA receptor. These sites are known as the NMDA binding site and the glycine binding site respectively. Think of it this way - just like how firing a nuclear missile requires two soldiers to turn two separate keys, so the NMDA receptor requires binding by two ligands to initiate its influence on the firing of a neuronal signal.
So to review, administration of DAA leads to it’s uptake into the hypothalamus and binding to the NMDA receptors there. And to activate the NMDA receptor you also require adequate levels of ligands that bind to the glycine site of the NMDA receptor. Now common sense would lead one to assume that by ingesting supplemental amounts of glycine would ensure that glycine site co-activation is ensured. However the scientific literature has shown that this method has limited efficacy.
The reason that glycine administration is not very effective at stimulating NMDA activity is not completely straight forward, but one reason is because it is efficiently removed from the synapses by the reuptake regulator Glycine Transporter 1 (GT1).
Interestingly, much of the science published on the subject of stimulaton of NMDA receptor activity revolves around the theory that NMDA receptor hypo-activity is a causative factor in schizophrenia. For years scientists have been investigating ways to stimulate NMDA activity as a means for treating schizophrenic patients. One of the most effective strategies has been through targeting the GT1 protein. And one of the most efficient means to do this is actually through supplementation with sarcosine.
Of course we aren’t concerned about treating schizophrenia here, what we are concerned with is maximally stimulating natural production of testosterone (or growth hormone) But the mechanism in question is exactly the same for both purposes. By blocking the re-uptake of glycine you increase the concentration of glycine in neuronal synapses, and therefore increase the influence of NMDA upon nerve transmission. In essence this is the exact way some anti-depressants (such as SSRIs) work, except the goal there is to increase binding and activating of serotonin or dopamine receptors, not NMDA receptors.
Blocking glycine reuptake is not the only mechanism through which sarcosine stimulates DAA activity. Sarcosine actually can itself bind to the glycine binding site of NMDA receptors. In fact, it binds with a higher affinity than even glycine. So basically it replaces glycine as well as serves as its own reuptake inhibitor. It totally solves the glycine co-activation issue in one shot.
Knowing all these facts you can see why sarcosine produces a rather dramatic effect on NMDA neuronal transmission compared to glycine itself, or other endogenous ligands for the glycine receptor such as d-serine.
To summarize, for d-aspartic acid to work to its maximum potential it must be taken with an efficient stimulator of the glycine binding site on the NMDA receptor. The most efficient non-drug stimulator we know of is the natural amino acid sarcosine.