I noticed that sarcosine is being included in some natural testosterone elevator products most notably E-Pharm Testforce 2. For instance on the following page at http://www.primordial-muscle.com/E-Pharm-Testforce-2_p_36.html?gdftrk=gdfV29243_a_7c2906_a_7c9157_a_7c733428007022, it mentions schizophrenia on why sarcosine is included in the product. It states:
Let me start with some background. 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 activation
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
stimulation 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