Destroy harmful blood fat that blocks up male blood flow
This washes the penile chambers clean from blood fat
Blood fat irritates the linings of the penile chambers in the male member:
These linings are called endothelium.
And there are at least 1,000 studies showing how blood fat causes what scientists call “endothelial dysfunction.”
The linings of the arteries and the linings in the penile chambers become swollen, inflamed, and angry when they are exposed to blood fat.
Then plaque begins to build up in the arteries, the arteries that you need to be nice and clear if you want to get good “rockiness” again…
Some of these arteries feeding blood to the male member are barely the width of a human hair.
So it doesn’t take much blood fat to clog up the arteries that you need down in the penile chambers.
Many men feel they are getting less and less blood flow down there as they get older…and it’s not their imagination!
Blood fat is reducing blood flow to the penile chambers and that’s why many men can’t get great erections anymore.
And it gets even worse…
… because the linings of the penile chambers and the linings of the arteries and organs are all made of this endothelium.
So it’s not only the male member that doesn’t get good blood flow, it’s also other crucial organs like the liver and the heart.
Luckily, you can stop this dangerous blood fat from spreading and make it commit mass suicide!
And that will not only clear the penile chambers, but it will also result in loss of flab…
L-Serine: a new nootropic that is safe and increases thinking and memory
The idea that individual amino acids can influence the brain is certainly not new.
Up to this point in time, however, the influence of amino acids on psychology has focused primarily on aromatic amino acids.
Tryptophan as the direct precursor for serotonin, L‑histidine for histamine, and L‑tyrosine for dopamine.
But serine hasn’t received much attention until only recently.
Although D‑serine was known to be a coagonist for the NMDA receptor as far back as 1988 (Kleckner, 1988), it wasn’t until four years later that it was found to be a natural metabolite (Hashimoto, 1992).
Since D‑amino acids weren’t thought to have a biological role at the time, the activity of D‑serine on the NMDA receptor was seen as unphysiological and something of interest only to chemical treatment designers.
‘Binding of the coagonist is an obligatory requirement for NMDA receptor/ channel activity, as the channel does not operate without it.’ ―Wolosker, 2007
Yet it is now known that D‑serine is naturally found in the brain in one‑third the concentration of L‑serine, and after being shown necessary for NMDA activity in the hippocampus it’d gradually become known as an important neuromodulator.
This is very important because NMDA receptors are known to control spatial learning and memory formation. This is the receptor type activated by piracetam, the original ‘nootropic treatment’ (Giurgea, 1972).
The NMDA receptor shapes hippocampal plasticity by mediating the influx of Ca2+, its second messenger that goes on to quickly disassemble and remodel the actin and microtubule cytoskeletons.
Microtubules are found inside every nerve surrounded by myelin running lengthwise, and are what mediate nerve impulses throughout the body.
Unmyelinated microtubules are also found inside every cell where they also occupy a structural role.
‘Ca2+ entry during NMDA receptor stimulation can trigger intracellular second messenger pathways leading to persistent changes of excitatory postsynaptic current […]’ ―Panatier, 2006
The structural remodeling mediated by NMDA receptors leads to neurite outgrowth (Pearce, 1987).
In this manner, agonists and co‑agonists such as piracetam and D‑serine could help form new brain connections.
And the theoretical expectations have played out — enough experimental evidence has accumulated on D‑serine since 1988 to conclude that it DOES have piracetam-like effects on cognition.
This is fortunate because its precursor is L‑serine: a humble, nonessential, straight‑chain, and safe amino acid available over‑the‑counter.
‘These results indicate that endogenous glutamate, possibly released by granule cells themselves, stimulated neurite outgrowth through activation of the NMDA class of glutamate receptors.’ ―Pearce, 1987
And besides being a precursor for the D‑isomer, it is also a significant precursor of acetylcholine via the Bremer Pathway.
- Serine is first incorporated into phosphatidylserine…
- Decarboxylated into phosphatidylethanolamine…
- Methylated three times into phosphatidylcholine…
- Hydrolyzed into free choline…
- And finally acetylated by choline acetyltransferase into acetylcholine.
And moreover, serine is the primary source of methyl groups in the brain.
The enzyme serine hydroxymethyltransferase transforms L‑serine into glycine, capturing its β‑carbon as a folate‑bound methyl group in the process.
So serine is one thing you can take, and quite safely, that will potentiate both cholinergic and glutamatergic systems at once. These are both central to cognition.
This may sound like a tall order for an “nonessential amino acid,” yet there is direct evidence of this occurring in humans:
This study had been conducted on healthy normal volunteers free of any current or prior psychological issues.
They had been given 2.1 grams of D‑serine or placebo followed by a battery of cognitive tests.
The specific tests were chosen on account of being affected by ketamine, the classic NMDA antagonist along with PCP.
You’d expect that if D‑serine were to have an effect, it would probably show up on tests known to be affected by NMDA receptor function.
And they were affected.
The test group demonstrated an improvement in multiple cognitive tests scores over placebo, which also increased some due to repetition.
This was a double‑blind trial using standardized tests so this data should reflect a real change.
Moreover, it was a crossover design, so every person eventually participated in both D‑serine and placebo groups.
Scores increased more than placebo in the Continuous Performance Test and the Rey Auditory Verbal Learning Test.
These parameters, improved by D‑serine, are classically associated with NMDA receptor activation and enhanced hippocampal plasticity.
Test scores in the D‑serine group also improved in the Category Fluency Test, the Digits Forward Task, and the Benton Visual Retention Test.
Since studies using NMDA receptor knockout mice show a general deficit in spatial memory (Tsien, 1996), any test dependent on integrating visual input should be improved by NMDA agents.
Although D‑serine is not as readily available as L‑serine, this is okay because the latter will readily become the former.
Humans express an enzyme called serine racemase.
This is a bidirectional enzyme that converts L‑serine into D‑serine, and vice versa, and is known to be expressed in the brain, liver, kidney, heart and skeletal muscle (Xia, 2004).
In the brain it is found highest in the hippocampus and corpus callosum (De Miranda, 2000), coincidentally two areas also dense in NMDA receptors.
‘In the four neurons tested, D-serine increased NMDA responses by 230.2% […]’ ―Panatier, 2006
The close proximity of this enzyme to NMDA receptors has not been overlooked.
This was an important finding leading to D‑serine, but not glycine, being recognized as the primary coagonist of this receptor.
Concentrations of D‑serine in the brain closely parallel NMDA receptors while those of glycine are increased in the brainstem (Schell, 1997).
Also giving D‑serine priority over glycine is its potency.
It has been shown that D‑serine binds the NMDA receptor about 3‑fold more strongly than glycine by some researchers (Matsui, 1995), and ~6‑fold more strongly by others (Furukawa, 2003).
Experiments using D‑amino acid oxidase have conclusively shown that D‑serine is the primary endogenous modulator of the NMDA receptor in certain brain regions (Panatier, 2006).
This is our natural piracetam‑like neuromodulator. Although glutamate is needed along with D‑serine to activate the NMDA receptor it’s nonspecific and also acts on a few others.
Glycine also activates more than one receptor (NMDA and GlyR), yet D‑serine is only known to have one target: The NMDA receptor.
It is also only known to have only one precursor, its L‑isomer, which could be necessary considering availability.
Studies before this showed serine racemase converts L‑ to D‑serine in the brain (Dunlop, 1997), but this was one of the first to show this also occurs after systemic administration.
After injecting rats with a stiff dose of L‑serine, about one gram per kilogram body weight, they demonstrated a substantial increase in brain D‑serine in all regions analyzed:
The brain exhibits a variable expression of serine racemase and D‑amino acid oxidase, the enzymes which create and destroy it, so you’d have to expect some variation of D‑serine across regions.
Serine racemase also has pyridoxal (B6) for a cofactor, so nutrition could determine D‑serine levels in a few ways.
Serine racemase is also powerfully inhibited by nitric oxide (Mustafa, 2006), so with certain treatments an immune activation could decrease it.
‘The increase in the levels of D‑ and L‑serine in the cortex and striatum after the L‑serine injection are in good agreement with previous reports.’ ―Hashimoto, 2002
Although these rats had been given a very high dose, you wouldn’t need to take so much to get an effect.
In vitro evidence shows that only small changes in brain D‑serine affect the NMDA receptor (Panatier, 2006).
Although it’s generally assumed that the brain produces D‑serine entirely from brain L‑serine, some could actually be formed in the plasma and this could cross the blood brain barrier.
It has been shown, in rats at least, that D‑serine has a 2- to 3‑fold greater brain uptake than L‑serine (Bauer, 2005).
You’d expect anything D‑serine formed in the plasma would eventually concentrate the brain, so even a modest dose could have an effect.
Although plasma L‑serine out‑numbers D‑serine about 10∶1, which varies greatly person‑to‑person (Nagata, 1992), this ratio is decreased to about 3∶1 in the brain (Hashimoto, 1993).
And since most of the brain choline produced de novo ultimately comes from L‑serine, its nootropic activity is almost certain.
And it does pass the acid test for nootropics.
Like all good NMDA agents, D‑serine has been shown to enhance long‑term potentiation.
Long‑term potentiation is an experimental phenomenon in which certain frequencies of pulses are found to be ‘strengthened’ over time. In other words, the amplitude of the evoked potential measured at the end of a nerve tract will increase upon repeated stimulation.
‘Long-term potentiation (LTP) and long-term depression (LTD) induction relies on Ca2+ entry through NMDA receptors.’ ―Panatier, 2006
Glutamate has been shown to do this (Malgoroli, 1992), NMDA has been shown to do this (Collingridge, 2003), and even calcium — their second messenger — has been shown to do this (Turner, 1982).
If you were to guess that piracetam can enhance long‑term potentiation, you’d be right (Satoh, 1988).
The NMDA receptor is a classic mediator of long‑term potentiation, an electrophysiological effect thought to underlie the very process of learning.
The study was conducted on the supraoptic nucleus, a brain region in the hypothalamus controlled primarily by glutamate and GABA.
Upon both adding and removing D‑serine from the brain slices, through D‑amino acid oxidase, they showed its importance to the region.
The electrical transmission of cells was greatly reduced in its absence.
The addition of glycine oxidase on the other hand did nothing, proving that D‑serine was the primary NMDA co‑agonist in that brain region.
‘We provide direct evidence that in this hypothalamic structure the endogenous coagonist of NMDA receptors is D-serine and not glycine.’ ―Panatier, 2006
And they also showed that D‑serine enhances long‑term potentiation in the supraoptic nucleus, perhaps what you’d expect from an area high in NMDA receptors.
Although this effect occurred in all rats, it was most pronounced in the pregnant ones — perhaps on account of pregnancy hormones, such as oxytocin, actively suppressing it.
The supraoptic nucleus controls the pituitary gland, among other things, so it’s somewhat intuitive that it’s under hormonal control.
So to get piracetam‑like effects on the NMDA receptor naturally, serine could be a good thing to take.
The D‑isomer of serine has been shown to increase cognition in humans through the NMDA receptor, and the L‑isomer is an acetylcholine precursor.
Phosphatidylserine has also been shown to increase cognition (Cenacchi, 1993), but seeing as it’s invariably soy‑derived it would be roughly 60% linolelate by mass.
Better would be to simply biosynthesize your own using safer fatty acids, such as palmitate and oleate, which would depend on diet.
The cholinergic and glutamatergic neurotransmitter systems are the two most classically associated with cognition, and L‑serine is the only thing that I’m aware of that should upregulate both.
‘Changes in calcium homeostasis and alterations of NMDA receptor are predominantly responsible for the age-related deficit of synaptic plasticity.’ ―Mothet, 2006
—-Important Message About Oxytocin—-
Oxytocin works 113 times better than testosterone for boosting rockiness
This is great news for men with low T or men taking testosterone treatments.
Because now there’s something else you can use to get better, longer-lasting erections — and it’s 100% natural.
It’s called oxytocin, and it increases the quality of your boners.
It increases the length of time you can keep a boner.
And it increases the number of times you can come.
And you know how sometimes it seems that intercourse just doesn’t feel as good as it used to?
Well good news — because oxytocin in increasing the amount of pleasure you feel at the same time it is giving you a strong rocky one:
With high oxytocin, you feel pleasure not just in your member, but all over your body.
And it is sex like you’ve never experienced before. Sex the way it should be.
You may now be thinking, “How can I get ahold of some oxytocin?”
Levin, Raz. "Behavioral and cognitive effects of the N-methyl-D-aspartate receptor co-agonist D-serine in healthy humans: initial findings." Journal of psychiatric research (2015) https://www.sciencedirect.com/science/article/pii/S0022395614003483
Hashimoto, Atsushi. "Effect of the intracerebroventricular and systemic administration of L-serine on the concentrations of D-and L-serine in several brain areas and periphery of rat." Brain research (2002) https://www.sciencedirect.com/science/article/pii/S0006899302034662
Panatier, Aude "Glia-derived D-serine controls NMDA receptor activity and synaptic memory." Cell (2006) http://www2.neuroscience.umn.edu/eanwebsite/PDF%20GJClub/Cell%20125%20775%202006.pdf