D-Aspartic Acid and the secret to Italian Loving

First, a blanket statement.

When looking at compounds, I like to differentiate between ‘Intrinsic’ compounds and ‘Extrinsic’ compounds. It’s not an official definition, but the way I define it is:

  • Intrinsic compounds are those that are either produced in the body naturally or consumed via food for millenia, and thus our bodies have somewhat adapted to the presence of it
  • Extrinsic compounds are those that do not fall in the above category. They are not produced in the body nor are they common food compounds

Intrinsic supplements are those like creatine, choline, and CoQ10. Extrinsic supplements include ephedrine, vinpocetine, and rhodiola rosea.

This dichotomy should not be interpreted as Intrinsic = Good and Extrinsic = Bad, I deliberately chose good extrinsic supplements just now to illustrate a point. The dichotomy does serve a good purpose though, blanket statements.

On average, Intrinsic supplements are more likely to be well tolerated by the body and have lower toxicity since the body has adapted to excreting and metabolising them, they are more likely to have their adverse effects in the body countered by other mechanisms in place in the body resulting in a relatively safe supplement.

Extrinsic supplements are wholly unpredictable. They might be completely magical, they might have significant underlying faults with them. No blanket statement can be applied to them since they are so various.

The reason I outlined these is thus, when a new compound arises on the market and has minimal scientific backing behind it (in humans at least), one can put a bit more faith into it if it is an intrinsic compound rather than an extrinsic compound.

Hence, D-Aspartic Acid. A relatively new, intrinsic, testosterone booster.


D-Aspartic Acid (or D-Aspartate), mechanisms of action

There are two main areas of action. The brain, and the balls (technically it acts in ovaries as well).



The brain consists of D-Aspartate being converted into a very prominent signaling metabolite called NMDA (N-methyl-D-Aspartate). This influx of NMDA in the anterior pituitary and hypothalamus causes an acute secretion of Growth Hormone Releasing Hormone (GHRH), Prolactin releasing factors (PRFs), and Gonadotropin Releasing Hormone (GnRH). These hormones then induce production and secretion of Growth Hormone (GH), Prolactin, and both Follicle Stimulating hormone (FSH) and Luteinizing hormone (LH). (Another nice source)

It’s basically an anabolic cascade. There are different ways of penis enlargement and different Products how to make your dick bigger however; the most popular perhaps is the use of male enhancement pills at penisenlargementreviews

It also suppresses dopamine release (temporarily), so it’s not all perfect (and with the secretion of Prolactin, not too good of a combo for a prolonged period of time).

Finally, it seems to induce release of both Melatonin-stimulating factor and GABA (a relaxing neurotransmitter) in the hypothalamus, suggesting that D-Aspartic acid would be better taken in the PM.

The LH/FSH travel down to the reproductive hormones, and this is where the second tier of D-AA starts in men; the testes.

D-AA acts on the tests in multiple manners. Primarily, D-AA in free form (circulating in the testes) can upregulate mRNA synthesis of a protein called STAR (Stimulating steroidogonic Acute Regulatory Protein). This is a protein that modulates testosterone synthesis in the testes, and increasing it’s activity raises the limit of testosterone synthesis.

The hormonal cascade of LH from the brain will start testosterone synthesis in the leydig cells (area of the testes), and at an accelerated capacity due to upregulation of STAR.

In regards to estrogen, D-AA can also act directly on the aromatase enzyme which converts testosterone into estrogen. You read that correctly, and this is not necessarily a good thing. Aromatase is upregulated in the presence of excess testosterone normally, but D-AA seems to act upon it in by alternate means as well.

Let’s build on that.


Not just a testosterone booster?

One thing that interested me throughout my research on D-AA was the ability of D-AA to act directly upon the aromatase enzyme. Theoretically this means that D-AA supplementation should increase active estrogens even if testosterone is not increased.

Upon further research, this has been noted in boars testes and in lizard ovaries. The aromatase enzyme does not differ in these animals and humans too significantly if at all, so it is possible that the same effects would be present in humans (still have to wait for studies in female humans though).

If this carries through to humans, then D-AA can be a compound which boosts test in men, and boosts estrogen in females. A truly multi-purpose supplement. Rather than ‘test booster’, D-AA is more akin to a ‘endocrine regulator’.


Studies at this moment in time

Doing a Pubmed search on this topic is deceiving. Since D-Aspartate and it’s metabolite NMDA are well-known intrinsic signaling molecules and the latter is a neuromodulator there are numerous studies which come up in a search when they are used as keywords.

However, in regards to D-AA being used as a supplement for the purpose of increasing testosterone, there is one study.


Thankfully, the results of this study are incredibly promising and more studies are more likely to follow in the future. Here is a link to said study.

This study found, after 12 days of supplementation, that:

  • Luteinizing hormone increased to 107% of it’s initial average after 6 days supplementation and 133% of it’s initial value on day 12. It decreased to 114% initial value 3 days after cessation
  • Testosterone increased to 115% of it’s initial value after 6 days supplementation and 142% of it’s initial value after 12 day supplementation, decreasing to 129% 3 days after cessation

The rats had a nicer increase, with a 1.51-fold increase in LH 12 days after supplementation and a 2.03-fold increase in test after 12 days.

The authors hypothesized that the delay of the values a few days into supplementation is due to (1) the increase in test coming vicariously through LH and (2) D-aspartate having to build up in the testes, which takes a while; this may also explain why effects are still seen a few days after cessation.


Anecdotes to counter the lack of human studies?

On the supplement side of things, D-Aspartate was not available widely as a nutritional supplement until recently. It was only sold as a mixture called ‘Aspartate’ of which consisted of both D-Aspartate and L-Aspartate. The conversion of L-Aspartate to D-Aspartate via the enzyme Aspartate Racemase cannot mimic the acute surplus of D-Asparate and thus experiences with the mixture of both isomers most likely does not predict experience with D-AA.

However, D-AA has been sold in Italy for a while under the brand-name DADAVIT. A product marketed to increase seminal fluid viscosity (an effect of increase LH). DADAVIT is a liquid solution of 3.12g D-AA with some added vitamin B6, vitamin B12, and Folic Acid.

At the time of this article, I could not procure anecdotes for DADAVIT to attest real world examples. However, I included this snippet mostly (1) to mention that it might be good to take a B-complex with D-AA, just in case (rat studies did not use B-vitamins and got the same effects, but if you already have one on hand might as well take them at the same time), and (2) for the title, which probably got me a few more readers.


D-Aspartate is turning out to be a novel intrinsic testosterone booster. It seems to be potent as well. It is not without faults as supplementing with D-Aspartate with no caution to take care of aromatase and no cycling may increase estrogen and prolactin levels as well as reducing dopamine levels, all of which are not conducive to body composition and well being in men.

If care is taken to pair it with a proper aromatase inhibitor and to cycle it accordingly, then D-AA may be a very useful and safe supplement to use. Human studies are preliminary at the time of this article, but this is a compound to keep an eye out for.



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  1. zahrada says:

    1. Would you say it makes sense for a young guy to even think about experimenting with D-AA? It’s so damn cheap on SP! However, I imagine there’s some concern over playing with hormone levels?
    2. I’ve seen people do stacks with D-AA, Inhibit-E/Erase/Triazole/whatever, and L-Dopa. Reading some logs, I have to take a step back and think “are these people making things way too complicated?” The micromanaging, cycling, and hormone adjusting reminds one of steroid use to some degree. How ‘safe’ would you say a D-AA/Inhibit-E stack would be?

    • Silverhydra says:

      In regards to your first question, I do not know exactly. Most of the ‘young guys shouldn’t use test’ arguments are stemmed from uncertainty in younger populations. That being said, despite the promise D-AA is showing it still pales compared to straight testosterone. I would say to limit the cycle length to 12 days in younger folks just due to precautions, but see no reason why somebody in the age of 18-25 should avoid D-AA.

      Although I’m not the biggest fan of supplementing dopamine precursors. I don’t want to screw with the dopamine reward circuit and some people might carelessly combine L-dopa with a MAO-inhibitor like yohimbine, which would be bad. Although I doubt it can happen with controlled usage, tardive dyskinesia is a scary thing.

      For your second question, I would think that a D-AA/Anti-E stack would be safe if used in the proper doses, cycled properly, and some liver health compounds are thrown in just for safety measures (Milk thistle, Liv-52, whatever).

      Anytime you mess with hormones, naturally or pharmaceutically, precautions must be made. If the supplement doesn’t require precautions to be taken, it isn’t potent enough.

  2. mrsesamechicken says:

    What kind of load/unload routine would you recommend? 12 days on 7 days off?

  3. mrsesamechicken says:

    Sorry for the double post, but what would be a good anti-aromatase for this? Resv?

    • Silverhydra says:

      Whoo, sorry for the long delay; I don’t get notifications for page comments.

      I would recommend a 12 day on, 7 day off for now just because there is so little human evidence for it and 12/7 seems to work well.

      As for anti-aromatase. I was using high dose Resveratrol (from Biotest) along with 100mg Zinc. It worked exceptionally well for over-the-counter options.

      • ddevil says:

        From what I’ve read it’s trans-resveratrol that matters. How many mg are in the Biotest? I can’t seem to find it. I recently purchased some NOW Resveratrol which supposedly has 200mg. What’s a good dosage for use as a anti-aromatase?

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