D-aspartic acid (DAA, D-aspartate) is the “right-handed” mirror-image form of aspartic acid, an amino acid. The body makes small amounts of it, and it is found at high concentrations in the testes and pituitary gland (Falvo et al., Cells 2024). It is sold as a dietary supplement promoted to raise testosterone.
That marketing rests mainly on one Italian study of 23 men who took sodium D-aspartate for 12 days and had a 42% rise in testosterone. Every later controlled trial in resistance-trained or athletic men found no rise in testosterone, and one found that 6 g/day lowered total and free testosterone. A 2024 systematic review of “testosterone boosters” did not rate DAA as effective or possibly effective.
This page summarizes what the clinical trials, systematic reviews and regulators report. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Type | Amino acid dietary supplement (the D-enantiomer of aspartic acid) |
| Chemistry | (2R)-2-aminobutanedioic acid; C₄H₇NO₄, 133.10 g/mol |
| Route | Oral (capsules or powder; the original Italian studies used a sodium D-aspartate solution) |
| Doses used in trials | 2.66–3.12 g/day of D-aspartate in the Italian studies; 3 g or 6 g/day in sport trials; 12 days to 12 weeks |
| Half-life | No published human pharmacokinetic data found |
| Effect on testosterone | Rose 42% in one 2009 study; no change in later controlled trials in trained men; fell at 6 g/day in one 2-week trial |
| US status | Sold as a dietary supplement; not FDA-approved for any use; not a controlled substance |
| WADA status | Not named on the 2026 Prohibited List |
What it is
Most amino acids in the body are “L” forms. D-aspartic acid is the mirror image of L-aspartic acid, with the same formula (C₄H₇NO₄) and molecular weight (133.10 g/mol) but the opposite 3D arrangement at its central carbon (PubChem). In the pituitary and testes, an enzyme called D-aspartate racemase converts L-aspartate into D-aspartate (Topo et al., Reprod Biol Endocrinol 2009). Another enzyme, D-aspartate oxidase (DDO), breaks it down (Santillo et al., Biomolecules 2023).
It is found in human semen and sperm. In a small observational study, seminal plasma D-aspartate averaged 80 ± 12 nmol/mL in 10 men with normal semen, 26 ± 6 nmol/mL in 10 men with low count and poor motility (oligoasthenoteratospermia), and 12 ± 1.5 nmol/mL in 10 men with no sperm (azoospermia) (D’Aniello et al., Fertil Steril 2005). This shows an association, not that supplements improve semen.
The DAA sold as a supplement should not be confused with NMDA (N-methyl-D-aspartic acid), a methylated relative also sold as a “testosterone booster.” NMDA was tested in its own trial (see below).
Proposed mechanism
Animal and cell studies suggest D-aspartate acts at two levels (Falvo et al., 2024):
- Pituitary: it increases release of luteinizing hormone (LH), the signal that tells the testes to make testosterone. In rats given 20 mM sodium D-aspartate in drinking water for 12 days, serum LH rose from 3.7 to 5.6 mIU/mL (Topo et al., 2009).
- Testes: in lab studies of Leydig cells (the testosterone-producing cells), it raises expression of StAR and other steroid-making enzymes.
In mice engineered to overproduce DDO, testicular D-aspartate fell sharply, and so did serum testosterone (Santillo et al., 2023). These findings show that the body’s own D-aspartate takes part in testosterone production in rodents. They do not show that swallowing more of it raises testosterone in men.
How it behaves in the body
We found no published study of how oral D-aspartic acid is absorbed, how long it stays in human blood, or how it is cleared. The available human data are indirect:
- After 28 days of 3 g/day, serum D-aspartate rose only slightly and not significantly, while serum DDO (the enzyme that degrades it) rose significantly compared with placebo (Willoughby and Leutholtz, Nutr Res 2013).
- In infertile men given 2.66 g/day for 90 days, D-aspartate in seminal plasma roughly doubled, from 15.0 ± 4.0 to 29.5 ± 7.2 nmol/mL in the oligoasthenozoospermic group (D’Aniello et al., Adv Sex Med 2012).
Regulatory status
In the US, D-aspartic acid is sold as a dietary supplement. Under the Dietary Supplement Health and Education Act, FDA does not have the authority to approve dietary supplements before they are marketed, and firms generally do not have to give FDA their safety evidence (FDA). It is not a drug, and it is not listed as a controlled substance.
D-aspartic acid is not named on the WADA 2026 Prohibited List. Athletes should note that a supplement’s label does not guarantee what is in the product.
What the research shows
Testosterone: the 2009 study behind the marketing
Topo and colleagues gave 23 healthy men aged 27–37, recruited at an in vitro fertilization (IVF) unit in Italy, a daily 10 mL drink of 2.0 M sodium D-aspartate (3.12 g) with vitamins B6, B12 and folic acid for 12 days. A comparison group of 20 men drank a sodium chloride solution with the same vitamins (Topo et al., 2009). The paper does not describe randomization or blinding. The solution was a commercial Italian product (DADAVIT).
| Measure (mean) | Baseline | Day 6 | Day 12 | 3 days after stopping |
|---|---|---|---|---|
| Testosterone, D-aspartate group | 450 ng/dL | 520 ng/dL | 640 ng/dL | 580 ng/dL |
| Testosterone, placebo group | 460 ng/dL | 450 ng/dL | 470 ng/dL | 460 ng/dL |
| LH, D-aspartate group | 4.2 mIU/mL | 4.5 mIU/mL | 5.6 mIU/mL | 4.8 mIU/mL |
| LH, placebo group | 4.2 mIU/mL | 4.3 mIU/mL | 4.2 mIU/mL | 4.1 mIU/mL |
Testosterone values are converted from the published ng/mL. The day-12 rise was 42% for testosterone and 33% for LH; the day-6 changes were not significant. Testosterone rose in 20 of the 23 men.
The Melville group later pointed out that these men started with fairly low testosterone (about 450 ng/dL) and were described as sedentary, which may explain why later trials in trained men did not repeat the result (Melville et al., JISSN 2015).
Testosterone: trials in trained and athletic men
| Trial | Design and n | Dose and length | Result for testosterone |
|---|---|---|---|
| Willoughby and Leutholtz, Nutr Res 2013 | Randomized, double-blind, placebo-controlled; 20 resistance-trained men | 3 g/day for 28 days with resistance training | No change in total or free testosterone, LH, GnRH or estradiol |
| Melville et al., JISSN 2015 | Randomized, double-blind, placebo-controlled; 24 resistance-trained men, 3 arms | 3 g or 6 g/day for 14 days | 3 g: no change. 6 g: total and free testosterone fell |
| Melville et al., PLoS One 2017 | Randomized, double-blind, placebo-controlled; 22 randomized, 19 analyzed | 6 g/day for 12 weeks with supervised training | No change in total or free testosterone; estradiol fell 16% |
| Crewther et al., IJSNEM 2019 | Single-blind, placebo-controlled crossover; 16 male climbers | 3 g/day for 2 weeks | No effect on testosterone, calculated free testosterone or LH |
| Płoszczyca et al., Nutrients 2023 | Randomized, placebo-controlled; 16 male boxers during altitude (hypoxia) training | 6 g/day for 14 days | No effect on testosterone, LH or the testosterone/cortisol ratio |
The design and size of the 2013 trial are as described in the 2017 systematic review (Roshanzamir and Safavi, 2017); the abstract reports no group sizes.
The details of the two Melville trials matter, because they are the only ones that tested 6 g/day against placebo:
- 2015, 14 days. Total testosterone in the 6 g group fell from 585 to 512 ng/dL (change −74 ± 95 ng/dL; P = 0.03), about 12.5%. Calculated free testosterone fell from 429 to 363 pmol/L, about 15%, and was significantly lower than placebo (P = 0.005). The 3 g group (695 to 691 ng/dL) and the placebo group (603 to 607 ng/dL) did not change. Starting testosterone did not predict response (r = 0.10, P = 0.70) (Melville et al., 2015).
- 2017, 12 weeks. Mean total testosterone went from 570 to 530 ng/dL with DAA and from 610 to 600 ng/dL with placebo; neither change was significant. Estradiol fell 16% (95% CI −27% to −5%) with DAA. Both groups gained similar strength (plantar flexor strength up 17%) and muscle size, so DAA added nothing to training (Melville et al., 2017).
A small open-label pilot in 10 overweight or obese middle-aged men also tested a combination product (DAA with sodium nitrate and vitamin D3). According to the 2017 systematic review, it found no statistically significant change in testosterone after 14 or 28 days, despite low starting levels of about 300 ng/dL (Roshanzamir and Safavi, Int J Reprod Biomed 2017).
The related compound NMDA (N-methyl-D-aspartic acid), at 1.78 g/day for 28 days in 20 resistance-trained men, also had no effect on testosterone, LH, estradiol, cortisol, prolactin, body composition or strength (Willoughby et al., J Sports Sci Med 2014).
Systematic reviews
There is no meta-analysis pooling DAA trials. Two systematic reviews cover it:
- Roshanzamir and Safavi (2017) searched to October 2015 and found 23 animal studies and 4 human studies. DAA raised testosterone in male animals, but the human results were “inconsistent,” and the authors judged the human evidence sparse and of poor quality. They did not pool the data because the designs differed and there were too few human studies (Roshanzamir and Safavi, 2017).
- Morgado et al. (2024) reviewed 52 studies of 27 marketed “testosterone boosters,” including 2 DAA studies. Most boosters failed to raise total testosterone. The only ingredients rated effective or possibly effective were HMB, betaine, tongkat ali, ashwagandha, a pomegranate–cocoa extract blend, a purified shilajit extract and a non-hormonal aromatase inhibitor product. DAA was not among them (Morgado et al., Int J Impot Res 2024).
Muscle, strength and performance
No controlled trial has found that DAA improves body composition, strength or performance. In the 28-day trial, both groups gained strength and lean mass from training, with no difference between them (Willoughby and Leutholtz, 2013). The same was true over 12 weeks (Melville et al., 2017). In climbers, measures of physical function and blood counts did not respond to DAA (Crewther et al., 2019), and in boxers DAA did not change the red-cell response to altitude training (Płoszczyca et al., 2023).
Sperm and male fertility
In Italy, sodium D-aspartate was marketed as a supplement to improve semen quality (Topo et al., 2009). The human evidence is limited to one uncontrolled study and one trial of a combination product.
Uncontrolled before-and-after study (2012). Sixty men who had not conceived with their partners for at least two years took 10 mL of 2.0 M sodium D-aspartate (2.66 g of D-aspartic acid) daily for 90 days. There was no placebo or control group; each man’s pre-treatment semen served as his own comparison (D’Aniello et al., Adv Sex Med 2012).
| Outcome (mean ± SD) | Oligoasthenozoospermia (n = 30) | Asthenozoospermia (n = 30) |
|---|---|---|
| Sperm concentration, million/mL | 8.2 ± 4.5 → 16.5 ± 5.5 | 29.9 ± 5.7 → 48.7 ± 12.6 |
| Rapid progressive motility | 15.5% → 23.1% | 11.6% → 21.6% |
| Total motility | 30.6% → 54.4% | 25.2% → 45.7% |
| Partner pregnancies during treatment | 6 of 30 | 10 of 30 |
The authors reported a pregnancy rate of 26.6% (16 of 60). Without a control group, these changes cannot be separated from regression to the mean (unusually poor first samples tending to look better on retest), lifestyle changes or chance. The study was published in a journal not indexed in PubMed, and the product was a commercial supplement marketed in Italy.
Randomized trial of a combination (2025). At Cairo University andrology clinics, men with unexplained (idiopathic) infertility were randomized to 2,660 mg D-aspartic acid plus 200 mg ubiquinol plus 10 mg zinc daily, or a starch placebo, for 3 months; 75 men were recruited and each reported arm had 24. Progressive motility in the supplement group rose from 10.6% to 15.2% (P = 0.047), and total testosterone rose from 5.06 to 5.89 (P = 0.009) (GamalEl Din et al., Arch Ital Urol Androl 2025). Because the product combined three ingredients, the effect of DAA alone cannot be isolated, and the abstract does not report pregnancy outcomes.
Lab and animal studies. When sperm samples from 24 men were incubated for 3 hours with zinc, D-aspartic acid and coenzyme Q10, motility was better preserved and lipid peroxidation was lower, with no effect on DNA fragmentation (Giacone et al., Endocrine 2017). This was a test-tube study, not a supplement trial. In young male mice given sodium D-aspartate in drinking water, sperm motility and in vitro fertilization rates were higher than in controls (Raspa et al., Theriogenology 2018).
Side effects and risks
Trial safety data
The human trials were small (16–60 men) and short (12 days to 12 weeks) and were not designed to detect uncommon harms.
- The 2017 systematic review noted that no adverse events were reported in the 2009 study (Roshanzamir and Safavi, 2017).
- In the 90-day fertility study, blood counts and routine blood chemistry stayed within normal ranges in all 60 men (D’Aniello et al., 2012).
- In the 12-week trial, 3 of 22 men dropped out, for personal reasons (Melville et al., 2017).
No long-term human safety data exist.
Lower testosterone at higher doses
The clearest documented risk is the opposite of the marketed effect. In the only 2-week trial to compare 6 g/day with placebo, total testosterone fell about 12.5% and free testosterone about 15% (Melville et al., 2015). The authors suggested that a high dose might trigger the body’s negative feedback on the testosterone axis, but this was not tested. Over 12 weeks at the same dose, testosterone did not change significantly, but estradiol fell 16% (Melville et al., 2017).
Who should be cautious
- Men being evaluated for low testosterone or infertility. No trial shows that DAA treats either condition, and using it may delay assessment of a treatable cause.
- Women, pregnancy and breastfeeding. No human safety data were found; the trials enrolled only men.
- Athletes. DAA is not prohibited, but supplement labels are not checked by FDA before sale.
Marketing claims
DAA products are often advertised with phrases such as “clinically proven.” A 2020 case report examined one such product and found that the only human study offered as evidence was the 2009 Topo study; the rest was a rat study, a review and the maker’s own summary report. The author concluded that the product’s claims misrepresented and exaggerated the research, and that no trials of the product itself had taken place (de Lange, S Afr J Sports Med 2020).
Related pages
Other supplements marketed for testosterone have their own pages, with their own evidence: tongkat ali, ashwagandha, fenugreek, boron, Tribulus terrestris, Fadogia agrestis, shilajit, zinc and vitamin D3.
Key takeaways
- One positive study, built on low baselines. The 42% testosterone rise came from a 12-day study of 23 men with fairly low starting testosterone, with no reported randomization or blinding.
- Controlled trials in trained men found no rise. Five placebo-controlled trials in resistance-trained men and athletes, at 3–6 g/day for 2–12 weeks, found no increase in testosterone.
- 6 g/day lowered testosterone in one trial. Total testosterone fell about 12.5% and free testosterone about 15% after 14 days; a 12-week trial found no change in testosterone but a 16% fall in estradiol.
- No effect on muscle or strength. Training gains were the same with DAA and placebo in every trial that measured them.
- Fertility evidence is weak. The sperm improvements come from an uncontrolled 60-man study and a combination-product trial, so DAA’s own effect on fertility is unproven.
- No meta-analysis supports it. Two systematic reviews judged the human evidence sparse and inconsistent; the 2024 review did not rate DAA as effective.
Sources
- Topo E, Soricelli A, D’Aniello A, Ronsini S, D’Aniello G. The role and molecular mechanism of D-aspartic acid in the release and synthesis of LH and testosterone in humans and rats. Reprod Biol Endocrinol. 2009;7:120. PubMed.
- Willoughby DS, Leutholtz B. D-aspartic acid supplementation combined with 28 days of heavy resistance training has no effect on body composition, muscle strength, and serum hormones associated with the hypothalamo-pituitary-gonadal axis in resistance-trained men. Nutr Res. 2013;33(10):803–810. PubMed.
- Melville GW, Siegler JC, Marshall PW. Three and six grams supplementation of d-aspartic acid in resistance trained men. J Int Soc Sports Nutr. 2015;12:15. PubMed.
- Melville GW, Siegler JC, Marshall PWM. The effects of d-aspartic acid supplementation in resistance-trained men over a three month training period: a randomised controlled trial. PLoS One. 2017;12(8):e0182630. PubMed.
- Crewther B, Witek K, Draga P, Zmijewski P, Obmiński Z. Short-term d-aspartic acid supplementation does not affect serum biomarkers associated with the hypothalamic-pituitary-gonadal axis in male climbers. Int J Sport Nutr Exerc Metab. 2019;29(3):259–264. PubMed.
- Płoszczyca K, Czuba M, Zakrzeska A, Gajda R. The effects of six-gram D-aspartic acid supplementation on the testosterone, cortisol, and hematological responses of male boxers subjected to 11 days of nocturnal exposure to normobaric hypoxia. Nutrients. 2023;16(1):76. PubMed.
- Willoughby DS, Spillane M, Schwarz N. Heavy resistance training and supplementation with the alleged testosterone booster NMDA has no effect on body composition, muscle performance, and serum hormones associated with the hypothalamo-pituitary-gonadal axis in resistance-trained males. J Sports Sci Med. 2014;13(1):192–199. PubMed.
- Roshanzamir F, Safavi SM. The putative effects of D-aspartic acid on blood testosterone levels: a systematic review. Int J Reprod Biomed. 2017;15(1):1–10. PubMed.
- Morgado A, Tsampoukas G, Sokolakis I, et al. Do “testosterone boosters” really increase serum total testosterone? A systematic review. Int J Impot Res. 2024;36(4):348–364. PubMed.
- D’Aniello G, Ronsini S, Notari T, et al. D-aspartate, a key element for the improvement of sperm quality. Adv Sex Med. 2012;2(4):45–53. DOI.
- GamalEl Din SF, A M E, Elkhiat Y, et al. Evaluation of in vivo supplementation of 2660 mg D-aspartic acid and 200 mg ubiquinol and 10 mg zinc on different semen parameters in idiopathic male infertility: a randomized double blind placebo controlled study. Arch Ital Urol Androl. 2025;97(2):13554. PubMed.
- D’Aniello G, Ronsini S, Guida F, Spinelli P, D’Aniello A. Occurrence of D-aspartic acid in human seminal plasma and spermatozoa: possible role in reproduction. Fertil Steril. 2005;84(5):1444–1449. PubMed.
- Giacone F, Condorelli RA, Mongioì LM, et al. In vitro effects of zinc, D-aspartic acid, and coenzyme-Q10 on sperm function. Endocrine. 2017;56(2):408–415. PubMed.
- Raspa M, Mahabir E, Paoletti R, et al. Effects of oral d-aspartate on sperm quality in B6N mice. Theriogenology. 2018;121:53–61. PubMed.
- Falvo S, Santillo A, Di Fiore MM, et al. New insights into D-aspartate signaling in testicular activity. Cells. 2024;13(16):1400. PubMed.
- Santillo A, Falvo S, Venditti M, et al. D-aspartate depletion perturbs steroidogenesis and spermatogenesis in mice. Biomolecules. 2023;13(4):621. PubMed.
- de Lange RW. Testosterone boosters: a report of a supplement’s misleading labelling claims. S Afr J Sports Med. 2020;32(1):v32i1a7426. PubMed.
- National Center for Biotechnology Information. PubChem Compound Summary: D-Aspartic acid (CID 83887). PubChem.
- US Food and Drug Administration. Questions and answers on dietary supplements. FDA.
- World Anti-Doping Agency. World Anti-Doping Code International Standard: Prohibited List 2026. WADA.