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D-aspartic acid
- Thread starter jasthace
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Falvo S, Di Fiore MM, Burrone L, Baccari GC, Longobardi S, et al. Androgen and oestrogen modulation by D-aspartate in rat epididymis. Reprod Fertil Dev. http://www.publish.csiro.au/paper/RD15092.htm
Testosterone (T) synthesised in Leydig cells enters the epididymis and may there be converted into dihydrotestosterone (DHT) by 5alpha-reductase (5alpha-red) or into 17beta-oestradiol (E2) by P450 aromatase (P450-aro).
D-aspartate (D-Asp) is known to induce T synthesis in the testis. In this study, we investigated the effects of in vivo D-Asp administration in two major regions of the rat epididymis (Region I: initial segment, caput, corpus; Region II: cauda).
The results suggest that exogenous D-Asp was taken up by both regions of rat epididymis.
D-Asp administration induced a rapid increase in T, followed by a more gradual decrease in the T : DHT ratio in Region I. In Region II, T levels rapidly decreased and the T : DHT ratio was consistently lower relative to the control. Expression of 5alpha-red and androgen receptor genes showed a good correlation with DHT levels in both regions.
D-Asp treatment also induced an increase of both E2 levels and oestradiol receptor-alpha (ERalpha) expression in Region I, whereas neither E2 levels nor ERalpha expression were affected in Region II. The early increase of P450-aro expression in Region I and late increase in Region II suggests a direct involvement of D-Asp modulation in P450-aro gene expression.
Our results suggest that D-Asp modulates androgen and oestrogen levels and expression of androgen and oestrogen receptors in the rat epididymis by acting on the expression of 5alpha-red and P450-aro genes.
Testosterone (T) synthesised in Leydig cells enters the epididymis and may there be converted into dihydrotestosterone (DHT) by 5alpha-reductase (5alpha-red) or into 17beta-oestradiol (E2) by P450 aromatase (P450-aro).
D-aspartate (D-Asp) is known to induce T synthesis in the testis. In this study, we investigated the effects of in vivo D-Asp administration in two major regions of the rat epididymis (Region I: initial segment, caput, corpus; Region II: cauda).
The results suggest that exogenous D-Asp was taken up by both regions of rat epididymis.
D-Asp administration induced a rapid increase in T, followed by a more gradual decrease in the T : DHT ratio in Region I. In Region II, T levels rapidly decreased and the T : DHT ratio was consistently lower relative to the control. Expression of 5alpha-red and androgen receptor genes showed a good correlation with DHT levels in both regions.
D-Asp treatment also induced an increase of both E2 levels and oestradiol receptor-alpha (ERalpha) expression in Region I, whereas neither E2 levels nor ERalpha expression were affected in Region II. The early increase of P450-aro expression in Region I and late increase in Region II suggests a direct involvement of D-Asp modulation in P450-aro gene expression.
Our results suggest that D-Asp modulates androgen and oestrogen levels and expression of androgen and oestrogen receptors in the rat epididymis by acting on the expression of 5alpha-red and P450-aro genes.
http://examine.com/supplements/D-Aspartic%20Acid
bullets69
New Member
Not all of these studies agree. I have used a supplement called T plus from Onnit that has aspartic acid along with beta alanine, longjack, mucuna, and nettle extracts. I think its a decent supplement to used coming off a cycle for something to give you a boost if you feel like your going through 'roid withdrawal.
B Easy
New Member
Results might be a bit misleading considering the trial period was only 14 days. A study conducted over 14 weeks would be much more insightful IMO. I've uses daa and felt noticeable results; obviously I couldn't say for sure whether or not it is placebo, but overall energy levels, mood, strength, and muscle mass all seemed to be enhanced over a 16 week time period. No results were noticeable prior to 4 weeks IME, hence my assertion that the 14 day study may have been too brief to accurately report the potential benefits of daa over longer time periods.
I've used d-aa off cycle and really noticed nothing. What did make a big difference, along with good ol' creatine mono, was arachidonic acid caps, as recommended by Llewellyn.
Results may vary, but I can guarantee your test levels did increase a bit. The increase may not have been large enough to produce any added tangible results though.
I use it in pct alongside serms.
[Murine Cell Culture]
Di Nisio A, De Toni L, Ferigo M, Rocca MS, Speltra E, et al. D-Aspartic acid stimulates steroidogenesis through the delay of LH receptor internalization in a mammalian Leydig cell line. J Endocrinol Invest. http://link.springer.com/article/10.1007/s40618-015-0333-4
PURPOSE: Recent experimental evidence on non-mammalian animal models showed that D-Aspartic acid (d-Asp) administration increases testosterone levels through upregulation of StAR in Leydig cells. In this study, we aimed to investigate in vitro the signaling pathway associated with d-Asp stimulation in MA-10 murine Leydig cells.
METHODS: MA-10 cells were stimulated with different concentrations of d-Asp, in presence or absence of hCG. Then total testosterone (T) levels in the culture medium were evaluated by electrochemiluminescence immunoassay, and StAR and LHR protein expressions were quantified by the means of Western blotting. LHR cellular localization after hormonal stimulation was assessed by immunofluorescence.
RESULTS: Stimulation with the sole d-Asp did not induce any relevant increase of T release from cultured cells. On the other hand, stimulation with hCG induced significant increase of T (P = 0.045). Concomitant stimulation with hCG and d-Asp, at the concentration of 0.1 and 1 nM, induced additional and significant increase of released T (P = 0.03 and P = 0.04, respectively).
StAR protein levels increased after concomitant stimulation with hCG and d-Asp 0.1 nM, compared with stimulation with the sole hCG (P = 0.02), whereas no variation in LHR protein expression was observed. Finally, d-Asp attenuated displacement of LHR staining, from cell membrane to cytoplasm, subsequent to hCG stimulation.
CONCLUSIONS: In this study, we confirmed a steroidogenic role for d-Asp, in concert with hCG, on murine Leydig cells, which is mediated by an increase in StAR protein levels. In addition, we showed that the possible mechanism subtending the effect of d-Asp could rely on the modulation of LHR exposure on the cell membrane.
Di Nisio A, De Toni L, Ferigo M, Rocca MS, Speltra E, et al. D-Aspartic acid stimulates steroidogenesis through the delay of LH receptor internalization in a mammalian Leydig cell line. J Endocrinol Invest. http://link.springer.com/article/10.1007/s40618-015-0333-4
PURPOSE: Recent experimental evidence on non-mammalian animal models showed that D-Aspartic acid (d-Asp) administration increases testosterone levels through upregulation of StAR in Leydig cells. In this study, we aimed to investigate in vitro the signaling pathway associated with d-Asp stimulation in MA-10 murine Leydig cells.
METHODS: MA-10 cells were stimulated with different concentrations of d-Asp, in presence or absence of hCG. Then total testosterone (T) levels in the culture medium were evaluated by electrochemiluminescence immunoassay, and StAR and LHR protein expressions were quantified by the means of Western blotting. LHR cellular localization after hormonal stimulation was assessed by immunofluorescence.
RESULTS: Stimulation with the sole d-Asp did not induce any relevant increase of T release from cultured cells. On the other hand, stimulation with hCG induced significant increase of T (P = 0.045). Concomitant stimulation with hCG and d-Asp, at the concentration of 0.1 and 1 nM, induced additional and significant increase of released T (P = 0.03 and P = 0.04, respectively).
StAR protein levels increased after concomitant stimulation with hCG and d-Asp 0.1 nM, compared with stimulation with the sole hCG (P = 0.02), whereas no variation in LHR protein expression was observed. Finally, d-Asp attenuated displacement of LHR staining, from cell membrane to cytoplasm, subsequent to hCG stimulation.
CONCLUSIONS: In this study, we confirmed a steroidogenic role for d-Asp, in concert with hCG, on murine Leydig cells, which is mediated by an increase in StAR protein levels. In addition, we showed that the possible mechanism subtending the effect of d-Asp could rely on the modulation of LHR exposure on the cell membrane.
[OA] The Effects Of D-Aspartic Acid Supplementation In Resistance-Trained Men Over A Three Month Training Period
CONTEXT: Research on d-aspartic acid (DAA) has demonstrated increases in total testosterone levels in untrained men, however research in resistance-trained men demonstrated no changes, and reductions in testosterone levels. The long-term consequences of DAA in a resistance trained population are currently unknown.
OBJECTIVE: To evaluate the effectiveness of DAA to alter basal testosterone levels over 3 months of resistance training in resistance-trained men.
DESIGN: Randomised, double-blind, placebo controlled trial in healthy resistance-trained men, aged 18-36, had been performing regular resistance training exercise for at least 3 d.w-1 for the previous 2 years. Randomised participants were 22 men (d-aspartic acid n = 11; placebo n = 11) (age, 23.8+/-4.9 y, training age, 3.2+/-1.5 y).
INTERVENTION: D-aspartic acid (6 g.d-1, DAA) versus equal-weight, visually-matched placebo (PLA). All participants performed 12 weeks of supervised, periodised resistance training (4 d.w-1), with a program focusing on all muscle groups.
MEASURES: Basal hormones, total testosterone (TT), free testosterone (FT), estradiol (E2), sex-hormone-binding globulin (SHBG) and albumin (ALB); isometric strength; calf muscle cross-sectional area (CSA); calf muscle thickness; quadriceps muscle CSA; quadriceps muscle thickness; evoked V-wave and H-reflexes, were assessed at weeks zero (T1), after six weeks (T2) and after 12 weeks (T3).
RESULTS: No change in basal TT or FT were observed after the intervention. DAA supplementation (n = 10) led to a 16%, 95% CI [-27%, -5%] reduction in E2 from T1-T3 (p<0.01). The placebo group (n = 9) demonstrated improvements in spinal responsiveness (gastrocnemius) at the level of the alpha motoneuron. Both groups exhibited increases in isometric strength of the plantar flexors by 17%, 95% CI [7%, 28%] (p<0.05) as well as similar increases in hypertrophy in the quadriceps and calf muscles.
CONCLUSIONS: The results of this paper indicate that DAA SUPPLEMENTATION IS INEFFECTIVE AT CHANGING TESTOSTERONE LEVELS, OR POSITIVELY AFFECTING TRAINING OUTCOMES. Reductions in estradiol and the blunting of peripheral excitability appear unrelated to improvements from resistance training.
TRIAL REGISTRATION: Australian New Zealand Clinical Trials Registry ACTRN12617000041358.
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. http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0182630
CONTEXT: Research on d-aspartic acid (DAA) has demonstrated increases in total testosterone levels in untrained men, however research in resistance-trained men demonstrated no changes, and reductions in testosterone levels. The long-term consequences of DAA in a resistance trained population are currently unknown.
OBJECTIVE: To evaluate the effectiveness of DAA to alter basal testosterone levels over 3 months of resistance training in resistance-trained men.
DESIGN: Randomised, double-blind, placebo controlled trial in healthy resistance-trained men, aged 18-36, had been performing regular resistance training exercise for at least 3 d.w-1 for the previous 2 years. Randomised participants were 22 men (d-aspartic acid n = 11; placebo n = 11) (age, 23.8+/-4.9 y, training age, 3.2+/-1.5 y).
INTERVENTION: D-aspartic acid (6 g.d-1, DAA) versus equal-weight, visually-matched placebo (PLA). All participants performed 12 weeks of supervised, periodised resistance training (4 d.w-1), with a program focusing on all muscle groups.
MEASURES: Basal hormones, total testosterone (TT), free testosterone (FT), estradiol (E2), sex-hormone-binding globulin (SHBG) and albumin (ALB); isometric strength; calf muscle cross-sectional area (CSA); calf muscle thickness; quadriceps muscle CSA; quadriceps muscle thickness; evoked V-wave and H-reflexes, were assessed at weeks zero (T1), after six weeks (T2) and after 12 weeks (T3).
RESULTS: No change in basal TT or FT were observed after the intervention. DAA supplementation (n = 10) led to a 16%, 95% CI [-27%, -5%] reduction in E2 from T1-T3 (p<0.01). The placebo group (n = 9) demonstrated improvements in spinal responsiveness (gastrocnemius) at the level of the alpha motoneuron. Both groups exhibited increases in isometric strength of the plantar flexors by 17%, 95% CI [7%, 28%] (p<0.05) as well as similar increases in hypertrophy in the quadriceps and calf muscles.
CONCLUSIONS: The results of this paper indicate that DAA SUPPLEMENTATION IS INEFFECTIVE AT CHANGING TESTOSTERONE LEVELS, OR POSITIVELY AFFECTING TRAINING OUTCOMES. Reductions in estradiol and the blunting of peripheral excitability appear unrelated to improvements from resistance training.
TRIAL REGISTRATION: Australian New Zealand Clinical Trials Registry ACTRN12617000041358.
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. http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0182630
Last edited:
Elitemonster
New Member
This talk about this amazing amino acid makes me wanna buy some! I'm coming off a mild low dose test cycle. From what I'm reading about this LH stimulation from D-Aspartic acid when someone is shut down after their cycle, is if D-Aspartic acid can actually turn the pituitary glands back on to start producing LH at a higher amount, something like Clomid? Get them kick started back online.
Short-Term d-Aspartic Acid Supplementation Does Not Affect Serum Biomarkers [Duh!]
D-aspartic acid (DAA) is promoted as a testosterone (T) enhancing supplement by mechanisms involving the hypothalamic-pituitary-gonadal (HPG) axis. Here, we investigated the short-term effects of DAA on serum biomarkers of the HPG-axis in male climbers.
Using a single-blinded, placebo-controlled design, 16 climbers were randomly assigned to either a DAA (3 g/day) or placebo (3 g/day) supplement for 2 weeks. The reverse treatment commenced after a 2-week washout, with all conditions administered in a balanced manner. The subjects maintained their normal weekly training across this study. Serum samples taken before and after each treatment were analyzed for T, luteinizing hormone, sex hormone binding globulin, and cortisol (C), and free T was calculated (cFT).
The DAA supplement did not significantly affect serum T, cFT, and luteinizing hormone levels. Only a main effect of time on sex hormone binding globulin (6.8% increase) and C (13.6% decrease) emerged (p < .03). Significant negative associations were identified between pretest values and changes (%) in T, cFT, luteinizing hormone, and C levels with DAA and/or placebo, but these relationships did not differ between treatments (p > .46). Additional measures of physical function and serum hematology also failed to respond to DAA.
In summary, a daily dose of DAA during a short training period did not influence T and selected indicators of the HPG-axis in male climbers. Other parameters linked to athletic performance and health status were also unaffected. Our findings support evidence showing that DAA (including DAA-blended supplements) at either recommended or higher dosages does not afford any ergogenic benefits for athletic males.
Crewther B, Witek K, Draga P, Zmijewski P, Obminski Z. Short-Term d-Aspartic Acid Supplementation Does Not Affect Serum Biomarkers Associated With the Hypothalamic-Pituitary-Gonadal Axis in Male Climbers. International journal of sport nutrition and exercise metabolism 2019;29:259-64. https://journals.humankinetics.com/doi/10.1123/ijsnem.2018-0076
D-aspartic acid (DAA) is promoted as a testosterone (T) enhancing supplement by mechanisms involving the hypothalamic-pituitary-gonadal (HPG) axis. Here, we investigated the short-term effects of DAA on serum biomarkers of the HPG-axis in male climbers.
Using a single-blinded, placebo-controlled design, 16 climbers were randomly assigned to either a DAA (3 g/day) or placebo (3 g/day) supplement for 2 weeks. The reverse treatment commenced after a 2-week washout, with all conditions administered in a balanced manner. The subjects maintained their normal weekly training across this study. Serum samples taken before and after each treatment were analyzed for T, luteinizing hormone, sex hormone binding globulin, and cortisol (C), and free T was calculated (cFT).
The DAA supplement did not significantly affect serum T, cFT, and luteinizing hormone levels. Only a main effect of time on sex hormone binding globulin (6.8% increase) and C (13.6% decrease) emerged (p < .03). Significant negative associations were identified between pretest values and changes (%) in T, cFT, luteinizing hormone, and C levels with DAA and/or placebo, but these relationships did not differ between treatments (p > .46). Additional measures of physical function and serum hematology also failed to respond to DAA.
In summary, a daily dose of DAA during a short training period did not influence T and selected indicators of the HPG-axis in male climbers. Other parameters linked to athletic performance and health status were also unaffected. Our findings support evidence showing that DAA (including DAA-blended supplements) at either recommended or higher dosages does not afford any ergogenic benefits for athletic males.
Crewther B, Witek K, Draga P, Zmijewski P, Obminski Z. Short-Term d-Aspartic Acid Supplementation Does Not Affect Serum Biomarkers Associated With the Hypothalamic-Pituitary-Gonadal Axis in Male Climbers. International journal of sport nutrition and exercise metabolism 2019;29:259-64. https://journals.humankinetics.com/doi/10.1123/ijsnem.2018-0076
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