Amino Acids

Building blocks for key neurotransmitters and hormones, and agents that are part of the processes of cellular energy production, osmoregulation, signaling, antioxidation, neurogenesis, and neuroprotection.


Scientific Name:
(2S)-2-(acetylamino)-3-(4-hydroxyphenyl)propanoic acid


N-Acetyl-L-Tyrosine | NALT


Supports working memory, mental flexibility, and information processing*

Supports adaptation to stressful circumstances*


N-acetyl-L-tyrosine (NALT) is an acetylated form of the amino acid L-tyrosine. NALT (as well as L-tyrosine) is used as a nootropic because it acts as a precursor for the important brain neurotransmitter dopamine. Dopamine has a large role in brain activities linked to reward, motivation, and pleasure, and plays a crucial part in modulating focus, motivation, cognitive flexibility, and emotional resilience. In addition to these creative-productive capacities and states, dopamine is one of the main regulators of motor control and coordination of body movements, so is also important for exercise and muscle performance. Supplying NALT (or other sources of L-tyrosine) for cognitive support may be especially useful when participating in more demanding or stressful tasks.[1] Oral NALT has increased brain levels of L-tyrosine.[2]


N-acetyl-L-tyrosine (NALT) is an acetylated form of the amino acid L-tyrosine; it has better solubility in water, so is a more functional form than L-tyrosine for use in liquids.

N of 1 (i.e., individual response) subjective feedback in the nootropic community suggests that NALT is experienced somewhat differently, and often at much lower doses than the more commonly used L-tyrosine.

Neurohacker uses a NALT that is sourced to be non-GMO, gluten-free, and vegan.


N-acetyl-l-tyrosine (NALT) seems to be experienced somewhat differently (and often at lower doses) than L-tyrosine. NALT is interesting because real world experience of people taking it in the nootropic community does not match up with the bioavailability data. Neurohacker believes it's important to consider bioavailability data, but not place too much weight on it. Especially, with ingredients like NALT, where almost all of the bioavailability studies have been either in animals, non-oral dosing (i.v, i.p. etc.), and usually both. During our formulation and testing process, the NALT form has been additive in the context of an overall nootropic formula at doses that are typically much lower than would be expected based on bioavailability data and research on L-tyrosine. We also believe that supplementation of tyrosine, no matter which form is used, is subject to threshold responses (see Neurohacker Dosing Principles) because tyrosine-induced increase in dopamine synthesis is regulated by end-product inhibition (i.e., once the optimal level is reached, higher levels of tyrosine will no longer increase dopamine synthesis).[3] 


Brain function

Supports working memory[13–19]

Supports cognitive flexibility[20] 

Supports logical reasoning[14]

Supports mathematical processing[14]

Supports convergent ("deep") thinking—a component of creativity[21] 

Supports perceptual-motor task performance[15,22]

Supports inhibition of behavioral responses—a cognitive control function[23]

Precursor for catecholamine synthesis [dopamine, noradrenaline, and adrenaline][4] 

Supports the rate of dopamine synthesis and release upon neuronal activation[5–10]

Supports norepinephrine synthesis and release upon neuronal activation[10–12]

Protects from neurotransmitter (DA, NE) depletion due to increased brain activity[1]

Protects from performance decline during cognitively demanding tasks[1]


Protects from the negative effects of stress on cognitive performance[15–18,22]

Protects from adverse behavioral responses to environmental stress[24]

Protects from stress-induced decreases in norepinephrine levels[25]

Protects from stress-induced increases in blood pressure[15,22] 

Supports global mood[26]


Mucuna Pruriens, Phenylalanine, Phenylethylamine, Hordenine, Phosphatidylserine, Rhodiola Rosea, Vitamin C



[1] B.J. Jongkees, B. Hommel, S. Kühn, L.S. Colzato, J. Psychiatr. Res. 70 (2015) 50–57.
[2] G. Topall, H. Laborit, J. Pharm. Pharmacol. 41 (1989) 789–791.
[3] S.C. Daubner, T. Le, S. Wang, Arch. Biochem. Biophys. 508 (2011) 1–12.
[4] J.D. Fernstrom, M.H. Fernstrom, J. Nutr. 137 (2007) 1539S–1547S; discussion 1548S.
[5] S.Y. Tam, J.D. Elsworth, C.W. Bradberry, R.H. Roth, J. Neural Transm. Gen. Sect. 81 (1990) 97–110.
[6] R.J. Wurtman, F. Larin, S. Mostafapour, J.D. Fernstrom, Science 185 (1974) 183–184.
[7] M.C. Scally, I. Ulus, R.J. Wurtman, J. Neural Transm. 41 (1977) 1–6.
[8] J.D. Milner, R.J. Wurtman, Neurosci. Lett. 59 (1985) 215–220.
[9] M.J. During, I.N. Acworth, R.J. Wurtman, J. Neurochem. 52 (1989) 1449–1454.
[10] T. Oishi, R.J. Wurtman, J. Neural Transm. 53 (1982) 101–108.
[11] S.K. Yeghiayan, S. Luo, B. Shukitt-Hale, H.R. Lieberman, Physiol. Behav. 72 (2001) 311–316.
[12] C.J. Gibson, R.J. Wurtman, Life Sci. 22 (1978) 1399–1405.
[13] L.S. Colzato, B.J. Jongkees, R. Sellaro, B. Hommel, Front. Behav. Neurosci. 7 (2013) 200.
[14] R.A. Magill, W.F. Waters, G.A. Bray, J. Volaufova, S.R. Smith, H.R. Lieberman, N. McNevin, D.H. Ryan, Nutr. Neurosci. 6 (2003) 237–246.
[15] J.B. Deijen, J.F. Orlebeke, Brain Res. Bull. 33 (1994) 319–323.
[16] C.R. Mahoney, J. Castellani, F.M. Kramer, A. Young, H.R. Lieberman, Physiol. Behav. 92 (2007) 575–582.
[17] C. O’Brien, C. Mahoney, W.J. Tharion, I.V. Sils, J.W. Castellani, Physiol. Behav. 90 (2007) 301–307.
[18] D. Shurtleff, J.R. Thomas, J. Schrot, K. Kowalski, R. Harford, Pharmacol. Biochem. Behav. 47 (1994) 935–941.
[19] J.R. Thomas, P.A. Lockwood, A. Singh, P.A. Deuster, Pharmacol. Biochem. Behav. 64 (1999) 495–500.
[20] L. Steenbergen, R. Sellaro, B. Hommel, L.S. Colzato, Neuropsychologia 69 (2015) 50–55.
[21] L.S. Colzato, A.M. de Haan, B. Hommel, Psychol. Res. 79 (2015) 709–714.
[22] J.B. Deijen, C.J. Wientjes, H.F. Vullinghs, P.A. Cloin, J.J. Langefeld, Brain Res. Bull. 48 (1999) 203–209.
[23] L.S. Colzato, B.J. Jongkees, R. Sellaro, W.P.M. van den Wildenberg, B. Hommel, Neuropsychologia 62 (2014) 398–402.
[24] L.E. Banderet, H.R. Lieberman, Brain Res. Bull. 22 (1989) 759–762.
[25] H. Lehnert, D.K. Reinstein, B.W. Strowbridge, R.J. Wurtman, Brain Res. 303 (1984) 215–223.
[26] L.A. Palinkas, K.R. Reedy, M. Smith, M. Anghel, G.D. Steel, D. Reeves, D. Shurtleff, H.S. Case, N. Van Do, H.L. Reed, Int. J. Circumpolar Health 66 (2007) 401–417.



Betaine | Trimethylglycine | TMG | Glycine Betaine


Supports NAD metabolism *
Supports liver health *
Supports cardiovascular health *
Supports aspects of sports performance *
Supports neurotransmitter and melatonin synthesis *


Betaine was originally found in sugar beets (Beta vulgaris), which is the source of its name. Betaines are a group of structurally similar compounds. But because the first betaine discovered was trimethylglycine (the type of betaine found in sugar beets), betaine is commonly used as a synonym for trimethylglycine (TMG), though TMG is more specifically called glycine betaine (there can be non-glycine containing betaines but they are not typically used as dietary supplements). Betaine is an amino acid derivative (i.e., it falls into the protein category). It is found in some foods—in addition to beet roots, other good sources include quinoa, spinach, lamb and wheat brain. Betaine can also be made in the body from choline. This is thought to be a main metabolic fate of dietary choline. However, according to the National Institute of Health most adults don’t get the recommended amount of choline in their diet, so relying on choline (which is also needed to produce phosphatidylcholine for cell membranes and the neurotransmitter acetylcholine) to make betaine can be akin to the saying “Robbing Peter to pay Paul.” Betaine is an important cofactor in methylation, a process that occurs in cells where methyl groups (-CH3) are donated for other processes in the body. These processes include (1) synthesizing neurotransmitters such as dopamine and serotonin, (2) making melatonin and CoQ10, (3) methylation of DNA for epigenetics, (4) remethylation of homocysteine[1] (which has a key role in cardiovascular health[2]), and (5) influencing S-Adenosyl Methionine (SAMe) and folate levels (since they are actively involved in methylation). Betaine is thought to be the source of up to 60% of the methyl groups required for the methylation of homocysteine[3]. Strategies that boost NAD can decrease betaine[4,5] (NAD metabolites are methylated for elimination). Because of this, experts recommend supplementing betaine when strategies are used to boost NAD. Betaine has been largely used to support heart and liver function, but more recently has been receiving attention as a possible ergogenic (i.e., sports performance) and nootropic. Some biohackers use betaine to support sleep.


Betaine sourcing is focused on ensuring it is Non-GMO, gluten-free and vegan.


Betaine plays a central role in methylation and is involved in the synthesis of important neurotransmitters (dopamine and serotonin) and the neurohormone melatonin. It is also something that can be decreased when higher doses of niacin equivalent compounds are supplemented. For these reasons, it can play a role in a variety of different types of formulations. The dose of betaine used in a formulation will vary depending upon the purpose it is being used for. In general, Neurohacker Collective believes it’s prudent to supplement betaine (or a choline source) when niacin equivalents are used in amounts significantly greater than the daily value (DV) to ensure against unintended depletion. When used to ensure against depletion a general rule of thumb is that approximately 1mg of betaine can be used for each mg of niacin equivalent supplemented. When used for supporting homocysteine metabolism, heart or liver health, as a nootropic or ergogenic (i.e., not simply to ensure against depletion), or for supporting sleep, higher doses may be used. Doses above 1500 mg a day may increase cholesterol levels, so, even in these other applications, Neurohacker Collective believes in using a more moderate dose of betaine, combined with other supportive nutrients.


Homocysteine metabolism

Methylates homocysteine to produce the amino acid L-methionine[1]
Regulates the blood levels of homocysteine (a risk factor for cardiovascular disease)[6–8]

NAD metabolome

Supports the demand for methyl groups caused by the metabolism of niacin equivalents (e.g., niacin, niacinamide, nicotinamide riboside, NMN)[9]
Supports the production of hepatic S-adenosylmethionine[10–12]
Balances the reduction in hepatic levels of S-adenosylmethionine (SAMe) caused by the metabolism of niacin equivalents[9]

Mitochondrial function

Supports mitochondrial size/density/number[13]
Supports mitochondrial respiratory capacity[14,15]
Supports fatty acid oxidation[13,16]
Supports electron transport chain and oxidative phosphorylation performance[15,17,18]
Supports mitochondrial dynamics—upregulates mitochondrial fusion[19]
Supports mitochondrial membrane potential[15,17]
Supports mitochondrial antioxidant defenses[17]
Supports mitochondrial function[17,20]

Brain function

Supports memory[21–25]
Down-regulates the expression of GABA transaminase [21]
Supports betaine-GABA transporters [24,25]
Supports neuronal mitochondrial performance [14]
Supports brain phospholipid metabolism [16]
Supports brain antioxidant defenses [23,25–27]

Liver function

Supports hepatic fatty acid metabolism [10–13,18,28]
Supports liver protective functions [17,20]
Supports liver antioxidant defenses [20]


Supports resistance training performance [29–33]
Supports anabolic signaling [34]

Gastrointestinal function

Supports intestinal digestive enzymes[35]
Supports gut microbiota[35–39]

Cell function

Osmolyte—regulates cell hydration[40]


Choline — Supplementation with choline sources can increase betaine levels[41,42]
S-Adenosyl Methionine (SAMe)— Supplementation with betaine can increase SAMe levels[43]
Folic acid in regulating homocysteine levels[7]
Melatonin —appears to have synergies when combined for gut health[44,45]


[1] P.M. Ueland, J. Inherit. Metab. Dis. 34 (2011) 3–15.
[2] M. Lever, P.M. George, J.L. Elmslie, W. Atkinson, S. Slow, S.L. Molyneux, R.W. Troughton, A.M. Richards, C.M. Frampton, S.T. Chambers, PLoS One 7 (2012) e37883.
[3] H. Pellanda, Clin. Chem. Lab. Med. 51 (2013) 617–621.
[4] W.-P. Sun, M.-Z. Zhai, D. Li, Y. Zhou, N.-N. Chen, M. Guo, S.-S. Zhou, Clin. Nutr. 36 (2017) 1136–1142.
[5] Y.-J. Tian, D. Li, Q. Ma, X.-Y. Gu, M. Guo, Y.-Z. Lun, W.-P. Sun, X.-Y. Wang, Y. Cao, S.-S. Zhou, Sheng Li Xue Bao 65 (2013) 33–38.
[6] M.R. Olthof, T. van Vliet, E. Boelsma, P. Verhoef, J. Nutr. 133 (2003) 4135–4138.
[7] G. Alfthan, K. Tapani, K. Nissinen, J. Saarela, A. Aro, Br. J. Nutr. 92 (2004) 665–669.
[8] G.R. Steenge, P. Verhoef, M.B. Katan, J. Nutr. 133 (2003) 1291–1295.
[9] M.F. McCarty, Med. Hypotheses 55 (2000) 189–194.
[10] A.J. Barak, H.C. Beckenhauer, M. Junnila, D.J. Tuma, Alcohol. Clin. Exp. Res. 17 (1993) 552–555.
[11] A.J. Barak, H.C. Beckenhauer, S. Badakhsh, D.J. Tuma, Alcohol. Clin. Exp. Res. 21 (1997) 1100–1102.
[12] S. Mukherjee, TOTRANSMJ 3 (2011) 1–4.
[13] L. Zhang, Y. Qi, Z. ALuo, S. Liu, Z. Zhang, L. Zhou, Food Funct. 10 (2019) 216–223.
[14] N.K. Singhal, S. Li, E. Arning, K. Alkhayer, R. Clements, Z. Sarcyk, R.S. Dassanayake, N.E. Brasch, E.J. Freeman, T. Bottiglieri, J. McDonough, J. Neurosci. 35 (2015) 15170–15186.
[15] I. Lee, Biochem. Biophys. Res. Commun. 456 (2015) 621–625.
[16] N. Abu Ahmad, M. Raizman, N. Weizmann, B. Wasek, E. Arning, T. Bottiglieri, O. Tirosh, A.M. Troen, FASEB J. 33 (2019) 9334–9349.
[17] M.J. Khodayar, H. Kalantari, L. Khorsandi, M. Rashno, L. Zeidooni, Biomed. Pharmacother. 103 (2018) 1436–1445.
[18] K.K. Kharbanda, S.L. Todero, A.L. King, N.A. Osna, B.L. McVicker, D.J. Tuma, J.L. Wisecarver, S.M. Bailey, Int. J. Hepatol. 2012 (2012) 962183.
[19] M. Jung Kim, Anim Cells Syst (Seoul) 22 (2018) 289–298.
[20] R. Heidari, H. Niknahad, A. Sadeghi, H. Mohammadi, V. Ghanbarinejad, M.M. Ommati, A. Hosseini, N. Azarpira, F. Khodaei, O. Farshad, E. Rashidi, A. Siavashpour, A. Najibi, A. Ahmadi, A. Jamshidzadeh, Biomed. Pharmacother. 103 (2018) 75–86.
[21] K. Kunisawa, K. Kido, N. Nakashima, T. Matsukura, T. Nabeshima, M. Hiramatsu, Eur. J. Pharmacol. 796 (2017) 122–130.
[22] K. Kunisawa, N. Nakashima, M. Nagao, T. Nomura, S. Kinoshita, M. Hiramatsu, Behav. Brain Res. 292 (2015) 36–43.
[23] C. Nie, H. Nie, Y. Zhao, J. Wu, X. Zhang, Neurosci. Lett. 615 (2016) 9–14.
[24] M. Miwa, M. Tsuboi, Y. Noguchi, A. Enokishima, T. Nabeshima, M. Hiramatsu, J. Neuroinflammation 8 (2011) 153.
[25] D. Ibi, A. Tsuchihashi, T. Nomura, M. Hiramatsu, Eur. J. Pharmacol. 842 (2019) 57–63.
[26] M. Alirezaei, Z. Khoshdel, O. Dezfoulian, M. Rashidipour, V. Taghadosi, J. Physiol. Sci. 65 (2015) 243–252.
[27] M. Alirezaei, G. Jelodar, P. Niknam, Z. Ghayemi, S. Nazifi, J. Physiol. Biochem. 67 (2011) 605–612.
[28] M.F. Abdelmalek, S.O. Sanderson, P. Angulo, C. Soldevila-Pico, C. Liu, J. Peter, J. Keach, M. Cave, T. Chen, C.J. McClain, K.D. Lindor, Hepatology 50 (2009) 1818–1826.
[29] J.F. Trepanowski, T.M. Farney, C.G. McCarthy, B.K. Schilling, S.A. Craig, R.J. Bloomer, J. Strength Cond. Res. 25 (2011) 3461–3471.
[30] J.R. Hoffman, N.A. Ratamess, J. Kang, A.M. Gonzalez, N.A. Beller, S.A.S. Craig, J. Strength Cond. Res. 25 (2011) 2235–2241.
[31] J.R. Hoffman, N.A. Ratamess, J. Kang, S.L. Rashti, A.D. Faigenbaum, J. Int. Soc. Sports Nutr. 6 (2009) 7.
[32] E.C. Lee, C.M. Maresh, W.J. Kraemer, L.M. Yamamoto, D.L. Hatfield, B.L. Bailey, L.E. Armstrong, J.S. Volek, B.P. McDermott, S.A. Craig, J. Int. Soc. Sports Nutr. 7 (2010) 27.
[33] J.L. Pryor, S.A. Craig, T. Swensen, J. Int. Soc. Sports Nutr. 9 (2012) 12.
[34] J.M. Apicella, E.C. Lee, B.L. Bailey, C. Saenz, J.M. Anderson, S.A.S. Craig, W.J. Kraemer, J.S. Volek, C.M. Maresh, Eur. J. Appl. Physiol. 113 (2013) 793–802.
[35] H. Wang, S. Li, S. Fang, X. Yang, J. Feng, Nutrients 10 (2018).
[36] Y. Qu, K. Zhang, Y. Pu, L. Chang, S. Wang, Y. Tan, X. Wang, J. Zhang, T. Ohnishi, T. Yoshikawa, K. Hashimoto, J. Affect. Disord. 272 (2020) 66–76.
[37] F. Wang, J. Xu, I. Jakovlić, W.-M. Wang, Y.-H. Zhao, Food Funct. 10 (2019) 6675–6689.
[38] V.M. Koistinen, O. Kärkkäinen, K. Borewicz, I. Zarei, J. Jokkala, V. Micard, N. Rosa-Sibakov, S. Auriola, A.-M. Aura, H. Smidt, K. Hanhineva, Microbiome 7 (2019) 103.
[39] B.U. Metzler-Zebeli, A. Ratriyanto, D. Jezierny, N. Sauer, M. Eklund, R. Mosenthin, Arch. Anim. Nutr. 63 (2009) 427–441.
[40] M.B. Burg, J.D. Ferraris, J. Biol. Chem. 283 (2008) 7309–7313.
[41] L.M. Fischer, K.-A. da Costa, L. Kwock, J. Galanko, S.H. Zeisel, Am. J. Clin. Nutr. 92 (2010) 1113–1119.
[42] J.M.W. Wallace, J.M. McCormack, H. McNulty, P.M. Walsh, P.J. Robson, M.P. Bonham, M.E. Duffy, M. Ward, A.M. Molloy, J.M. Scott, P.M. Ueland, J.J. Strain, Br. J. Nutr. 108 (2012) 1264–1271.
[43] R. Deminice, R.P. da Silva, S.G. Lamarre, K.B. Kelly, R.L. Jacobs, M.E. Brosnan, J.T. Brosnan, Amino Acids 47 (2015) 839–846.
[44] M.R. Werbach, Altern. Ther. Health Med. 14 (2008) 54–58.
[45] R. de S. Pereira, J. Pineal Res. 41 (2006) 195–200.


L-Tryptophan Common Name


Top Benefits of L-Tryptophan

  • Supports cell energy generation*
  • Supports healthy aging*
  • Supports healthy sleep and body clock function*
  • Supports prosocial behaviors*

What is L-Tryptophan?

L-Tryptophan is an essential amino acid. The body cannot synthesize it: it must be obtained from the diet. It functions as a metabolic precursor (i.e., substrate) for the synthesis of nicotinamide adenine dinucleotide (NAD), an important coenzyme found in all living cells—NAD is used for mitochondrial energy production and activation of the important sirtuin healthspan pathways. NAD can be made by any molecule which contains a niacin or nicotinamide (vitamin B3) molecule. L-Tryptophan is unique because it’s the only other way to build NAD that doesn’t start from vitamin B3. L-Tryptophan is also the precursor for the synthesis of the neurotransmitter serotonin and the neurohormone melatonin, which regulates sleep-wake cycles and nighttime body clock functions. In addition to these three main molecules, L-tryptophan is involved in making many other important intermediate molecules. Giving extra L-tryptophan allows the body to use it where it is needed most … at that time and over the next 12-16 hours. In general, giving extra L-tryptophan with breakfast supports both daytime mood (presumably via supporting serotonin function) and nightly sleep (presumably via supporting melatonin function). Giving some extra L-tryptophan also helps support body clock, orienting many of it’s daytime functions earlier in the day. L-tryptophan supplementation may support prosocial behaviors. Low-to-modest doses of L-tryptophan prior to bed may support healthier sleep cycles.

Neurohacker’s L-Tryptophan Sourcing

L-Tryptophan is used as a precursor (i.e., substrate) by the body to make NAD, serotonin, and melatonin. Our main reason for including it in a formulation would be to support biosynthesis of one or more of these important molecules.

In general, L-tryptophan is additive with other strategies for making NAD (such as the non-flushing form (niacinamide) and flushing form (niacin) of vitamin B3, so it can be useful to stack the two together in formulations.

L-Tryptophan sourcing is focused on identifying and purchasing from a reputable supplier and ensuring it is NON-GMO, gluten-free and vegan.

L-Tryptophan Dosing Principles and Rationale

L-Tryptophan is generally considered to be dose-dependent (see Neurohacker Dosing Principles) in the range it’s commonly dosed (between several hundred mg to several grams or more a day). It’s been estimated that an average adult diet provides about 800-1000 mg/day of L-tryptophan. In studies that have looked at augmenting the breakfast meal with L-tryptophan, amounts less than the amount in an average diet have been sufficient to produce positive subjective responses during the day, with sleep that night, and with overall body clock function. When taken prior to bed, a dose close to ¼ the daily average intake has been sufficient to support healthier deep sleep. These studies are consistent with L-tryptophan supplementation supporting healthier function when given in amounts that are less than what would be found in an average diet. 

L-Tryptophan Key Mechanisms

NAD(P) synthesis

  • L-tryptophan is a substrate in the de novo NAD+ synthesis pathway via the kynurenine pathway (KP)[1]
  • NAD+ can be converted to the coenzyme NADP+ by the enzyme NAD kinase[2]
  • NAD(H) and NADP(H) are key molecules in essential redox pathways of cellular metabolism and energy production[3]
  • NAD(H) is essential for the production of ATP through the citric acid cycle and oxidative phosphorylation[3]
  • NADP(H) is essential in many anabolic metabolic reactions, including DNA and RNA synthesis[3]
  • NADP(H) is a cofactor for some cytochrome P450 enzymes that detoxify xenobiotics[4]
  • NADPH also acts as a cofactor for glutathione reductase, the enzyme used to maintain reduced glutathione (GSH) levels[3]
  • NAD(H) and NADP(H) are essential for healthy aging[3]

Brain function

  • L-tryptophan is a precursor for serotonin (a neurotransmitter) and melatonin (a neurohormone) synthesis[5]
  • Upregulates the rate of serotonin synthesis[6,7]
  • Promotes social behavior[8,9]

Exercise performance (ergogenic effect)

  • Supports power output[10,11]
  • Delays time to exertion[10,11]

Social Cognition

  • Supports healthier social interactions[12–14]
  • Promotes charitable behaviors[15]


  • Nicotinic acid (niacin) and nicotinamide (niacinamide) as substrates for NAD synthesis. 


[1] A. A.-B. Badawy, Int. J. Tryptophan Res. 10, 1178646917691938 (2017).
[2] G. Magni et al., Cell. Mol. Life Sci. 61, 19–34 (2004).
[3] W. Ying, Antioxid. Redox Signal. 10, 179–206 (2008).
[4] D. S. Riddick et al., Drug Metab. Dispos. 41, 12–23 (2013).
[5] L. Palego, L. Betti, A. Rossi, G. Giannaccini, J. Amino Acids. 2016, 8952520 (2016).
[6] J. D. Fernstrom, Physiol. Rev. 63, 484–546 (1983).
[7] J. D. Fernstrom, J. Nutr. Biochem. 1, 508–517 (1990).
[8] L. Steenbergen, B. J. Jongkees, R. Sellaro, L. S. Colzato, Neurosci. Biobehav. Rev. 64, 346–358 (2016).
[9] S. N. Young, Philos. Trans. R. Soc. Lond. B Biol. Sci. 368, 20110375 (2013).
[10] C. Javierre, R. Segura, J. L. Ventura, A. Suárez, J. M. Rosés, Int. J. Neurosci. 120, 319–327 (2010).
[11] R. Segura, J. L. Ventura, Int. J. Sports Med. 9, 301–305 (1988).
[12] D.S. Moskowitz, G. Pinard, D.C. Zuroff, L. Annable, S.N. Young, Neuropsychopharmacology. 25, 277–289 (2001).
[13] A. Nantel-Vivier, R.O. Pihl, S.N. Young, S. Parent, S.A. Bélanger, R. Sutton, M.-E. Dubois, R.E. Tremblay, J.R. Séguin, PLoS One. 6 (2011) e20304.
[14] K. Hogenelst, R.A. Schoevers, M. Aan Het Rot, Int. J. Neuropsychopharmacol. 18 (2015).
[15] L. Steenbergen, R. Sellaro, L.S. Colzato, Front. Psychol. 5, 1451 (2014).


Scientific Name:
2-aminoethanesulphonic acid




Supports brain function *

Supports cognitive function *

Supports mood *

Supports antioxidant defenses *

Supports cardiovascular function *


Taurine is an organic amino sulfonic acid naturally produced in our body.  It has nootropic and neuroprotective actions and can improve memory and has anxiolytic effects.


Brain function

Supports synaptic long-term potentiation 1

Modulates GABAergic neurotransmission 2–5

Modulates glycinergic neurotransmission 6

Upregulates BDNF production 5

Cognitive function

Supports short-term memory 5


Supports mood 6–9

Antioxidant defenses

Downregulates reactive oxygen species (ROS) production 10

Downregulates ROS by supporting mitochondrial protein synthesis 11,12

Upregulates antioxidant defenses 13–16

Protects tissues from oxidative damage 8,16–18

Cardiovascular function

Protects vascular endothelial cells 8,19

Protects cardiac muscle cells 17,18

Supports the generation of new blood vessels (angiogenesis) 20

Supports healthy blood flow 19


Supports healthy insulin sensitivity and glucose metabolism 13,21,22



1. del Olmo N, Suárez LM, Orensanz LM, et al. Role of taurine uptake on the induction of long-term synaptic potentiation. Eur J Neurosci. 2004;19(7):1875-1886. doi:10.1111/j.1460-9568.2004.03309.x

2. Kuriyama K, Hashimoto T. Interrelationship between Taurine and GABA. In: Schaffer S, Lombardini JB, Huxtable RJ, eds. Taurine 3: Cellular and Regulatory Mechanisms. Boston, MA: Springer US; 1998:329-337. doi:10.1007/978-1-4899-0117-0_41

3. Bureau MH, Olsen RW. Taurine acts on a subclass of GABAA receptors in mammalian brain in vitro. Eur J Pharmacol. 1991;207(1):9-16. doi:10.1016/S0922-4106(05)80031-8

4. Kontro P, Oja SS. Interactions of taurine with GABAB binding sites in mouse brain. Neuropharmacology. 1990;29(3):243-247.

5. Caletti G, Almeida FB, Agnes G, Nin MS, Barros HMT, Gomez R. Antidepressant dose of taurine increases mRNA expression of GABAA receptor α2 subunit and BDNF in the hippocampus of diabetic rats. Behav Brain Res. 2015;283:11-15. doi:10.1016/j.bbr.2015.01.018

6. Zhang CG, Kim S-J. Taurine induces anti-anxiety by activating strychnine-sensitive glycine receptor in vivo. Ann Nutr Metab. 2007;51(4):379-386. doi:10.1159/000107687

7. Iio W, Matsukawa N, Tsukahara T, Toyoda A. The effects of oral taurine administration on behavior and hippocampal signal transduction in rats. Amino Acids. 2012;43(5):2037-2046. doi:10.1007/s00726-012-1282-2

8. Caletti G, Olguins DB, Pedrollo EF, Barros HMT, Gomez R. Antidepressant effect of taurine in diabetic rats. Amino Acids. 2012;43(4):1525-1533. doi:10.1007/s00726-012-1226-x

9. Toyoda A, Iio W. Antidepressant-like effect of chronic taurine administration and its hippocampal signal transduction in rats. Adv Exp Med Biol. 2013;775:29-43. doi:10.1007/978-1-4614-6130-2_3

10. Wu QD, Wang JH, Fennessy F, Redmond HP, Bouchier-Hayes D. Taurine prevents high-glucose-induced human vascular endothelial cell apoptosis. Am J Physiol. 1999;277(6):C1229-C1238. doi:10.1152/ajpcell.1999.277.6.C1229

11. Jong CJ, Azuma J, Schaffer S. Mechanism underlying the antioxidant activity of taurine: prevention of mitochondrial oxidant production. Amino Acids. 2012;42(6):2223-2232. doi:10.1007/s00726-011-0962-7

12. Schaffer SW, Azuma J, Mozaffari M. Role of antioxidant activity of taurine in diabetes. Can J Physiol Pharmacol. 2009;87(2):91-99. doi:10.1139/Y08-110

13. Nandhini ATA, Thirunavukkarasu V, Ravichandran MK, Anuradha CV. Effect of taurine on biomarkers of oxidative stress in tissues of fructose-fed insulin-resistant rats. Singapore Med J. 2005;46(2):82-87.

14. Devamanoharan PS, Ali AH, Varma SD. Oxidative stress to rat lens in vitro: protection by taurine. Free Radic Res. 1998;29(3):189-195.

15. Guz G, Oz E, Lortlar N, et al. The effect of taurine on renal ischemia/reperfusion injury. Amino Acids. 2007;32(3):405-411. doi:10.1007/s00726-006-0383-1

16. Tabassum H, Parvez S, Rehman H, Dev Banerjee B, Siemen D, Raisuddin S. Nephrotoxicity and its prevention by taurine in tamoxifen induced oxidative stress in mice. Hum Exp Toxicol. 2007;26(6):509-518. doi:10.1177/0960327107072392

17. Hanna J, Chahine R, Aftimos G, et al. Protective effect of taurine against free radicals damage in the rat myocardium. Exp Toxicol Pathol. 2004;56(3):189-194. doi:10.1016/j.etp.2004.08.004

18. Kingston R, Kelly CJ, Murray P. The therapeutic role of taurine in ischaemia-reperfusion injury. Curr Pharm Des. 2004;10(19):2401-2410.

19. Moloney MA, Casey RG, O’Donnell DH, Fitzgerald P, Thompson C, Bouchier-Hayes DJ. Two weeks taurine supplementation reverses endothelial dysfunction in young male type 1 diabetics. Diab Vasc Dis Res. 2010;7(4):300-310. doi:10.1177/1479164110375971

20. Baek Y-Y, Cho DH, Choe J, et al. Extracellular taurine induces angiogenesis by activating ERK-, Akt-, and FAK-dependent signal pathways. Eur J Pharmacol. 2012;674(2-3):188-199. doi:10.1016/j.ejphar.2011.11.022

21. Nandhini ATA, Thirunavukkarasu V, Anuradha CV. Taurine modifies insulin signaling enzymes in the fructose-fed insulin resistant rats. Diabetes Metab. 2005;31(4 Pt 1):337-344.

22. Nandhini ATA, Anuradha CV. Taurine modulates kallikrein activity and glucose metabolism in insulin resistant rats. Amino Acids. 2002;22(1):27-38.


L-carnitine Common Name


Top Benefits of L-carnitine

  • Supports mitochondrial function*
  • Supports healthy metabolism of fats*
  • Supports healthy heart function*
  • Supports healthy aging*

What is L-carnitine?

L-carnitine is an important molecule because it’s needed to convert fat into energy. The name carnitine is derived from Latin “carnus” (flesh), because it was originally found in meat extracts. Animal products such as meat, poultry, fish, and milk are the best food sources, with redder meats tending to have higher levels of L-carnitine. Adults eating animal products consume about 60–180 milligrams of carnitine per day.[1] The human body can make carnitine from lysine using other micronutrients as cofactors. Adults eating a variety of animal products get about 75% of the daily carnitine needs filled from the diet, so only need to make about 25% of what they use.[2] Vegans get noticeably less (about 10–12 milligrams),[1] with vegetarians getting a bit more than vegans because of eating dairy products. In both cases, because the diet is limited in L-carnitine, they may need to make as much as 90% of their daily needs.[2] While the human body can make carnitine from lysine, it may not always be able to make sufficient amounts to meet demands. This has led to it being thought of as a “conditionally essential” nutrient. L-carnitine’s most important role is in mitochondrial fat metabolism—it is used to transport long-chain fatty acids across the mitochondrial membrane for breakdown by mitochondrial β-oxidation. This transportation function allows fats and oils from our diet to be used for energy production and enhances mitochondria potential to burn fat. This function is especially important in tissues and organs that use a lot of fat as an energy source, including the heart and skeletal muscles. 

Neurohacker’s L-carnitine Sourcing

L-Carnitine is used by the body to transport long-chain fatty acids (fats) so they can be broken down and used to make cellular energy (ATP).

In general, L-carnitine is additive with other strategies used for supporting mitochondrial function (i.e., mitochondrial nutrients like CoQ10 and lipoic acid).

Carnitine can also be supplemented as acetyl-L-carnitine (ALCAR). While both ALCAR and L-carnitine support the same functions, in general, the ALCAR form tends to be used in research more for brain and nervous system support, while the L-carnitine form has been researched more for supporting heart and skeletal muscles. But both forms support all tissues.

L-carnitine sourcing is focused on ensuring it is NON-GMO, gluten-free and vegan.

L-carnitine Dosing Principles and Rationale

L-carnitine is generally considered to be dose-dependent (see Neurohacker Dosing Principles) in the range it’s commonly dosed (between 500 mg to several grams a day). These higher supplemental doses are pharmacological (i.e., substantially higher than what the body gets from the diet and makes daily), while a lower dose would be more physiological. We opted for a dose slightly higher than the daily physiological amount, because, like most nutrients, L-carnitine isn’t perfectly absorbed. 

L-carnitine Key Mechanisms

Mitochondrial function and structure

  • Supports fatty acid β-oxidation[3]
  • Protects from mitochondrial dysfunction[4]
  • Promotes the production of ATP[5]
  • Supports mitochondrial structure[5]


  • Supports healthy insulin sensitivity[6–8]
  • Downregulates fat accumulation and blood / liver lipid levels[5]

Healthy aging and protective effects

  • Downregulates oxidative stress and reactive oxygen species production[4,9]
  • Protects against neurotoxic agents[4]
  • Supports cardiovascular function[10–12]
  • Supports liver function[5]
  • Upregulates telomerase activity and telomere length[13,14]
  • Delays aging of mesenchymal stem cells[13–15]


  • Lipoic acid – support  mitochondrial function[16]
  • Creatine and L-leucine – support muscle function and structure[17]


[1] C. J. Rebouche, Ann. N. Y. Acad. Sci. 1033, 30–41 (2004).
[2] C. J. Rebouche, The FASEB Journal. 6, 3379–3386 (1992).
[3] D. W. Foster, Ann. N. Y. Acad. Sci. 1033, 1–16 (2004).
[4] D. Elinos-Calderón et al., Exp. Brain Res. 197, 287–296 (2009).
[5] K. Kon et al., Hepatol. Res. 47, E44–E54 (2017).
[6] M. Malaguarnera et al., Am. J. Gastroenterol. 105, 1338–1345 (2010).
[7] A. Molfino et al., JPEN J. Parenter. Enteral Nutr. 34, 295–299 (2010).
[8] B. Capaldo, R. Napoli, P. Di Bonito, G. Albano, L. Saccà, Diabetes Res. Clin. Pract. 14, 191–195 (1991).
[9] G. Guerreiro et al., J. Cell. Biochem. (2018), doi:10.1002/jcb.27332.
[10] J. J. DiNicolantonio, C. J. Lavie, H. Fares, A. R. Menezes, J. H. O’Keefe, Mayo Clin. Proc. 88, 544–551 (2013).
[11] Y. Suzuki, M. Narita, N. Yamazaki, Jpn. Heart J. 23, 349–359 (1982).
[12] A. Kobayashi, Y. Masumura, N. Yamazaki, Jpn. Circ. J. 56, 86–94 (1992).
[13] R. Farahzadi, E. Fathi, S. A. Mesbah-Namin, N. Zarghami, Tissue Cell. 54, 105–113 (2018).
[14] R. Farahzadi, S. A. Mesbah-Namin, N. Zarghami, E. Fathi, Int J Stem Cells. 9, 107–114 (2016).
[15] H. Mobarak, E. Fathi, R. Farahzadi, N. Zarghami, S. Javanmardi, Vet. Res. Commun. 41, 41–47 (2017).
[16] S. Savitha, K. Sivarajan, D. Haripriya, V. Kokilavani, C. Panneerselvam, Clin. Nutr. 24, 794–800 (2005).
[17] M. Evans et al., Nutr. Metab. . 14, 7 (2017).


N-acetylcysteine Common Name

N-acetylcysteine | acetylcysteine | NAC

Top Benefits of N-acetylcysteine

  • Supports the production of glutathione*
  • Upregulates antioxidant defenses*
  • Supports liver detoxification*
  • Supports healthy immune function*
  • Supports healthy gut microbiota*

What is N-acetylcysteine?

N-acetylcysteine (NAC), a sulfur-containing amino acid, is the acetylated form of L-cysteine. The acetylation increases bioavailability compared to cysteine. NAC increases body stores of L-cysteine, which, along with glutamine and glycine, is used to make an important detoxification and antioxidant molecule called “glutathione.”[1] This ability to support production of glutathione is NAC’s main mechanism of action.[2] L-cysteine availability limits the rate of glutathione production (it is thought to be rate-limiting).[3] Supplying NAC allows the body to restore intracellular glutathione levels when demand has been increased or under circumstances when it is lower (such as older age or increased toxin exposure) in tissues throughout the body (including the brain, liver, and muscles). The combination of NAC and glycine appears to be additive,[4,5] which makes sense since both are used in glutathione production. NAC promotes glutathione-related antioxidant defenses, which helps protect cells and mitochondria against free radicals, cell membrane damage, damage from metals and toxins, and other oxidative stress-related and aging issues. 

Neurohacker’s N-acetylcysteine Sourcing

NAC is used as a precursor (i.e., substrate) by the body to make glutathione. It’s this mechanism that’s our reason for including it.

In general, NAC is additive with glycine (another glutathione substrate), so it can be useful to stack the two together in formulations.

NAC sourcing is focused on identifying and purchasing from a reputable supplier and ensuring it is NON-GMO, gluten-free and vegan.

N-acetylcysteine Dosing Principles and Rationale

NAC is generally considered to be dose-dependent (see Neurohacker Dosing Principles) in the range it’s commonly dosed (between 400-2400 mg a day). But, side-effects of NAC also go up with higher doses. Since our use is solely to augment the supply of molecular precursors to make glutathione, and not to use NAC as part of a clinical treatment protocol, we opted to use a very low dose, primarily to gain some benefits of having a glutathione precursor (if it’s needed) while being at a dose that’s sufficiently low enough to minimize the risk of producing unwanted effects.

N-acetylcysteine Key Mechanisms

Antioxidant defenses

  • Upregulates glutathione levels in the plasma[6]
  • Upregulates glutathione levels in red blood cells[7]
  • Crosses the blood brain barrier and upregulates glutathione levels in the brain[6,8,9]

Mitochondrial function

  • Protects from mitochondrial dysfunction[10]
  • Supports mitochondrial biogenesis[11]
  • Supports mitophagy (mitochondrial autophagy)[12]

Brain function

  • Supports neuroprotection (secondary to boosting glutathione and antioxidant defenses)[13,14]
  • Protects auditory system from fatigue and noise-induced hearing loss[15–18]

Immune system and cell signaling

  • Supports balanced immune mechanisms and cell signaling[19,20]
  • Protects from age-related cellular responses and immune function declines (immunosenescence)[19,21–23]

Gut microbiota

  • Downregulates gut oxidative stress[24–26]
  • Regulates the composition of the gut microbiota[24,26]
  • Regulates gut microbial metabolism[24,25]
  • Supports gut barrier function[24]


[1] G. Wu, Y.-Z. Fang, S. Yang, J. R. Lupton, N. D. Turner, J. Nutr. 134, 489–492 (2004).
[2] K. R. Atkuri, J. J. Mantovani, L. A. Herzenberg, L. A. Herzenberg, Curr. Opin. Pharmacol. 7, 355–359 (2007).
[3] S. C. Lu, Biochim. Biophys. Acta. 1830, 3143–3153 (2013).
[4] S. Xie, W. Zhou, L. Tian, J. Niu, Y. Liu, Fish Shellfish Immunol. 55, 233–241 (2016).
[5] K. A. Cieslik et al., J. Gerontol. A Biol. Sci. Med. Sci. 73, 1167–1177 (2018).
[6] M. J. Holmay et al., Clin. Neuropharmacol. 36, 103–106 (2013).
[7] S. Kasperczyk, M. Dobrakowski, A. Kasperczyk, A. Ostałowska, E. Birkner, Clin. Toxicol. . 51, 480–486 (2013).
[8] S. A. Farr et al., J. Neurochem. 84, 1173–1183 (2003).
[9] O. M. Dean et al., Neurosci. Lett. 499, 149–153 (2011).
[10] O. E. Aparicio-Trejo et al., Free Radic. Biol. Med. 130, 379–396 (2018).
[11] W.-C. Lee, L.-C. Li, J.-B. Chen, H.-W. Chang, ScientificWorldJournal. 2015, 620826 (2015).
[12] V. S. Van Laar et al., Neurobiol. Dis. 74, 180–193 (2015).
[13] M. Günther et al., J. Clin. Neurosci. 22, 1477–1483 (2015).
[14] E. Olakowska, W. Marcol, A. Właszczuk, I. Woszczycka-Korczyńska, J. Lewin-Kowalik, Adv. Clin. Exp. Med. 26, 1329–1334 (2017).
[15] C.-Y. Lin et al., Hear. Res. 269, 42–47 (2010).
[16] A.-C. Lindblad, U. Rosenhall, A. Olofsson, B. Hagerman, Noise Health. 13, 392–401 (2011).
[17] M. E. Hoffer, C. Balaban, M. D. Slade, J. W. Tsao, B. Hoffer, PLoS One. 8, e54163 (2013).
[18] R. Kopke et al., Hear. Res. 323, 40–50 (2015).
[19] L. Arranz, C. Fernández, A. Rodríguez, J. M. Ribera, M. De la Fuente, Free Radic. Biol. Med. 45, 1252–1262 (2008).
[20] A. Perl et al., Metabolomics. 11, 1157–1174 (2015).
[21] B. Purwanto, D. H. Prasetyo, Acta Med. Indones. 44, 140–144 (2012).
[22] F. Saddadi, S. Alatab, F. Pasha, M. R. Ganji, T. Soleimanian, Saudi J. Kidney Dis. Transpl. 25, 66 (2014).
[23] A. Jeremias et al., Heart Int. 4, e7 (2009).
[24] J. Zheng et al., J. Diabetes (2018), doi:10.1111/1753-0407.12795.
[25] C. Wan et al., OMICS. 21, 540–549 (2017).
[26] C. C. Xu et al., J. Anim. Sci. 92, 1504–1511 (2014).


Scientific Name:


L-Theanine | L-γ-Glutamylethylamide | 5-N-Ethyl-Glutamine


  • Supports cognitive function*
  • Supports relaxed mood*
  • Supports stress resilience*
  • Supports sleep*
  • Supports general immune health*


L-theanine is a calming amino acid that naturally occurs in green tea. It is used as a nootropic because it supports focused attention, mental alertness, and a calm, relaxed sense of mental energy. L-theanine is often used with caffeine in nootropic stacks, because the combination supports task switching, accuracy, and focus. L-theanine promotes alpha brain waves (α-waves), which are thought of as a marker of relaxation[1]. This brain state also reduces the perception of stress. L-theanine has a few other lesser known functional actions. L-theanine can be broken down into glutamate, which is a building block for glutamatergic signaling (i.e., the glutamate-GABA pathway) and for glutathione, an antioxidant used for detoxification. And L-theanine, because of another metabolite, primes specialized immune cells—gamma delta T cells—that help the immune system respond more efficiently to new antigens and have enhanced immune memory.* The best dietary sources of L-theanine are green and black tea (made from Camellia sinensis): L-theanine comprises up to 50% of total amino acids in tea leaves.


L-theanine is non-GMO, gluten-free, and vegan.


L-theanine has been studied clinically over a fairly wide range of doses, with the most common range being 100-400 mg. Evidence suggests a threshold response (see Neurohacker Dosing Principles) when L-theanine is given by itself (i.e., the best responses occur when it’s dosed within a range as opposed to more being better). That said, the dose of L-theanine used in a Neurohacker formulation can vary significantly depending upon what other ingredients it’s combined with and the intent of the formulation. Neurohacker looks for additive or synergistic ingredient combinations. In some cases, ingredients tend to be most complimentary when used at certain ratios. L-theanine falls into this category. As an example, when used as part of a nootropic formula combined with a source of caffeine, L-theanine might be dosed to provide about double the dose of caffeine and/or theobromine (i.e., ~2:1 ratio). But when used in combination with GABA before bedtime for supporting sleep, it might be dosed at as little as 20% of the GABA dose (i.e., 1:5 ratio). Following an oral dose, the amount of L-theanine in the brain increase within the first hour (i.e., it’s able to cross the blood-brain barrier,[2] so in general, L-Theanine has fairly quick onset and is often experienced within 30-45 minutes of taking it. 


Brain function

Supports attention[3–5]

Supports memory[4–7]

Supports learning[8]

Supports executive function[4,9]

Supports faster reaction times[3]

Supports alpha (α) brain waves (α-waves are associated with relaxation, selective attention, and mental alertness)[1,3,10–13]

Supports hippocampal activity[14]

Supports dopamine signaling[15–21]

Supports serotonin signaling[21]

Supports GABA levels in the brain[21]

Binds to glutamate receptors (with low affinity)[22–24]

Supports hippocampal neurogenesis [6]

Supports brain-derived neurotrophic factor (BDNF)[6,24,25] 

Supports neuroprotective functions[7,8,26–28]

Mood and stress

Supports a calm/relaxed mood[4,8,9,13,14,29–32]

Supports a positive mental-emotional bias[4,9]

Modulates psychological and physiological stress responses[33]

Supports healthy behavioral and cognitive responses to stress[26,34]

Reduces fight or flight nervous system activity (i.e., promotes relaxation response)[33]


Supports sleep efficiency and quality[4,9,35,36]

Counters some of caffeine’s effects on deep sleep[37]


Supports innate immunity[38–40]

Supports adaptive immunity[38,40,41]

Supports gamma delta T cell function[42,43]

Modulates immune signaling[38,44]

Gastrointestinal function

Supports gut microbiota[45]

Supports amino acid absorption[46]

Healthy aging and longevity

Pro-longevity (Caenorhabditis elegans)[47]


Caffeine in cognitive performance[48–51]

GABA for supporting sleep quality[52]

L-Cysteine in support of general immune health[53–59]

Green tea extracts in support of general immune health[60,61]


[1] L.R. Juneja, D.-C. Chu, T. Okubo, Y. Nagato, H. Yokogoshi, Trends Food Sci. Technol. 10 (1999) 199–204.
[2] T. Terashima, J. Takido, H. Yokogoshi, Biosci. Biotechnol. Biochem. 63 (1999) 615–618.
[3] A. Higashiyama, H.H. Htay, M. Ozeki, L.R. Juneja, M.P. Kapoor, J. Funct. Foods 3 (2011) 171–178.
[4] S. Hidese, M. Ota, C. Wakabayashi, T. Noda, H. Ozawa, T. Okubo, H. Kunugi, Acta Neuropsychiatr. 29 (2017) 72–79.
[5] S.-K. Park, I.-C. Jung, W.K. Lee, Y.S. Lee, H.K. Park, H.J. Go, K. Kim, N.K. Lim, J.T. Hong, S.Y. Ly, S.S. Rho, J. Med. Food 14 (2011) 334–343.
[6] A. Takeda, K. Sakamoto, H. Tamano, K. Fukura, N. Inui, S.W. Suh, S.-J. Won, H. Yokogoshi, Cell. Mol. Neurobiol. 31 (2011) 1079–1088.
[7] T.I. Kim, Y.K. Lee, S.G. Park, I.S. Choi, J.O. Ban, H.K. Park, S.-Y. Nam, Y.W. Yun, S.B. Han, K.W. Oh, J.T. Hong, Free Radic. Biol. Med. 47 (2009) 1601–1610.
[8] K. Unno, K. Fujitani, N. Takamori, F. Takabayashi, K.-I. Maeda, H. Miyazaki, N. Tanida, K. Iguchi, K. Shimoi, M. Hoshino, Free Radic. Res. 45 (2011) 966–974.
[9] S. Hidese, S. Ogawa, M. Ota, I. Ishida, Z. Yasukawa, M. Ozeki, H. Kunugi, Nutrients 11 (2019).
[10] C.H. Song, J.H. Jung, J.S. Oh, K.S. Kim, Korean Journal of Nutrition 36 (2003) 918–923.
[11] M. Gomez-Ramirez, B.A. Higgins, J.A. Rycroft, G.N. Owen, J. Mahoney, M. Shpaner, J.J. Foxe, Clin. Neuropharmacol. 30 (2007) 25–38.
[12] A.C. Nobre, A. Rao, G.N. Owen, Asia Pac. J. Clin. Nutr. 17 Suppl 1 (2008) 167–168.
[13] D.J. White, S. de Klerk, W. Woods, S. Gondalia, C. Noonan, A.B. Scholey, Nutrients 8 (2016).
[14] S. Ogawa, M. Ota, J. Ogura, K. Kato, H. Kunugi, Psychopharmacology 235 (2018) 37–45.
[15] H. Yokogoshi, M. Kobayashi, M. Mochizuki, T. Terashima, Neurochem. Res. 23 (1998) 667–673.
[16] T. Yamada, T. Terashima, T. Okubo, L.R. Juneja, H. Yokogoshi, Nutr. Neurosci. 8 (2005) 219–226.
[17] T. Yamada, T. Terashima, S. Kawano, R. Furuno, T. Okubo, L.R. Juneja, H. Yokogoshi, Amino Acids 36 (2009) 21–27.
[18] J. Yao, X.-N. Shen, H. Shen, M. Wu, Zhonghua Yu Fang Yi Xue Za Zhi 46 (2012) 635–639.
[19] M. Shen, Y. Yang, Y. Wu, B. Zhang, H. Wu, L. Wang, H. Tang, J. Chen, Phytotherapy Research 33 (2019) 412–421.
[20] G. Zhu, S. Yang, Z. Xie, X. Wan, Neuropharmacology 138 (2018) 331–340.
[21] P.J. Nathan, K. Lu, M. Gray, C. Oliver, J. Herb. Pharmacother. 6 (2006) 21–30.
[22] H. Yokogoshi, M. Kobayashi, M. Mochizuki, T. Terashima, Neurochemical Research 23 (1998) 667–673.
[23] T. Kakuda, A. Nozawa, A. Sugimoto, H. Niino, Biosci. Biotechnol. Biochem. 66 (2002) 2683–2686.
[24] C. Wakabayashi, T. Numakawa, M. Ninomiya, S. Chiba, H. Kunugi, Psychopharmacology 219 (2012) 1099–1109.
[25] C. Miodownik, R. Maayan, Y. Ratner, V. Lerner, L. Pintov, M. Mar, A. Weizman, M.S. Ritsner, Clin. Neuropharmacol. 34 (2011) 155–160.
[26] X. Tian, L. Sun, L. Gou, X. Ling, Y. Feng, L. Wang, X. Yin, Y. Liu, Brain Res. 1503 (2013) 24–32.
[27] T. Sumathi, D. Asha, G. Nagarajan, A. Sreenivas, R. Nivedha, Environ. Toxicol. Pharmacol. 42 (2016) 99–117.
[28] M. Takeshima, I. Miyazaki, S. Murakami, T. Kita, M. Asanuma, J. Clin. Biochem. Nutr. 59 (2016) 93–99.
[29] K. Lu, M.A. Gray, C. Oliver, D.T. Liley, B.J. Harrison, C.F. Bartholomeusz, K.L. Phan, P.J. Nathan, Human Psychopharmacology: Clinical and Experimental 19 (2004) 457–465.
[30] M.S. Ritsner, C. Miodownik, Y. Ratner, T. Shleifer, M. Mar, L. Pintov, V. Lerner, J. Clin. Psychiatry 72 (2011) 34–42.
[31] K. Unno, N. Tanida, N. Ishii, H. Yamamoto, K. Iguchi, M. Hoshino, A. Takeda, H. Ozawa, T. Ohkubo, L.R. Juneja, H. Yamada, Pharmacol. Biochem. Behav. 111 (2013) 128–135.
[32] A. Yoto, M. Motoki, S. Murao, H. Yokogoshi, J. Physiol. Anthropol. 31 (2012) 28.
[33] K. Kimura, M. Ozeki, L.R. Juneja, H. Ohira, Biol. Psychol. 74 (2007) 39–45.
[34] H. Tamano, K. Fukura, M. Suzuki, K. Sakamoto, H. Yokogoshi, A. Takeda, Brain Res. Bull. 95 (2013) 1–6.
[35] M. Ozeki, L.R. Juneja, S. Shirakawa, J. Physiol. Anthropol. 23 (2004) 58.
[36] M.R. Lyon, M.P. Kapoor, L.R. Juneja, Altern. Med. Rev. 16 (2011) 348–354.
[37] H.-S. Jang, J.Y. Jung, I.-S. Jang, K.-H. Jang, S.-H. Kim, J.-H. Ha, K. Suk, M.-G. Lee, Pharmacology Biochemistry and Behavior 101 (2012) 217–221.
[38] A. Juszkiewicz, A. Glapa, P. Basta, E. Petriczko, K. Żołnowski, B. Machaliński, J. Trzeciak, K. Łuczkowska, A. Skarpańska-Stejnborn, J. Int. Soc. Sports Nutr. 16 (2019) 7.
[39] M. Lei, J. Zuo, M. Li, Q. Gu, C. Hu, Chin. Med. J. 127 (2014) 1545–1549.
[40] N.H. Kim, H.J. Jeong, H.M. Kim, Amino Acids 42 (2012) 1609–1618.
[41] C. Li, H. Tong, Q. Yan, S. Tang, X. Han, W. Xiao, Z. Tan, Med. Sci. Monit. 22 (2016) 662–669.
[42] A.B. Kamath, L. Wang, H. Das, L. Li, V.N. Reinhold, J.F. Bukowski, Proc. Natl. Acad. Sci. U. S. A. 100 (2003) 6009–6014.
[43] J.F. Bukowski, S.S. Percival, Nutr. Rev. 66 (2008) 96–102.
[44] C. Li, Q. Yan, S. Tang, W. Xiao, Z. Tan, Biomed Res. Int. 2018 (2018) 1497097.
[45] M. Saeed, X. Yatao, Z. Tiantian, R. Qian, S. Chao, Poult. Sci. 98 (2019) 842–854.
[46] Q. Yan, H. Tong, S. Tang, Z. Tan, X. Han, C. Zhou, Biomed Res. Int. 2017 (2017) 9747256.
[47] K. Zarse, S. Jabin, M. Ristow, Eur. J. Nutr. 51 (2012) 765–768.
[48] C.F. Haskell, D.O. Kennedy, A.L. Milne, K.A. Wesnes, A.B. Scholey, Biol. Psychol. 77 (2008) 113–122.
[49] S.J.L. Einöther, V.E.G. Martens, J.A. Rycroft, E.A. De Bruin, Appetite 54 (2010) 406–409.
[50] T. Giesbrecht, J.A. Rycroft, M.J. Rowson, E.A. De Bruin, Nutr. Neurosci. 13 (2010) 283–290.
[51] G.N. Owen, H. Parnell, E.A. De Bruin, J.A. Rycroft, Nutr. Neurosci. 11 (2008) 193–198.
[52] S. Kim, K. Jo, K.-B. Hong, S.H. Han, H.J. Suh, Pharm. Biol. 57 (2019) 65–73.
[53] K. Miyagawa, Y. Hayashi, S. Kurihara, A. Maeda, Geriatr. Gerontol. Int. 8 (2008) 243–250.
[54] S. Kawada, K. Kobayashi, M. Ohtani, C. Fukusaki, J. Strength Cond. Res. 24 (2010) 846–851.
[55] S. Murakami, S. Kurihara, N. Koikawa, A. Nakamura, K. Aoki, H. Yosigi, K. Sawaki, M. Ohtani, Biosci. Biotechnol. Biochem. 73 (2009) 817–821.
[56] S. Murakami, S. Kurihara, C.A. Titchenal, M. Ohtani, J. Int. Soc. Sports Nutr. 7 (2010) 23.
[57] S. Kurihara, S. Shibahara, H. Arisaka, Y. Akiyama, J. Vet. Med. Sci. 69 (2007) 1263–1270.
[58] S. Kurihara, T. Shibakusa, K.A. Tanaka, Springerplus 2 (2013) 635.
[59] S. Kurihara, T. Hiraoka, M. Akutsu, E. Sukegawa, M. Bannai, S. Shibahara, J. Amino Acids 2010 (2010) 307475.
[60] C.A. Rowe, M.P. Nantz, J.F. Bukowski, S.S. Percival, Journal of the American College of Nutrition 26 (2007) 445–452.
[61] K. Matsumoto, H. Yamada, N. Takuma, H. Niino, Y.M. Sagesaka, BMC Complement. Altern. Med. 11 (2011) 15.


Scientific Name:

Acetyl-L-Carnitine is an acetylated form of L-carnitine with anti-aging, neuroprotective and nootropic effects. It decreases fatigue and improves attention, memory, learning and executive function.

Scientific Name:


  • The acetylated version of L-Carnitine can cross the blood brain barrier thereby providing better cognitive benefits[1]
  • In the brain, it originates Acetyl-CoA that can bind to choline to increase the production of Acetylcholine[1]
  • Synergistic with choline donors
  • Can increase the release of Noradrenaline and Serotonin[2]
  • Increases synaptic plasticity[3]
  • Potent cerebral antioxidant activity – can prevent and repair oxidative damage to neurons[4]
  • Increases energy production by mitochondria[5]
  • Can decrease toxicity associated with excessive excitatory neurotransmitter release and cellular waste accumulation[4]

[1] Nałecz KA, et al (2004). Carnitine: transport and physiological functions in the brain. Mol Aspects Med, 25(5-6):551-67.
[2] Smeland OB, et al (2012). Chronic acetyl-L-carnitine alters brain energy metabolism and increases noradrenaline and serotonin content in healthy mice. Neurochem Int, 61(1):100-7.
[3] Laschi R, et al (1990). Ultrastructural aspects of aging rat hippocampus after long-term administration of acetyl-L-carnitine. Int J Clin Pharmacol Res, 10(1-2):59-63.
[4] Zanelli SA, et al (2005). Mechanisms of ischemic neuroprotection by acetyl-L-carnitine. Ann N Y Acad Sci, 1053:153-61.
[5] Reuter SE & Evans AM (2012). Carnitine and acylcarnitines: pharmacokinetic, pharmacological and clinical aspects. Clin Pharmacokinet, 51(9):553-72.


Scientific Name:

DLPA is a mixture of two forms of the essential amino acid phenylalanine, the naturally occurring L-phenylalanine and the synthetic D-phenylalanine with nootropic effects. DLPA enhances mood and can increases alertness and improve memory and learning.

Scientific Name:


  • DL-Phenylalanine crosses the blood-brain barrier easily
  • Increases the production of dopamine and noradrenalin – mood enhancer
  • Decreases chronic pain by blocking the action of enkephalinase[1]
  • Binds to Glutamate AMPA receptors improving synaptic communication –memory and learning enhancement[2]

[1] Russell AL & McCarty MF (2000). DL-phenylalanine markedly potentiates opiate analgesia – an example of nutrient/pharmaceutical up-regulation of the endogenous analgesia system. Med Hypotheses, 55(4):283-8. doi: 10.1054/mehy.1999.1031
[2] Hill RA, et al (1997). Structure–activity studies for alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropanoic acid receptors: acidic hydroxyphenylalanines. J Med Chem, 40(20):3182-91. doi: