Supports cell energy generation *
Supports healthy aging *
Supports healthy sleep*
Supports mood *
Supports prosocial behaviors *
L-Tryptophan is an essential amino acid. The body cannot synthesize it: it must be obtained from the diet. It’s been known for decades that L-tryptophan has niacin equivalent activity in the body (i.e., we can make the NAD+ molecules from it). L-tryptophan is unique because it’s the only way to build NAD+ that doesn’t start from one of the older or newer vitamin B3’s. L-tryptophan does this by a de novo synthesis pathway, which creates a niacin molecule through a series of biological reactions (many other important molecules are also created in this process). In the morning, most L-tryptophan—as much as 95%—is used in this pathway. L-tryptophan has enhanced aspects of exercise performance when taken before working out, presumably because of this role in cellular energy production. At night, while most L-tryptophan is still funneled into the de novo pathway, relatively more gets directed to a different pathway, 5-hydroxytryptophan (5-HTP) → serotonin → melatonin. This alternate pathway is involved in regulating sleep-wake cycles and nighttime body clock functions. This alternate pathway might be why low-to-moderate doses of L-tryptophan supports skills that fall into the social cognitive domain: these include prosocial behaviors like cooperation, empathy, getting along with others, and altruism. Since this alternate pathway can be used to make the neurohormone melatonin, L-tryptophan has been used to support healthier sleep cycles. Giving extra L-tryptophan allows the body to use it where it is needed most 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 early in the day also helps support the body clock, orienting many of its daytime functions earlier in the day. L-tryptophan supplementation may support prosocial behaviors. Low-to-modest doses of L-tryptophan in the evening may support healthier sleep cycles.*
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.
One of our formulating principles is to determine whether there is a serving range, in which many of the benefits occur and above which there appears to be diminishing returns (i.e., a threshold), and to provide a serving within this threshold range (see Neurohacker Dosing Principles). We consider L-tryptophan to be one of these threshold compounds, because many of the benefits appear to occur at a low amount, and in some functional areas a worse response may occur at higher amounts. As an example, in a comparative study for sleep, the lowest amount used produced a healthier deep sleep response than the higher amount . 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 lower than that 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. 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 is a substrate in the de novo NAD+ synthesis pathway via the kynurenine pathway (KP) 
NAD+ can be converted to the coenzyme NADP+ by the enzyme NAD kinase 
NAD(H) and NADP(H) are key molecules in essential redox pathways of cellular metabolism and energy production 
NAD(H) is essential for the production of ATP through the citric acid cycle and oxidative phosphorylation 
NADP(H) is essential in many anabolic metabolic reactions, including DNA and RNA synthesis 
NADP(H) is a cofactor for some cytochrome P450 enzymes that detoxify xenobiotics 
NADPH also acts as a cofactor for glutathione reductase, the enzyme used to maintain reduced glutathione (GSH) levels 
NAD(H) and NADP(H) are essential for healthy aging 
Supports brain function*
L-tryptophan is a precursor for serotonin (a neurotransmitter) and melatonin (a neurohormone) synthesis 
Substrate for serotonin synthesis [7,8]
Substrate for melatonin synthesis 
Supports sleep [1,10–17]
Supports social cognition*
Promotes social behaviors [18,19]
Supports prosocial interactions [19–24]
Promotes charitable behaviors 
Supports a healthy mood*
Supports emotional processing and mental energy 
Supports a positive mental-emotional bias [12,27–29]
Supports a calm mood [12,27,30]
Supports healthy functional connectivity between the default mode network and emotion-related brain regions 
Promotes exercise performance*
Supports power output [32,33]
Delays time to exertion [32,33]
Nicotinic acid (niacin) and nicotinamide (niacinamide) as substrates for NAD synthesis
*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.
E. Hartmann, C.L. Spinweber, J. Nerv. Ment. Dis. 167 (1979) 497–499.
A.A.-B. Badawy, Int. J. Tryptophan Res. 10 (2017) 1178646917691938.
G. Magni, A. Amici, M. Emanuelli, G. Orsomando, N. Raffaelli, S. Ruggieri, Cell. Mol. Life Sci. 61 (2004) 19–34.
W. Ying, Antioxid. Redox Signal. 10 (2008) 179–206.
D.S. Riddick, X. Ding, C.R. Wolf, T.D. Porter, A.V. Pandey, Q.-Y. Zhang, J. Gu, R.D. Finn, S. Ronseaux, L.A. McLaughlin, C.J. Henderson, L. Zou, C.E. Flück, Drug Metab. Dispos. 41 (2013) 12–23.
L. Palego, L. Betti, A. Rossi, G. Giannaccini, J. Amino Acids 2016 (2016) 8952520.
J.D. Fernstrom, Physiol. Rev. 63 (1983) 484–546.
J.D. Fernstrom, J. Nutr. Biochem. 1 (1990) 508–517.
S. Esteban, C. Nicolaus, A. Garmundi, R.V. Rial, A.B. Rodríguez, E. Ortega, C.B. Ibars, Mol. Cell. Biochem. 267 (2004) 39–46.
R.J. Wyatt, K. Engelman, D.J. Kupfer, D.H. Fram, A. Sjoerdsma, F. Snyder, Lancet 2 (1970) 842–846.
C.F. George, T.W. Millar, P.J. Hanly, M.H. Kryger, Sleep 12 (1989) 345–353.
R. Bravo, S. Matito, J. Cubero, S.D. Paredes, L. Franco, M. Rivero, A.B. Rodríguez, C. Barriga, Age 35 (2013) 1277–1285.
A.N. Nicholson, B.M. Stone, Electroencephalogr. Clin. Neurophysiol. 47 (1979) 539–545.
H.S. Schmidt, Bull. Eur. Physiopathol. Respir. 19 (1983) 625–629.
C. Hudson, S.P. Hudson, T. Hecht, J. MacKenzie, Nutr. Neurosci. 8 (2005) 121–127.
J.G. Lindsley, E.L. Hartmann, W. Mitchell, Sleep 6 (1983) 247–256.
K. Demisch, J. Bauer, K. Georgi, Pharmacopsychiatry 20 (1987) 245–248.
L. Steenbergen, B.J. Jongkees, R. Sellaro, L.S. Colzato, Neurosci. Biobehav. Rev. 64 (2016) 346–358.
S.N. Young, Philos. Trans. R. Soc. Lond. B Biol. Sci. 368 (2013) 20110375.
D.S. Moskowitz, G. Pinard, D.C. Zuroff, L. Annable, S.N. Young, Neuropsychopharmacology 25 (2001) 277–289.
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.
K. Hogenelst, R.A. Schoevers, M. Aan Het Rot, Int. J. Neuropsychopharmacol. 18 (2015).
M. aan het Rot, D.S. Moskowitz, G. Pinard, S.N. Young, J. Psychiatry Neurosci. 31 (2006) 253–262.
H. Cerit, R.J. Schuur, E.R.A. de Bruijn, W. Van der Does, Front. Psychol. 6 (2015) 1012.
L. Steenbergen, R. Sellaro, L.S. Colzato, Front. Psychol. 5 (2014) 1451.
M.H. Mohajeri, J. Wittwer, K. Vargas, E. Hogan, A. Holmes, P.J. Rogers, R. Goralczyk, E.L. Gibson, Br. J. Nutr. 113 (2015) 350–365.
G. Lindseth, B. Helland, J. Caspers, Arch. Psychiatr. Nurs. 29 (2015) 102–107.
S.E. Murphy, C. Longhitano, R.E. Ayres, P.J. Cowen, C.J. Harmer, Psychopharmacology 187 (2006) 121–130.
R.N. Herrington, A. Bruce, E.C. Johnstone, M.H. Lader, Psychol. Med. 6 (1977) 673–678.
D.J. Bowen, B. Spring, E. Fox, J. Behav. Med. 14 (1991) 97–110.
Y.I. Deza‐Araujo, P.T. Neukam, M. Marxen, D.K. Müller, T. Henle, M.N. Smolka, Hum. Brain Mapp. 40 (2019) 1844–1855.
C. Javierre, R. Segura, J.L. Ventura, A. Suárez, J.M. Rosés, Int. J. Neurosci. 120 (2010) 319–327.
R. Segura, J.L. Ventura, Int. J. Sports Med. 9 (1988) 301–305.