Acetyl-L-Carnitine (ALCAR) is an acetylated form of L-carnitine. The major difference between ALCAR and L-carnitine is that ALCAR more readily crosses the blood-brain barrier, which is why it tends to be the preferred form for use in brain and nervous system support. The bioavailability of ALCAR is thought to be higher than that of L-carnitine. The name carnitine is derived from Latin “carnus” (flesh) because it was originally found in meat extracts. Adults eating animal products consume about 60–180 milligrams of carnitine per day [1]. Vegans get noticeably less (about 10–12 milligrams) [1], with vegetarians getting a bit more than vegans because of eating dairy products. The carnitine in ALCAR and L-carnitine supports the same functions. The most important role of carnitine 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 mitochondrial potential to burn fat. Unlike L-carnitine, which does not contain an acetyl group, ALCAR can support acetylcholine synthesis, because the acetyl group in ALCAR can be delivered to coenzyme A to yield acetyl-CoA, which in turn can be used for the synthesis of the neurotransmitter acetylcholine. Acetyl-CoA can also be used for cell energy production as it is the primary substrate for the Krebs cycle in mitochondria, essential for the production of ATP. Accordingly, ALCAR has been shown to enhance cholinergic neurotransmission and support brain energy metabolism in several studies; it has also shown significant neuroprotective effects [2–5].*


Supports brain function *

Supports mood *

Supports energy metabolism *

Supports healthy aging *


ALCAR supplies carnitine, which 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). It is also a source of acetyl groups that can be used to make acetylCoA. 

While ALCAR and L-carnitine support the same mitochondrial functions, the ALCAR form tends to be preferentially used in research for brain and nervous system support.

ALCAR is NON-GMO and vegan.


ALCAR is generally considered to be dose-dependent (see Qualia Dosing Principles) in the range it’s commonly dosed (between 500 and 2000 mg). Because of the acetyl group in its structure, 500 mg of ALCAR supplies roughly 400 mg of carnitine. 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, though still greater than what’s supplied in the diet. We opted for a serving on the lower end of the usual supplementation range because ALCAR is additive with other ingredients used in our formulation for supporting brain health, which means that a lower serving should be sufficient to obtain the desired benefits. The serving used is sufficient to ensure that even persons with very low dietary intake of carnitine, such as vegans and vegetarians, consume adequate carnitine.* 


Supports brain function and cognitive performance*

Supports cognitive function* [6–10]

Supports mental energy and may help counter mental fatigue* [11,12]

Supports cholinergic neurotransmission* [3,4,13,14]

Supports brain energy metabolism* [4,15–22]

Supports dopamine release* [23,24]

Supports noradrenaline levels* [15]

Supports serotonin levels* [15]

Supports synaptic plasticity* [25,26]

Supports neuronal membrane lipid/phospholipid metabolism* [4,16,27]

Supports neuroprotective functions* [4,8,21,22,28–35] 

Supports neural cytokine signaling* [8,30,31]  

Supports mood*

Supports positive affect* [36–43] 


Promotes physical strength and resistance*

Supports energy and may help counter fatigue* [11,44]

Supports muscle fuel metabolism* [45]

Supports mitochondrial function*

Supports mitochondrial function and structure* [10,32,33,46]

Supports mitochondrial biogenesis* [47]


Promotes healthy aging and longevity*

Supports cerebral metabolism during aging* [19]

Supports mitochondrial function during aging* [10,33,48]

*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.


[1]C.J. Rebouche, Ann. N. Y. Acad. Sci. 1033 (2004) 30–41.

[2]H. Kuratsune, Y. Watanabe, K. Yamaguti, G. Jacobsson, M. Takahashi, T. Machii, H. Onoe, K. Onoe, K. Matsumura, S. Valind, T. Kitani, B. Långström, Biochem. Biophys. Res. Commun. 231 (1997) 488–493.

[3]K.A. Nałecz, D. Miecz, V. Berezowski, R. Cecchelli, Mol. Aspects Med. 25 (2004) 551–567.

[4]L.L. Jones, D.A. McDonald, P.R. Borum, Prog. Lipid Res. 49 (2010) 61–75.

[5]D.W. Foster, Ann. N. Y. Acad. Sci. 1033 (2004) 1–16.

[6]J.O. Brooks 3rd, J.A. Yesavage, A. Carta, D. Bravi, Int. Psychogeriatr. 10 (1998) 193–203.

[7]M. Malaguarnera, M. Vacante, M. Motta, M. Giordano, G. Malaguarnera, R. Bella, G. Nunnari, L. Rampello, G. Pennisi, Metab. Brain Dis. 26 (2011) 281–289.

[8]S. Singh, A. Mishra, N. Srivastava, R. Shukla, S. Shukla, Mol. Neurobiol. 55 (2018) 583–602.

[9]S.A. Montgomery, L.J. Thal, R. Amrein, Int. Clin. Psychopharmacol. 18 (2003) 61–71.

[10]B.N. Ames, J. Liu, Ann. N. Y. Acad. Sci. 1033 (2004) 108–116.

[11]M. Malaguarnera, M.P. Gargante, E. Cristaldi, V. Colonna, M. Messano, A. Koverech, S. Neri, M. Vacante, L. Cammalleri, M. Motta, Arch. Gerontol. Geriatr. 46 (2008) 181–190.

[12]R.C.W. Vermeulen, H.R. Scholte, Psychosomatic Medicine 66 (2004) 276–282.

[13]V. Dolezal, S. Tucek, J. Neurochem. 36 (1981) 1323–1330.

[14]S. Tucek, in: S.-M. Aquilonius, P.-G. Gillberg (Eds.), Progress in Brain Research, Elsevier, 1990, pp. 467–477.

[15]O.B. Smeland, T.W. Meisingset, K. Borges, U. Sonnewald, Neurochem. Int. 61 (2012) 100–107.

[16]T. Aureli, A. Miccheli, R. Ricciolini, M.E. Di Cocco, M.T. Ramacci, L. Angelucci, O. Ghirardi, F. Conti, Brain Res. 526 (1990) 108–112.

[17]T. Aureli, M.E. Di Cocco, C. Puccetti, R. Ricciolini, M. Scalibastri, A. Miccheli, C. Manetti, F. Conti, Brain Res. 796 (1998) 75–81.

[18]C. Ori, U. Freo, G. Pizzolato, M. Dam, Brain Res. 951 (2002) 330–335.

[19]U. Freo, M. Dam, C. Ori, Brain Res. 1259 (2009) 32–39.

[20]R.F. Villa, F. Ferrari, A. Gorini, Neurochem. Res. 36 (2011) 1372–1382.

[21]T. Aureli, A. Miccheli, M.E. Di Cocco, O. Ghirardi, A. Giuliani, M.T. Ramacci, F. Conti, Brain Res. 643 (1994) 92–99.

[22]R.E. Rosenthal, R. Williams, Y.E. Bogaert, P.R. Getson, G. Fiskum, Stroke 23 (1992) 1312–7; discussion 1317–8.

[23]H. Sershen, L.G. Harsing Jr, M. Banay-Schwartz, A. Hashim, M.T. Ramacci, A. Lajtha, J. Neurosci. Res. 30 (1991) 555–559.

[24]L.G. Harsing Jr, H. Sershen, E. Toth, A. Hashim, M.T. Ramacci, A. Lajtha, Eur. J. Pharmacol. 218 (1992) 117–121.

[25]R. Laschi, L. Badiali de Giorgi, F. Bonvicini, L. Centurione, Int. J. Clin. Pharmacol. Res. 10 (1990) 59–63.

[26]K. Kocsis, R. Frank, J. Szabó, L. Knapp, Z. Kis, T. Farkas, L. Vécsei, J. Toldi, Neuroscience 332 (2016) 203–211.

[27]T. Aureli, M.E. Di Cocco, G. Capuani, R. Ricciolini, C. Manetti, A. Miccheli, F. Conti, Neurochem. Res. 25 (2000) 395–399.

[28]S.A. Zanelli, N.J. Solenski, R.E. Rosenthal, G. Fiskum, Ann. N. Y. Acad. Sci. 1053 (2008) 153–161.

[29]Y. Liu, R.E. Rosenthal, P. Starke-Reed, G. Fiskum, Free Radic. Biol. Med. 15 (1993) 667–670.

[30]S. Afshin-Majd, K. Bashiri, Z. Kiasalari, T. Baluchnejadmojarad, R. Sedaghat, M. Roghani, Biomed. Pharmacother. 89 (2017) 1–9.

[31]H. Keshavarz-Bahaghighat, M.R. Sepand, M.H. Ghahremani, M. Aghsami, N. Sanadgol, A. Omidi, V. Bodaghi-Namileh, O. Sabzevari, Biol. Trace Elem. Res. 184 (2018) 422–435.

[32]L. Nicassio, F. Fracasso, G. Sirago, C. Musicco, A. Picca, E. Marzetti, R. Calvani, P. Cantatore, M.N. Gadaleta, V. Pesce, Exp. Gerontol. 98 (2017) 99–109.

[33]G. Forloni, N. Angeretti, S. Smiroldo, J. Neurosci. Res. 37 (1994) 92–96.

[34]M.A. Virmani, V. Caso, A. Spadoni, S. Rossi, F. Russo, F. Gaetani, Ann. N. Y. Acad. Sci. 939 (2006) 162–178.

[35]S. Singh, A. Mishra, S.K. Mishra, S. Shukla, Neurochem. Int. 108 (2017) 388–396.

[36]S. Chiechio, P.L. Canonico, M. Grilli, Int. J. Mol. Sci. 19 (2017).

[37]N. Veronese, B. Stubbs, M. Solmi, O. Ajnakina, A.F. Carvalho, S. Maggi, Psychosom. Med. 80 (2018) 154–159.

[38]S.-M. Wang, C. Han, S.-J. Lee, A.A. Patkar, P.S. Masand, C.-U. Pae, J. Psychiatr. Res. 53 (2014) 30–37.

[39]G. Garzya, D. Corallo, A. Fiore, G. Lecciso, G. Petrelli, C. Zotti, Drugs Exp. Clin. Res. 16 (1990) 101–106.

[40]E. Tempesta, L. Casella, C. Pirrongelli, L. Janiri, M. Calvani, L. Ancona, Drugs Exp. Clin. Res. 13 (1987) 417–423.

[41]R. Zanardi, E. Smeraldi, Eur. Neuropsychopharmacol. 16 (2006) 281–287.

[42]G. Bersani, G. Meco, A. Denaro, D. Liberati, C. Colletti, R. Nicolai, F.S. Bersani, A. Koverech, Eur. Neuropsychopharmacol. 23 (2013) 1219–1225.

[43]P. Leombruni, M. Miniotti, F. Colonna, C. Sica, L. Castelli, M. Bruzzone, S. Parisi, E. Fusaro, P. Sarzi-Puttini, F. Atzeni, R.G. Torta, Clin. Exp. Rheumatol. 33 (2015) S82–5.

[44]M. Malaguarnera, R. Bella, M. Vacante, M. Giordano, G. Malaguarnera, M.P. Gargante, M. Motta, A. Mistretta, L. Rampello, G. Pennisi, Scand. J. Gastroenterol. 46 (2011) 750–759.

[45]B.T. Wall, F.B. Stephens, D. Constantin-Teodosiu, K. Marimuthu, I.A. Macdonald, P.L. Greenhaff, J. Physiol. 589 (2011) 963–973.

[46]A. Gorini, A. D’Angelo, R.F. Villa, Neurochemical Research 23 (1998) 1485–1491.

[47]P. Cassano, A.G. Sciancalepore, V. Pesce, M. Flück, H. Hoppeler, M. Calvani, L. Mosconi, P. Cantatore, M.N. Gadaleta, Biochim. Biophys. Acta 1757 (2006) 1421–1428.

[48]V. Calabrese, A.M. Giuffrida Stella, M. Calvani, D.A. Butterfield, J. Nutr. Biochem. 17 (2006) 73–88.