Lipoic Acid
Common Names
Lipoic acid | R-Lipoic acid | alpha-Lipoic acid | α-Lipoic acid | ALA | Thioctic acid
Top Benefits of Lipoic Acid
Supports cellular energy creation*
Supports mitochondrial efficiency*
Supports healthy metabolism*
Supports antioxidant defenses*
Supports circadian rhythms*
What Is Lipoic Acid?
Lipoic acid is an important mitochondrial compound because it’s used in helper molecules (i.e., enzymes) for the metabolic processes that convert food energy into cellular energy (ATP). Lipoic acid is often characterized as an antioxidant, though in living systems it plays a larger role supporting the body’s own antioxidant defenses, upregulating important cellular defense molecules like glutathione and preserving Nrf2 function. It’s also involved in cellular signaling, especially with AMPK, considered a master cellular energy sensor and regulator. Lipoic acid was originally discovered in the 1930s and has been used as a nutrient since the late 1950s. While lipoic acid is found in many foods, amounts obtained in the diet are very low. The richest food sources are organ meats (e.g., kidney, liver) and vegetables such as spinach and broccoli. Mitochondria can make lipoic acid starting from a medium chain fat called caprylic acid (also called octanoic acid), which is found in some foods (e.g., milk, coconut) and can also be made in the body. Many animals and human studies report functional benefits when diets are supplemented with extra lipoic acid. This suggests there are circumstances where the amount made inside cells and supplied by foods in the diet are insufficient to optimize health.*
Qualia Lipoic Acid Sourcing
We use Bio-Enhanced®, Stabilized R-Lipoic Acid (sodium R-alpha-lipoic acid), the most bioavailable and potent form of lipoic acid.
Created by GeroNova Research, Inc., a leader in lipoic acid research.
Most lipoic acid in vitamins is a 50/50 mix of the R-(natural) and S-(unnatural) enantiomers. Only the R-lipoic acid is found in our body and used as a cofactor in human enzymes.
Supplementation with Bio-Enhanced®, Stabilized R-Lipoic Acid results in much higher lipoic acid blood levels compared to lipoic acid.[1]
Bio-Enhanced is a registered trademark of GeroNova Research, Inc.
Lipoic Acid Dosing Principles and Rationale
Lipoic acid is generally considered to be dose-dependent (see Neurohacker Dosing Principles) in the range it’s commonly dosed. Higher supplemental doses are typically used when it is given as a single nutrient, while much lower doses are used when it is given in combination with other mitochondrial nutrients (e.g., CoQ10, PQQ, L-carnitine). Lower doses can also be used when using the more bioavailable stabilized R-lipoic acid or when combining lipoic acid with other ingredients that act as bioenhancers, such as piperine from black pepper.*
Lipoic Acid Key Mechanisms
Supports mitochondrial biogenesis*
Supports mitochondrial mass [2]
Supports mitochondrial DNA (mtDNA) [2]
Supports peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) [2–5]
Supports nuclear transcription factors of mitochondrial biogenesis (nuclear respiratory factor 1 [NRF1], NRF2, mitochondrial transcription factor [TFAM]) [2,3,5–7]
Promotes brown-like features in adipose tissue [2]
Supports mitochondrial structure and function*
Cofactor for pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase [8]
Supports the NAD+ pool and the NAD+/NADH ratio [6,9]
Supports complex I-V function [5,7,10]
Supports oxidative phosphorylation and ATP production [4,5,7]
Supports fatty acid β-oxidation [9,11]
Supports membrane potential [7,12]
Supports signaling pathways*
Supports AMPK signaling [4–7,9,11,13–18]
Supports liver kinase B1 (LKB1) signaling [6,18]
Supports FOXO1 activity [6]
Supports peroxisome proliferator-activated receptor alpha (PPARα) signaling [4,19]
Supports the cAMP/CREB signaling pathway [3]
Supports healthy metabolic function*
Supports healthy insulin sensitivity [11,15,20–25]
Supports GLUT4 activity [13,22,26]
Supports healthy fat levels and blood/liver lipid levels [6,14,15]
Supports adiponectin levels [15]
Supports antioxidant defenses*
Supports antioxidant enzymes [3,20,23,27]
Replenishes glutathione (GSH) levels [7,12,22,27]
Counters oxidative stress and reactive oxygen species production [12,23,27,28]
Supports general health and wellbeing*
Supports neuroprotective functions [7,27,29,30]
Supports healthy vascular function [3]
Supports healthy cardiac structure [17]
Supports healthy blood pressure [23]
Supports healthy liver function [10]
Promotes healthy aging and longevity*
Supports SIRT1 activity [2,5,6,9]
Supports SIRT3 activity [10]
Supports uncoupling protein 1 (UCP1) activity [2]
Supports telomerase activity [3]
Supports healthy DNA structure [3]
Influences mTOR signaling [4,13]
Supports circadian rhythms*
Influences genes associated with governing circadian rhythms in the liver [31]
Modulates the expression patterns of circadian clock proteins in the liver [19]
Complementary ingredients*
Coenzyme Q10 – support of mitochondrial function [32–34]
Carnitine — in attenuating the age-associated decline in mitochondrial enzyme activities [35]
Creatine – support of mitochondrial function [32]
Inositol – insulin sensitivity [36]
Piperine and curcumin – additive effects when combined [37]
*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, cure, or prevent any disease.
REFERENCES
[1]D.A. Carlson, A.R. Smith, S.J. Fischer, K.L. Young, L. Packer, Altern. Med. Rev. 12 (2007) 343–351.
[2]M. Fernández-Galilea, P. Pérez-Matute, P.L. Prieto-Hontoria, M. Houssier, M.A. Burrell, D. Langin, J.A. Martínez, M.J. Moreno-Aliaga, Biochim. Biophys. Acta 1851 (2015) 273–281.
[3]S. Xiong, N. Patrushev, F. Forouzandeh, L. Hilenski, R.W. Alexander, Cell Rep. 12 (2015) 1391–1399.
[4]Z. Li, C.M. Dungan, B. Carrier, T.C. Rideout, D.L. Williamson, Lipids 49 (2014) 1193–1201.
[5]T. Jiang, F. Yin, J. Yao, R.D. Brinton, E. Cadenas, Aging Cell 12 (2013) 1021–1031.
[6]Y. Yang, W. Li, Y. Liu, Y. Sun, Y. Li, Q. Yao, J. Li, Q. Zhang, Y. Gao, L. Gao, J. Zhao, J. Nutr. Biochem. 25 (2014) 1207–1217.
[7]G. Song, Z. Liu, L. Wang, R. Shi, C. Chu, M. Xiang, Q. Tian, X. Liu, Food Funct. 8 (2017) 4657–4667.
[8]A. Solmonson, R.J. DeBerardinis, J. Biol. Chem. 293 (2018) 7522–7530.
[9]W.-L. Chen, C.-H. Kang, S.-G. Wang, H.-M. Lee, Diabetologia 55 (2012) 1824–1835.
[10]Z. Liu, J. Guo, H. Sun, Y. Huang, R. Zhao, X. Yang, Biochimie 116 (2015) 52–60.
[11]W.J. Lee, K.-H. Song, E.H. Koh, J.C. Won, H.S. Kim, H.-S. Park, M.-S. Kim, S.-W. Kim, K.-U. Lee, J.-Y. Park, Biochem. Biophys. Res. Commun. 332 (2005) 885–891.
[12]T.M. Hagen, R.T. Ingersoll, J. Lykkesfeldt, J. Liu, C.M. Wehr, V. Vinarsky, J.C. Bartholomew, A.B. Ames, FASEB J. 13 (1999) 411–418.
[13]Y. Wang, X. Li, Y. Guo, L. Chan, X. Guan, Metabolism 59 (2010) 967–976.
[14]K.-G. Park, A.-K. Min, E.H. Koh, H.S. Kim, M.-O. Kim, H.-S. Park, Y.-D. Kim, T.-S. Yoon, B.K. Jang, J.S. Hwang, J.B. Kim, H.-S. Choi, J.-Y. Park, I.-K. Lee, K.-U. Lee, Hepatology 48 (2008) 1477–1486.
[15]P.L. Prieto-Hontoria, P. Pérez-Matute, M. Fernández-Galilea, J. Alfredo Martínez, M.J. Moreno-Aliaga, Eur. J. Nutr. 52 (2013) 779–787.
[16]M. Fernández-Galilea, P. Pérez-Matute, P.L. Prieto-Hontoria, N. Sáinz, M. López-Yoldi, M. Houssier, J.A. Martínez, D. Langin, M.J. Moreno-Aliaga, Obesity 22 (2014) 2210–2215.
[17]J.E. Lee, C.-O. Yi, B.T. Jeon, H.J. Shin, S.K. Kim, T.S. Jung, J.Y. Choi, G.S. Roh, Cardiovasc. Diabetol. 11 (2012) 111.
[18]P.-Y. Cheng, Y.-M. Lee, M.-T. Chung, Y.-C. Shih, M.-H. Yen, Am. J. Hypertens. 25 (2012) 152–158.
[19]D. Keith, L. Finlay, J. Butler, L. Gómez, E. Smith, R. Moreau, T. Hagen, Biochem. Biophys. Res. Commun. 450 (2014) 324–329.
[20]H. Ansar, Z. Mazloom, F. Kazemi, N. Hejazi, Saudi Med. J. 32 (2011) 584–588.
[21]S. Jacob, P. Ruus, R. Hermann, H.J. Tritschler, E. Maerker, W. Renn, H.J. Augustin, G.J. Dietze, K. Rett, Free Radical Biology and Medicine 27 (1999) 309–314.
[22]A. Rudich, A. Tirosh, R. Potashnik, M. Khamaisi, N. Bashan, Diabetologia 42 (1999) 949–957.
[23]A. El Midaoui, J. de Champlain, Hypertension 39 (2002) 303–307.
[24]S. Jacob, P. Ruus, R. Hermann, H.J. Tritschler, E. Maerker, W. Renn, H.J. Augustin, G.J. Dietze, K. Rett, Free Radic. Biol. Med. 27 (1999) 309–314.
[25]S. Jacob, R.S. Streeper, D.L. Fogt, J.Y. Hokama, H.J. Tritschler, G.J. Dietze, E.J. Henriksen, Diabetes 45 (1996) 1024–1029.
[26]M. Khamaisi, R. Potashnik, A. Tirosh, E. Demshchak, A. Rudich, H. Tritschler, K. Wessel, N. Bashan, Metabolism 46 (1997) 763–768.
[27]A.O. Abdel-Zaher, R.H. Abdel-Hady, W.M. Abdel Moneim, S.Y. Salim, Exp. Toxicol. Pathol. 63 (2011) 161–165.
[28]B.A. Maddux, W. See, J.C. Lawrence Jr, A.L. Goldfine, I.D. Goldfine, J.L. Evans, Diabetes 50 (2001) 404–410.
[29]O. Tirosh, C.K. Sen, S. Roy, M.S. Kobayashi, L. Packer, Free Radic. Biol. Med. 26 (1999) 1418–1426.
[30]J.T. Greenamyre, M. Garcia-Osuna, J.G. Greene, Neurosci. Lett. 171 (1994) 17–20.
[31]L.A. Finlay, A.J. Michels, J.A. Butler, E.J. Smith, J.S. Monette, R.F. Moreau, S.K. Petersen, B. Frei, T.M. Hagen, Am. J. Physiol. Regul. Integr. Comp. Physiol. 302 (2012) R587–97.
[32]M.C. Rodriguez, J.R. MacDonald, D.J. Mahoney, G. Parise, M.F. Beal, M.A. Tarnopolsky, Muscle Nerve 35 (2007) 235–242.
[33]A. Abadi, J.D. Crane, D. Ogborn, B. Hettinga, M. Akhtar, A. Stokl, L. MacNeil, A. Safdar, M. Tarnopolsky, PLoS ONE 8 (2013) e60722.
[34]S. Silvestri, P. Orlando, T. Armeni, L. Padella, F. Brugè, G. Seddaiu, G.P. Littarru, L. Tiano, J. Clin. Biochem. Nutr. 57 (2015) 21–26.
[35]S. Savitha, K. Sivarajan, D. Haripriya, V. Kokilavani, C. Panneerselvam, Clin. Nutr. 24 (2005) 794–800.
[36]I. Capasso, E. Esposito, N. Maurea, M. Montella, A. Crispo, M. De Laurentiis, M. D’Aiuto, G. Frasci, G. Botti, M. Grimaldi, E. Cavalcanti, G. Esposito, A. Fucito, G. Brillante, G. D’Aiuto, G. Ciliberto, Trials 14 (2013) 273.
[37]F. Di Pierro, R. Settembre, J. Pain Res. 6 (2013) 497–503.