• Supports antioxidant defenses
      • Supports circadian rhythms
      • Supports mitochondrial efficiency
      • Supports healthy metabolism
      • Supports cellular energy creation


ATP is the cellular energy that arises from the metabolic process that converts food energy into cellular energy (lipids). Lipoic acid is a crucial component of mitochondria.


It is traditionally thought of as an antioxidant, but its role in living systems is to support the body's own antioxidant defenses, as well as upregulate important molecules involved in cell defense, such as glutathione and Nrf2.


A major regulator and sensor of cellular energy, AMPK, is also involved in its signaling.


As a nutrient, lipoic acid has been used since the 1950s after first being discovered in the 1930s.

Many foods contain lipoic acid, but the amount obtained from diet is very low. Vegetables like spinach and broccoli as well as organ meats (e.g., kidney, liver) provide the most nutrients.


Lipoic acid can be made by mitochondria using a medium chain fat called caprylic acid (also known as octanoic acid), which is found in some foods (e.g., milk, coconut) and can also be synthesized in the body.


Several studies have reported beneficial effects of adding extra lipoic acid to animal and human diets.


Accordingly, there are times when the amount produced inside cells and supplied by foods in the diet are insufficient to ensure optimal health.


Mitochondrial biogenesis


  • Upregulates mitochondrial mass[2]
  • Upregulates mitochondrial DNA (mtDNA)[2]
  • Upregulates peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC1α)[2–5]
  • Upregulates nuclear transcription factors of mitochondrial biogenesis (nuclear respiratory factor 1 [NRF1], NRF2, mitochondrial transcription factor [TFAM])[2, 3, 5–7]
  • Induces brown-like features in adipose tissue[2]


Mitochondrial structure and function


  • Cofactor for pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase[8]
  • Upregulates the NAD+ pool and the NAD+ : NADH ratio[6,9]
  • Protects from complex I-V inhibition[5,7,10]
  • Promotes oxidative phosphorylation and ATP production[4,5,7]
  • Promotes fatty acid β-oxidation[9,11]
  • Supports membrane potential[7,12]


Signaling pathways


  • Upregulates AMPK signaling[4–7,9,11,13–18]
  • Upregulates liver kinase B1 (LKB1) signaling[6,18]
  • Upregulates FOXO1 activity[6]
  • Upregulates peroxisome proliferator-activated receptor alpha (PPARα) signaling[4,19]
  • Upregulates the cAMP/CREB signaling pathway[3]




    • Supports healthy insulin sensitivity[11,15,20–25]
    • Upregulates GLUT4 activity[13,22,26]
    • Downregulates fat accumulation and blood/liver lipid levels[6,14,15]
    • Upregulates adiponectin levels[15]


Antioxidant defenses


    • Upregulates antioxidant enzymes (catalase [CAT], glutathione peroxidase [GPx])[3,20,23,27]
    • Replenishes glutathione (GSH) levels[7,12,22,27]
    • Downregulates oxidative stress and reactive oxygen species production[12,23,27,28]


Protective effects


    • Neuroprotective against neurotoxic agents[7,27,29,30]
    • Protects vascular function[3]
    • Protects cardiac structure[17]
    • Supports healthy blood pressure[23]
    • Protects liver function[10]


Healthy aging and longevity


    • Upregulates SIRT-1 activity[2,5,6,9]
    • Upregulates SIRT-3 activity[10]
    • Upregulates uncoupling protein 1 (UCP1) activity[2]
    • Stimulates telomerase activity / protects from telomere dysfunction[3]
    • Protects DNA from damage[3]
    • Downregulates mTOR signaling[4,13]


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[32–35]
    • Creatine – support of mitochondrial function[32–35]
    • Inositol – insulin sensitivity[36]
    • Piperine and curcumin – additive effects when combined[37]


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[3] S. Xiong, N. Patrushev, F. Forouzandeh, L. Hilenski, R. W. Alexander, Cell Rep. 12, 1391–1399 (2015).
[4] Z. Li, C. M. Dungan, B. Carrier, T. C. Rideout, D. L. Williamson, Lipids. 49, 1193–1201 (2014).
[5] T. Jiang, F. Yin, J. Yao, R. D. Brinton, E. Cadenas, Aging Cell. 12, 1021–1031 (2013).
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[10] Z. Liu et al., Biochimie. 116, 52–60 (2015).
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[12] T. M. Hagen et al., FASEB J. 13, 411–418 (1999).
[13] Y. Wang, X. Li, Y. Guo, L. Chan, X. Guan, Metabolism. 59, 967–976 (2010).
[14] K.-G. Park et al., Hepatology. 48, 1477–1486 (2008).
[15] P. L. Prieto-Hontoria, P. Pérez-Matute, M. Fernández-Galilea, J. Alfredo Martínez, M. J. Moreno-Aliaga, Eur. J. Nutr. 52, 779–787 (2013).
[16] M. Fernández-Galilea et al., Obesity . 22, 2210–2215 (2014).
[17] J. E. Lee et al., Cardiovasc. Diabetol. 11, 111 (2012).
[18] P.-Y. Cheng, Y.-M. Lee, M.-T. Chung, Y.-C. Shih, M.-H. Yen, Am. J. Hypertens. 25, 152–158 (2012).
[19] D. Keith et al., Biochem. Biophys. Res. Commun. 450, 324–329 (2014).
[20] H. Ansar, Z. Mazloom, F. Kazemi, N. Hejazi, Saudi Med. J. 32, 584–588 (2011).
[21] S. Jacob et al., Free Radical Biology and Medicine. 27, 309–314 (1999).
[22] A. Rudich, A. Tirosh, R. Potashnik, M. Khamaisi, N. Bashan, Diabetologia. 42, 949–957 (1999).
[23] A. El Midaoui, J. de Champlain, Hypertension. 39, 303–307 (2002).
[24] S. Jacob et al., Free Radic. Biol. Med. 27, 309–314 (1999).
[25] S. Jacob et al., Diabetes. 45, 1024–1029 (1996).
[26] M. Khamaisi et al., Metabolism. 46, 763–768 (1997).
[27] A. O. Abdel-Zaher, R. H. Abdel-Hady, W. M. Abdel Moneim, S. Y. Salim, Exp. Toxicol. Pathol. 63, 161–165 (2011).
[28] B. A. Maddux et al., Diabetes. 50, 404–410 (2001).
[29] O. Tirosh, C. K. Sen, S. Roy, M. S. Kobayashi, L. Packer, Free Radic. Biol. Med. 26, 1418–1426 (1999).
[30] J. T. Greenamyre, M. Garcia-Osuna, J. G. Greene, Neurosci. Lett. 171, 17–20 (1994).
[31] L. A. Finlay et al., Am. J. Physiol. Regul. Integr. Comp. Physiol. 302, R587–97 (2012).
[32] M. C. Rodriguez et al., Muscle Nerve. 35, 235–242 (2007).
[33] S. Savitha, K. Sivarajan, D. Haripriya, V. Kokilavani, C. Panneerselvam, Clin. Nutr. 24, 794–800 (2005).
[34] A. Abadi et al., Supplementation with α-Lipoic Acid, CoQ10, and Vitamin E Augments Running Performance and Mitochondrial Function in Female Mice. PLoS ONE. 8 (2013), p. e60722.
[35] S. Silvestri et al., J. Clin. Biochem. Nutr. 57, 21–26 (2015).
[36] I. Capasso et al., Trials. 14, 273 (2013).
[37] F. Di Pierro, R. Settembre, J. Pain Res. 6, 497–503 (2013).

*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.