3 Bottles of Brain First-Aid: NAC (N-Acetyl Cysteine) by Feed a Brain


Several studies show the safety and efficacy of NAC for many different conditions including infectious disease, respiratory infection, and… what peaks my interest is that when NAC is given before or immediately after a head injury brain injury, the effects are reduced by up to 78%! [1]

NAC is a conditionally essential amino acid that is absolutely life-saving in certain situations and has been shown to be neuroprotective immediately following brain injury.

While NAC an indirect antioxidant as a component of glutathione, the brain and body’s master antioxidant, it is also a direct antioxidant on its own… making it a fast acting treatment to reduce the effects of brain injury.

It is even approved in large doses (140mg/kg of body weight) by the FDA for acetaminophen toxicity. For this reason, it is often found in most hospitals. [5]


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N-acetylcysteine (NAC): Brain First Aid

[1] N-acetylcysteine reduces lipopolysaccharide-sensitized hypoxic-ischemic brain injury

Wang, X., Svedin, P., Nie, C., Lapatto, R., Zhu, C., Gustavsson, M., . . . Mallard, C. (2007). N-acetylcysteine reduces lipopolysaccharide-sensitized hypoxic-ischemic brain injury. Annals of Neurology,61(3), 263-271. doi:10.1002/ana.21066


NAC (200mg/kg) provided marked neuroprotection with up to 78% reduction of brain injury in the pre+post-HI treatment group and 41% in the early (0 hour) post-HI treatment group, which was much more pronounced protection than another free radical scavenger, melatonin. Protection by NAC was associated with the following factors: (1) reduced isoprostane activation and nitrotyrosine formation; (2) increased levels of the antioxidants glutathione, thioredoxin-2, and (3) inhibition of caspase-3, calpain, and caspase-1 activation.

[2] Sensory neuroprotection, mitochondrial preservation, and therapeutic potential of n-acetyl-cysteine after nerve injury

Hart, A., Terenghi, G., Kellerth, J., & Wiberg, M. (2004). Sensory neuroprotection, mitochondrial preservation, and therapeutic potential of n-acetyl-cysteine after nerve injury. Neuroscience,125(1), 91-101. doi:10.1016/j.neuroscience.2003.12.040

NAC (150 mg/kg/day) almost totally eliminated the extensive neuronal loss found in controls both 2 weeks (no treatment 21% loss, NAC 3%, P=0.03) and 2 months after axotomy (no treatment 35% loss, NAC 3%, P=0.002). Glial cell death was reduced (mean number TUNEL positive cells 2 months after axotomy: no treatment 51/ganglion pair, NAC 16/ganglion pair), and mitochondrial architecture was preserved. The effects were less profound when a lower dose was examined (30 mg/kg/day), although significant neuroprotection still occurred. This provides evidence of the importance of mitochondrial dysregulation in axotomy-induced neuronal death in the peripheral nervous system, and suggests that NAC merits investigation in CNS trauma. NAC is already in widespread clinical use for applications outside the nervous system; it therefore has immediate clinical potential in the prevention of primary sensory neuronal death, and has therapeutic potential in other neuropathological systems.

[3] Amelioration of Acute Sequelae of Blast Induced Mild Traumatic Brain Injury by N-Acetyl Cysteine: A Double-Blind, Placebo-Controlled Study

Hoffer, M. E., Balaban, C., Slade, M. D., Tsao, J. W., & Hoffer, B. (2013). Amelioration of Acute Sequelae of Blast Induced Mild Traumatic Brain Injury by N-Acetyl Cysteine: A Double-Blind, Placebo Controlled Study. PLoS ONE,8(1). doi:10.1371/journal.pone.0054163

This study was a randomized double blind, placebo-controlled study that was conducted on active duty service members at a forward deployed field hospital in Iraq. All symptomatic U.S. service members who were exposed to significant ordnance blast and who met the criteria for mTBI were offered participation in the study and 81 individuals agreed to participate. Individuals underwent a baseline evaluation and then were randomly assigned to receive either N-acetyl cysteine (NAC) or placebo for seven days. Each subject was re-evaluated at 3 and 7 days. Outcome measures were the presence of the following sequelae of mTBI: dizziness, hearing loss, headache, memory loss, sleep disturbances, and neurocognitive dysfunction. The resolution of these symptoms seven days after the blast exposure was the main outcome measure in this study. Logistic regression on the outcome of ‘no day 7 symptoms’ indicated that NAC treatment was significantly better than placebo (OR = 3.6, p = 0.006). Secondary analysis revealed subjects receiving NAC within 24 hours of blast had an 86% chance of symptom resolution with no reported side effects versus 42% for those seen early who received placebo

The 4 gram loading dose was witnessed and then bottles were name labeled and given to the subject’s corpsman, medic or a nurse (for subjects remaining at TQ). Beginning 18–24 hours after the loading dose, subjects were given 4 grams daily (in two divided doses of 2 gm morning and night) for 4 days. The dose was then reduced to 3 gm daily [in two divided doses of 1.5 gm morning and night]. Every dose was witnessed by a corpsman, medic, nurse, or doctor.

This study, conducted in an active theatre of war, demonstrates that NAC, a safe pharmaceutical countermeasure, has beneficial effects on the severity and resolution of sequelae of blast induced mTBI.

[4] Early, Transient Increase in Complexin I and Complexin II in the Cerebral Cortex following Traumatic Brain Injury Is Attenuated by N-Acetylcysteine

Yi, J., Hoover, R., Mcintosh, T. K., & Hazell, A. S. (2006). Early, Transient Increase in Complexin I and Complexin II in the Cerebral Cortex following Traumatic Brain Injury Is Attenuated by N-Acetylcysteine. Journal of Neurotrauma,23(1), 86-96. doi:10.1089/neu.2006.23.86

The early, transient increase in the injured cortex was completely blocked by N-acetylcysteine (NAC) administered 5 min following trauma, suggesting an involvement of oxidative stress. Neuronal loss was also reduced in the injured hemisphere with post-TBI NAC treatment. Our findings suggest a dysregulation of both inhibitory and excitatory neurotransmission following traumatic injury that is responsive to antioxidant treatment. These alterations in complexin levels may also play an important role in neuronal cell loss following TBI, and thus contribute to the pathophysiology of cerebral damage following brain injury.

[5] CETYLEV (acetylcysteine) effervescent tablets for oral solution Initial U.S. Approval: 1963

Drugs@FDA: FDA-Approved Drugs. (n.d.). Retrieved December 04, 2020, from


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Weight 0.126 kg
Dimensions 9 × 9 × 14 cm


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