Patients’ Own N-Acetyl-Cysteine
N-Acetyl-Cysteine (known as NAC) is absolutely essential for creating a key antioxidant, Glutathione, and for keeping Vitamins C and E in their active forms.
Many leading Chronic Fatigue Syndrome and Fibromyalgia researchers and doctors believe that Glutathione deficiency may be one of the major root causes of CFS and Fibromyalgia making the addition of a N-Acetyl-Cysteine supplement for these diseases of paramount importance.
When combined with L-Glutamine, N-Acetyl-Cysteine can help to significantly increase glutathione levels, making this combination of supplements ideal for Chronic Fatigue Syndrome and Fibromyalgia patients. NAC is also a popular choice for ME/CFS patients as it has the ability to increase time to muscle fatigue as well as reduce post-exertional malaise.
The Chronic Fatigue Syndrome specialists Dr Teitelbaum and Dr Downing-Orr recommend taking an NAC supplement for CFS/ME.
The science behind treating CFS and Fibro with N-Acetyl-Cysteine
NAC increases glutathione and reduces CFS symptoms
A recent study by Cornell University and the Mount Sinai Medical Center in New York assessed whether supplementing Chronic Fatigue Syndrome patients with N-Acetyl-Cysteine (1,800 mg) daily for 4 weeks would increase cortical glutathione compared to baseline. The authors previously reported a 36% deficit of glutathione in patients with Chronic Fatigue Syndrome compared to healthy controls. In this study, cortical glutathione levels were 15% lower in Chronic Fatigue Syndrome patients than in healthy controls. Following 4 weeks of daily NAC supplementation, cortical glutathione levels rose significantly in Chronic Fatigue Syndrome patients to match the healthy controls. Finally, N-Acetyl-Cysteine supplementation markedly improved symptoms in Chronic Fatigue Syndrome patients.
NAC reduces inflammation and leads to clinical improvement or remission in CFS and Fibro
A 2008 study published in the peer-reviewed Neuroendocrinology Letters analysed inflammatory markers and Fibromyalgia and Chronic Fatigue Syndrome rating, before and after intake of natural anti-inflammatory and anti-oxidative substances (NAIOSs), including L-glutamine, N-acetyl-cysteine and zinc, in conjunction with a leaky gut diet during 10-14 months. They found that intake of those NAIOSs significantly reduced inflammation resulting from leaky gut. Up to 24 of the 41 patients showed a significant clinical improvement or remission 10-14 months after intake of NAIOSs.
N-Acetyl-Cysteine improves athletic performance and could reduce post-exertional malaise
A 1994 placebo controlled study assessed the effect of N-Acetyl-Cysteine on healthy volunteers undergoing an extended fatiguing bout of electrical stimulation of the ankle dorsiflexors. They found that NAC significantly increased force output of approximately 15% after 3 minutes of repetitive contractions which persisted throughout the 30 minute protocol. The authors concluded that N-Acetyl-Cysteine resulted in improved performance suggestive of oxidative stress having a causal role in the fatigue process. As post-exertional malaise is one of the key symptoms found in CFS, this study suggests N-Acetyl-Cysteine supplementation may attenuate this.
Medved et al. (2004) investigated the effects of N-Acetyl-Cysteine on muscle cysteine, cystine, and glutathione and on time to fatigue during prolonged, submaximal exercise in endurance athletes. The study found that N-Acetyl-Cysteine improved performance in well-trained individuals, with enhanced muscle cysteine and glutathione availability a likely mechanism.
N-Acetyl-Cysteine delays fatigue and supports glutathione homeostasis
After observing N-Acetyl-Cysteine inhibiting fatigue during other tasks, Matuszczak et al. (2005) tested its effects during a handgrip exercise. They found that during repetitive submaximal efforts, NAC delayed fatigue (130% baseline) and inhibited glutathione oxidation. They go on to conclude that the data indicates that N-Acetyl-Cysteine supports glutathione homeostasis in exercising humans and may delay muscle fatigue during repetitive handgrip exercise. The findings support oxidative stress as a causal factor in human muscle fatigue and argue for larger translational studies to define NAC effects on human performance.
Intense exercise leads to post-exercise lymphocytopenia and immunosuppression, possibly by triggering lymphocyte apoptosis. Quadrilatero et al. (2004) tested the role of oxidative stress on exercise-induced lymphocyte apoptosis by administering N-Acetyl-Cysteine and measured apoptosis in intestinal lymphocytes (IL) from exhaustively exercised animals. N-Acetyl-Cysteine injection in mice maintained intracellular glutathione levels, prevented phosphatidylserine externalization, mitochondrial membrane depolarization, and loss of IL immediately and 24 h after exercise. These data suggest that lymphocyte apoptosis precedes post-exercise lymphocytopenia and may be due to oxidative stress.