For CATARACTS, it has been found that the amino acid cysteine, in the N-Acetyl Cysteine form, is effective for cataract prevention and treatment. Cysteine is a key building block for the powerful antioxidant glutathione, which is the first line of defense to protect the lens from free radical accumulation and damage to its lipids and proteins.

Oxidative stress is an imbalance between excessive formation of damaging reactive oxygen derivatives versus their insufficient removal or neutralization. If antioxidant defenses become depleted in the lens, then there is a build-up of excessive oxidants and cataracts can form. If glutathione levels drop, oxidative stress increases, and the lens can be damaged and become less transparent. Glutathione is a potent antioxidant that occurs in particularly high amounts in the lens and is a key protector against cataract development. Glutathione is also essential for enzyme systems within the lens that help prevent cataracts.

Polyunsaturated fatty acids in the lens are also vulnerable to free radical attacks. If they become oxidized by free radicals and suffer lipid peroxidation, then a chain reaction results in by-products which injure the lens. Excess calcium in the lens is another factor that causes lens proteins to precipitate and break down, leading to cataract.

Research shows that N-acetyl Cysteine, known as NAC, works in several ways to prevent cataract formation, halt its progression, and sometimes reverse cataracts. NAC prevents oxidative stress by boosting glutathione in the lens. It restores normal enzyme functions. NAC supplies cysteine for making glutathione, helping the lens convert cystine into valuable cysteine, and it enhances the production of glutathione from its precursors. NAC can decrease lipid peroxidation in the lens by providing good amounts of glutathione, which allows helpful enzymes to remove hurtful hydroperoxides.

A 2017 study sought to evaluate the efficacy of NAC eye drops in the prevention and reversal of cataracts. Researchers looked at oxidative stress parameters such as glutathione, lipid peroxidation, and calcium levels. The results were exciting and show that NAC has the potential to significantly improve vision and decrease the burden of cataract-related loss of function. Prevention and reversal of early-stage cataract formation could have a global impact especially in high-risk populations.¹˒²

A fascinating study in 2009 investigated the role of oxidative stress in premature aging and the development of age-related pathologies including cataracts. Chronic oxidative stress and resulting accelerated aging was induced by disruption of the body’s circadian clock which has significant impact on shift workers. Researchers were able to overcome these deficits by NAC supplementation over the lifespan of the subjects. This reduced the development of cataracts.³

In clinical trials, treatment with NAC prevented calcium build-up in the lens, and thus prevented disorganizing of lens proteins and loss of transparency. When the lens calcium levels stay close to normal, the lens keeps its transparency.⁴

We choose a high potency NAC for our patients to reduce the risk of developing cataracts because it helps to restore the lens’s natural defense against oxidative stress.

Recommendation: N-acetyl cysteine (NAC), 600 mg 2 to 4 times daily, or 1,200 mg per dose once or twice per day, or as directed by your healthcare provider.

References

  1. Maddirala, Yasaswi, et al. “Prevention and reversal of selenite-induced cataracts by N-acetylcysteine amide in Wistar rats.” BMC Ophthalmology 17.1 (2017): 54.
  2. Pascolini D, Mariotti SP. Global estimates of visual impairment: 2010. Br J Ophthalmol. 2012;96(5):614–618.
  3. Kondratov, Roman V., et al. “Antioxidant N-acetyl-L-cysteine ameliorates symptoms of premature aging associated with the deficiency of the circadian protein BMAL1.” Aging (Albany NY) 1.12 (2009): 979.
  4. Aydin B, Yagci R, Yilmaz FM, Erdurmus M, Karadag R, Keskin U, et al. Prevention of selenite-induced cataractogenesis by N-acetylcysteine. Curr Eye Res. 2009;34(3):196–201.
  5. Taylor A, Jacques PF, Epstein EM. Relations among aging, antioxidant status, and cataract. Am J Clin Nutr. 1995;62(6 Suppl):1439S–1447S.
  6. Spector A. Oxidative stress-induced cataract: mechanism of action. FASEB J. 1995;9(12):1173–1182.
  7. Lou MF. Redox regulation in the lens. Prog Retin Eye Res. 2003;22(5):657–682.
  8. Age-Related Eye Disease Study Research Group. Risk factors associated with age-related nuclear and cortical cataract: a case-control study in the age-related eye disease study, AREDS Report No. 5. Ophthalmology. 2001;108(8):1400–1408.
  9. Taylor A, Davies KJ. Protein oxidation and loss of protease activity may lead to cataract formation in the aged lens. Free Radic Biol Med. 1987;3(6):371–377.
  10. Penugonda S, Mare S, Goldstein G, Banks WA, Ercal N. Effects of N-acetylcysteine amide (NACA), a novel thiol antioxidant against glutamate-induced cytotoxicity in neuronal cell line PC12. Brain Res. 2005;1056(2):132–138.