For CATARACTS, research confirms that acetyl-L-carnitine (ALC) maintains a healthy balance of minerals including calcium in the lens, protects against disarray of lens fibers via its antioxidant actions, and lessens the impact of high blood sugar on the eye. Acetyl-L-carnitine is of significant value for reducing cataract risk or progression and protecting the lens and ocular tissues from free radical injury. It is especially helpful for individuals with high blood sugar levels.
Current research is clarifying the exact mechanisms of action of acetyl-L-carnitine and indicates that acetyl-L-carnitine’s efficacy may be related to both neural transmission activity and its ability to enhance cellular energy metabolism.¹
In addition, ALC is a powerful antioxidant that protects the lens from free radical damage, stabilizes cell membranes, and boosts energy production within cells. Oxygen free radicals are byproducts of the body’s metabolism and energy production. Most of these oxygen radicals are safely contained within the membrane folds of mitochondria, but about 2 percent get free, generating toxins that endanger the entire cell. Antioxidants “loan out” extra particles or molecules to stabilize oxygen free radicals. Recent research shows that acetyl L-carnitine can protect the eye and lens from peroxidation while at the same time enhancing the activity of other antioxidants.
Due to the unique structural and physiological properties of the eye lens, it is an organ that is vulnerable to oxidative stress and related complications. Age-related deterioration of the function of intraocular tissues is the prime cause of ocular pathologies. There is growing interest in the role of ALC for blocking or slowing the progress of this deterioration.
Preliminary research on human ocular tissue indicates that carnitine is differentially distributed within the eye with the highest concentrations reported in the iris, ciliary body, and the choroid-retina. ALC is involved in numerous physiological reactions, including sugar aerobic metabolism, oxidative phosphorylation, fatty acid oxidation and osmosis.
Bringing benefits for the whole eye, in patients with age-related macular degeneration (AMD), acetyl-L-carnitine improved four parameters of visual function, including visual field mean defect, visual acuity, foveal sensitivity, and ocular fundus alterations. ALC has also demonstrated antioxidant properties in models of oxidative damage showing its potential for use in additional age-related ocular pathologies, such as cataracts, glaucoma, and dry eye syndrome.²
One study proposed that ALC plays a key role in maintaining homeostasis in the lens: keeping a normal intercellular communication and stable calcium levels. Calcium homeostasis is achieved by a balance between inward leak and an outward ‘push’ of calcium by a plasma membrane pump. Noting this, researchers were able to show that ALC helped prevent a breakdown in homeostatic lens regulation, leading to increased lenticular calcium levels.³
Acetyl-L-carnitine can protect the lens from sugar-related damage. The eyes of people with diabetes or high blood sugar are especially at risk for ALC depletion. An excessive amount of glucose in the serum, which worsens with age, increases the formation of damaging protein-sugar complexes known as Advanced Glycosylation End-products (AGEs). These AGEs are seen as a benchmark of aging: they can accumulate in the lens of the eye and trigger or worsen cataracts. Studies looking at the effects of ALC immersed lens tissues in a glucose solution with ALC or with plain L-carnitine for about two weeks. In that short time, ALC reduced glycation by a striking 42%. ALC also helped the formation of antibodies to AGEs, so the body could clear the AGEs more efficiently. It was shown that ALC can protect lens tissue from glycation-mediated protein damage. Thus, ALC is potentially an effective solution to reduce the risk of cataract development and progression in people with high blood sugar, and to prevent the resulting blindness.⁴
Clinical studies have found that ALC can help keep glucose levels stable and in a normal range, perhaps by encouraging the body to use glucose and remove it from the blood stream, and by enhancing the conversion of glucose into its storage form, glycogen.
A recent study investigated acetyl-L-carnitine’s protective role regarding oxidative stress in the nervous system. The researchers found that pretreatment with acetyl-L-carnitine reduced protein oxidation and lipid peroxidation, while also enhancing the activity of other antioxidants at the same time.⁵
Acetyl-L-carnitine (ALC) is made up of acetic acid bound to the amino acid carnitine which carries long-chain fatty acids into the energy-producing mitochondria. Acetyl-L-carnitine can mimic the major neurotransmitter acetylcholine which declines with age and especially with neurological disorders. As well as protecting the eye — which derives from brain tissue when we are embryos — ALC can increase the number of nerve cells in growing brains, boost cellular ATP production, and prolong the healthy lifespan of neurons by boosting the brain’s inherent growth factors that usually decline with age.
In our clinic, patients with early cataracts or who wish to protect their lens use acetyl-L-carnitine to support the overall health of their eyes, helping to preserve their vision for as long as possible and to slow down progression of cataracts. Diabetic people report stabilizing of cataracts in their regular eye exams. With its antioxidant properties, patients with cataracts or other age-related lens-degeneration problems appreciate ALC as a proactive step to protect their eyesight.
Recommendation: Acetyl-L-carnitine 1,000 mg to 1,500 mg per day, fine to be taken with food, or as directed by your health care provider.
References
- Abdul HM, Calabrese V, et al. Acetyl-L-carnitine-induced up-regulation of heat shock proteins protects cortical neurons against amyloid-beta peptide 1-42-mediated oxidative stress and neurotoxicity: implications for Alzheimer’s disease. J Neurosci Res. 2006 Aug 1;84(2):398–408.
- Pescosolido, Nicola, Barbara Imperatrice, and Panagiotis Karavitis. “The aging eye and the role of L-carnitine and its derivatives.” Drugs in R & D 9.1 (2008): 3–14.
- Muralidharan AR, Leema G, et al. “Deciphering the potential efficacy of acetyl-L-carnitine (ALCAR) in maintaining connexin-mediated lenticular homeostasis.” Molecular Vision 18 (2012): 2076.
- Swamy-Mruthinti S, Carter AL. Acetyl-L-carnitine decreases glycation of lens proteins: in vitro studies. Exp Eye Res 1999 Jul;69(1):109–15.
- Elanchezhian R, Sakthivel M, Geraldine P, Thomas PA. The effect of acetyl-L-carnitine on lenticular calpain activity in prevention of selenite-induced cataractogenesis. Exp Eye Res. 2009;88(5):938–944.
- Geraldine P, Sneha BB, Elanchezhian R, et al. Prevention of selenite-induced cataractogenesis by acetyl-L-carnitine: an experimental study. Exp Eye Res. 2006;83(6):1340–1349.
- Elanchezhian R, Ramesh E, Sakthivel M, et al. Acetyl-L-carnitine prevents selenite-induced cataractogenesis in an experimental animal model. Curr Eye Res. 2007;32(11):961–971.