Role of Acetyl L Carnitine for Neuropathy Sufferers

(Newswire.net — November 16, 2019) Darien, CT –Acetyl-L-carnitine (ALC) is produced by the human brain, liver, and kidney. Although similar in molecular structure it shouldn’t be confused with acetylcholine This molecule is an acetyl-group donor and plays an important role in mitochondrial energy homeostasis and detoxification. ALC has been shown to strengthen the actions of Nerve Growth Factor, a neuropeptide primarily involved in the regulation of growth, maintenance, proliferation, and survival of certain target neurons that promotes peripheral nerve regeneration. ALC demonstrated a neuroprotective function in animal models of diabetic neuropathy. ALC has antiapoptotic effects in that it helps reduce cell death in peripheral mononeuropathy trials. ALC has demonstrated antioxidant activity and ramps up acetylcholine production.

So it hard to understand how learned medical professionals still say that nothing can be done to treat peripheral neuropathy. Lyrica and Cymbalta are the typical first line of treatment but at what cost of human suffering. Does a diabetic really need to deal with weight gain, blurry vision, and balance problems? Common sense dictates that a nutritional approach to treating the symptoms of peripheral neuropathy will allow the body to help itself. Whereas the Big Pharma approach is palliative at best. Do patients who are immunocompromised need more medication then they already have to take? More medicine does not always equate to more health. They contribute to a healthy bottom line for the drug companies.

ALC has gained a growing clinical interest in treating different forms of chronic-pain neuropathy, not only for treatment but also for pain prevention. Less pain can quickly add up to more activity and better balance. Studies done show dramatic improvements over a 3 month period using ALC. Patients were given 50 mg intramuscular injections of ALC for 10 days followed by 110 days of oral supplementation of 500mg ALC. These symptom improvements were detected after the first 10 days of intramuscular treatment and persisted throughout the 4-month treatment period. All sensory neurophysiological measures significantly improved including the Neuropathic Pain Symptom Inventory. The fact that the improvements lasted makes for an even more compelling argument that ALC supplementation should be a first-round defense against peripheral neuropathy.

A lack of carnitine reduces energy synthesis by impairing fatty acid degradation in diabetics. The studies indicate ALC operates via several mechanisms, inducing regeneration of injured nerve fibers, reducing oxidative stress, promoting DNA synthesis in mitochondria, and increasing Nerve Growth Factor concentrations in neurons, thus promoting nerve plasticity. I hope I made a strong argument for including Acetyl-L-carnitine into a treatment plan for peripheral neuropathy sufferers.