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Acetyl-L-carnitine improves diabetic neuropathy
The researchers evaluated 1,257 patients who had participated in one of two 52 week randomized trials of 500 or 1000 milligrams acetyl-L-carnitine, or a placebo three times per day. Subjects were evaluated for nerve conduction velocity and vibratory threshold before treatment and at the end of the study. Two hundred forty-five patients underwent nerve biopsies at the study’s onset and conclusion. Neuropathy symptoms were assessed at both time points.
Comparison of biopsy results determined that treatment with acetyl-L-carnitine increased the number of nerve fibers and regenerating nerve fiber clusters. While nerve conduction velocity did not improve, vibration perception increased. Clinical symptoms also improved in groups treated with acetyl-L-carnitine compared to placebo. Participants who received 1,000 milligrams acetyl-L-carnitine thrice daily demonstrated significant improvement in pain at the study’s midpoint and conclusion. Those who experienced the greatest pain relief were those who had the shortest duration of diabetes, showing that neuropathy needs to be treated early in the course of the disease. The authors of the report suggest longer trials initiated at an earlier stage of diabetic neuropathy.
One predominant theory of neuropathy in diabetic rats involves abnormalities in what is called the polyol pathway. Polyol stands for polyhydroxy alcohols. While most of the cells in the body require insulin in order to transport glucose across the cell membrane, nerve cells are different. Membranes of nerve cells and their capillaries have insulin-independent glucose transport; that is, insulin is not required for glucose to pass into the cells. Since there is an excess of glucose in the bloodstream of diabetics, this glucose can easily be absorbed into nerve cells. In nerve cells, this glucose gets converted to sorbitol (a sugar alcohol) by an enzyme known as aldose reductase. The sorbitol cannot easily get out of the cell and consequently it accumulates, causing free-radical damage to nerves and blood vessels. This causes a decrease in an intracellular nutrient known as myo-inositol that is partly responsible for nerve conduction.
There is also an increase in free radicals such as peroxides and decreased nitric oxide production (a blood vessel-relaxing messenger), which, of course, leads to increased oxidative stress and the need for increased antioxidants. The amino acid taurine is also depleted (Hansen 2000). Terada et al. (1998) suggest that there is a close relationship between increased polyol pathway activity and carnitine deficiency in the development of diabetic neuropathy and that an aldose reductase inhibitor, a carnitine analog, and alpha-lipoic acid have therapeutic potential for the treatment of diabetic neuropathy (Terada et al. 1998).
Acetyl-L-carnitine arginate capsules
Acetl-L-carnitine arginate is a patented form of carnitine that stimulates the growth of neurites in the brain. Studies show that acetyl-L-carnitine arginate stimulates the growth of new neurites by 19.5 percent, as much as nerve growth factor itself. Acetyl-L-carnitine arginate acts together with acetyl-L-carnitine to increase neurite growth.
Taurine is a conditionally essential amino acid produced from cysteine by the body and found abundantly in the body, particularly throughout the excitable tissues of the central nervous system, where it is thought to have a regulating influence. However, taurine is deficient in many diets and may be considered conditionally essential under certain circumstances.
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