Acetyl-L-carnitine improves diabetic neuropathy
Diabetic polyneuropathy is a painful complication of diabetes that results from damage to the nerves by high levels of blood glucose. The condition can lead to cardiac arrhythmias, foot ulcers and even amputations. In the January 2005 issue of the American Diabetes Association journal Diabetes Care (http://care.diabetesjournals.org), it was revealed that acetyl-L-carnitine not only improves the symptoms of diabetic neuropathy, but also helps regenerate nerve fibers and vibration perception.

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.

Neuropathy
The most important factor that contributes to the development of diabetic neuropathy is the blood sugar level. Tightly controlled blood sugar and insulin levels will often prevent the onset of diabetic polyneuropathy. Elevated blood sugar levels will of course add to free-radical generation and the production of what are termed glycosylated proteins that cause accelerated aging. Diabetic neuropathy is most frequently seen in developed countries. Neuropathy causes more hospitalizations than any other type of diabetic complication, and it is estimated that 50-70% of all amputations in the United States, not related to trauma, are due to diabetic neuropathy. Inadequate glycemic control is by far the most significant risk factor for developing diabetic neuropathy, the risk decreasing steadily and predictably as control becomes tighter, but other risk factors have also been identified including:

• Advanced age and increased duration of diabetes
• Greater height, due to greater neuronal length as well as greater pressures in the lower extremities
• High diastolic blood pressure
• Reduced HDL-cholesterol and elevated triglycerides, characteristic of diabetic hyperlipidemia, carry elevated risks of 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).

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The Life Extension Foundation would like to take this opportunity to wish everyone a safe and healthy new year.

For longer life,

Dayna Dye
Editor, Life Extension Update
ddye@lifeextension.com
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