Acetyl-L-Carnitine:
The Lesser Known Cousin
Acetyl-L-carnitine (ALC) is the powerful but lesser known cousin of L-carnitine (LC), a natural cellular amino acid synthesized by the body. LC is required for the conversion of fat, one of three types of cellular fuel, to chemical energy. LC functions as a vehicle to transport subunits of fat, fatty acids, into the specialized cellular structures, the mitochondria, for conversion to a chemical form of energy. A deficiency in LC, common in vegetarians (vegans), aging, and those who use certain prescribed drugs, results in a tired physical and mental state.
How is it different?
Structurally, the difference between the ALC and LC is that ALC is an LC molecule that also contains an attached acetic acid group. This structural difference is small, but it produces a considerable difference in the biochemical properties of the molecule and, consequently, in its effects on metabolism.ALC can substitute for LC in fat metabolism; however, as described below, recent studies have resulted in identification of several biological characteristics that are unique to ALC.
The acetyl group on ALC can be donated to a specific acceptor molecule, choline, to form the neurotransmitter acetylcholine, which helps restore nerve function. . This activity is believed to be at least partly responsible for the improved mental function that results from ALC supplementation in patients with cognitive disorders, including Alzheimer's disease, Parkinson's disease, Chronic Fatigue Syndrome, and other disorders of the nervous system. Additional studies supporting a neuroprotective role for ALC are those demonstrating an improvement in symptoms of peripheral nerve damage common to diabetic patients.
The acetyl group can also be utilized for the production of energy in the Krebs cycle. This donation increases the availability of an important cofactor (CoA) required for the conversion of carbohydrates to energy. Sufficient amounts of carnitine, derived from ALC, are necessary to transport, toxic, non-metabolizable, short-chain fatty acids, out of the mitochondria, and thus to free up the cofactor, CoA. A deficiency in ALC promotes a corresponding decrease in this cofactor, and consequently impaired energy production from both fats and carbohydrates, thus affecting energy levels in all cells of the body.
ALC, but not LC, protects the mitochondria. A recent finding demonstrated that a deficiency in ALC affects the structure and energy-producing capacity of the mitochondria. The mitochondria are responsible for producing virtually all the energy required by the cell. Therefore any subtle change in their structure can have a tremendous effect on the cell's energy reserves. ALC has been demonstrated to revitalize mitochondria by restoring levels of a key mitochondrial component, a phospholipid known as cardiolipin, which is susceptible to age-associated reduction in levels. Cardiolipin can be envisioned as the glue that secures and organizes, or better yet, orchestrates, the energy-producing machinery of the mitochondria.
The acetic acid group on ALC allows it to enter the mitochondria more readily than LC and consequently more rapidly perform its beneficial effects An additional enzyme must act on LC before it can enter the mitochondria.
How can it affect physical and mental state?
These characteristics raise some questions. First, why would a deficiency in a fat-burning chemical affect our physical as well as mental state? The two systems of the body requiring the most energy are the muscular and nervous systems. It has been estimated that for normal function and health, the brain requires every day the amount of energy present in a quarter pound of sugar. A lack of energy in brain and muscle tissues will be exhibited as impaired physical and mental activity. If the deficiency persists for a sufficient period of time, it can lead to disease.
Although the brain normally does not use fat for energy, (it prefers glucose from carbohydrates), except under conditions of fasting or starvation, it nevertheless can be adversely affected by a deficiency in ALC, because of all 5 of the numbered items described above.
Where does it come from?
Although the cells of the body do produce this important chemical, it is widely believed that the major source of the compound is derived from the diet. Meat, lamb especially, is the major dietary source of ALC, and the basis for why vegans can be deficient in ALC, since plants contain insignificant amounts.
Studies with animals have recently demonstrated a gradual decline in plasma levels of ALC with age, which correlates with age-associated energy decline. Additional studies with humans have indicated a steady decline in ALC, beginning with the fourth decade of life. This too is correlated with energy decline. This decline in plasma ALC may be a reflection of inefficient absorption from the diet and/or reduced synthesis. Both are believed to be responsible for the lower levels of ALC as we age. In view of the age-associated decline in the ability of the body to synthesize and absorb ALC, use of dietary supplements to ensure adequate ALC is a growing trend in healthy aging.
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Originally Posted by Shredder
